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Bioengineering, Science, Stanford News

Stanford bioengineer Karl Deisseroth wins 2016 Breakthrough Prize in Life Sciences

Stanford bioengineer Karl Deisseroth wins 2016 Breakthrough Prize in Life Sciences

Karl D at Clark - big

Updated 11-9-15: Lloyd Minor, MD, dean of Stanford’s medical school, provided comment last evening on Karl Deisseroth’s win. “The human brain has been called the most complicated object in the universe, but that hasn’t daunted Karl’s quest to understand it,” said Lloyd Minor, MD, dean of the School of Medicine. “If anything it seems the challenge has inspired him to develop techniques to see inside this most important of black boxes. This passion to understand the mind, combined with his intelligence and creativity, led to his pioneering role in creating optogenetics.”


11-8-15: We just learned that Stanford Medicine’s Karl Deisseroth, MD, PhD, has received the $3 million 2016 Breakthrough Prize in Life Sciences, an award designed to “honor transformative advances toward understanding living systems and extending human life.” Deisseroth was given the prize for his work in optogenetics, a technique using light to control the activity of the brain.

The award was presented tonight at a private black-tie, red-carpet ceremony in nearby Mountain View, Calif. “The suffering of the mentally ill and the mysteries of the brain are so deep that, to make progress, we need to take big risks and even blind leaps,” Deisseroth said after accepting his award from actress Kate Hudson. “The members of my lab have taken a leap: borrowing genes from microbes to control the brain.”

Congratulations, Dr. Deisseroth!

Previously: Inside the brain of optogenetics pioneer Karl Deisseroth, Stanford’s Karl Deisseroth awarded prestigious Albany Prize, Breaking through scientific barriers: Stanford hosts 2015 Breakthrough Prize winners, Lightning strikes twice: Optogenetics pioneer Karl Deisseroth’s newest technique renders tissues transparent, yet structurally intact and An in-depth look at the career of Stanford’s Karl Deisseroth, “a major name in science”
Related: Head lights and Optogenetics earns Stanford professor Karl Deisseroth the Keio prize in medicine
Photo by Steve Fisch

Ethics, In the News, NIH, Research, Science, Science Policy, Stanford News, Stem Cells

Stanford researchers protest NIH funding restrictions

penSeven Stanford researchers, including Irving Weissman, MD, who directs Stanford’s Institute for Stem Cell Biology and Regenerative Medicine, and David Magnus, PhD, director of Stanford’s Center for Biomedical Ethics, have joined with four other prominent scientists to urge the lifting of a recent and unexpected ban on funding by the National Institutes of Health for research that involves placing human stem cells into early-stage, non-human embryos. Their comments will be published tomorrow in a letter to Science.

As I describe in our release:

At issue is the growing field of research that seeks to understand how human pluripotent stem cells, which can become any cell type, may integrate and contribute to the development of a nonhuman animal, such as a laboratory mouse. Pluripotent stem cells can be isolated from human embryos or created in a lab from adult human cells, in which case they’re known as induced pluripotent stem cells. Once obtained, these versatile cells can be injected into an early-stage animal embryo and studied as the embryo develops into an adult animal.

Tracking where these cells go and how they function in the growing embryo and the adult animal can help researchers understand early stages of human development that can’t be studied any other way. (Although researchers can and do study the development of fertilized human eggs, the study period is restricted to only a few days after fertilization for ethical reasons.)

In addition to investigating human development, the research is expected to lead to significant advances in disease modeling, drug testing and even transplantation. As cardiologist and one of the co-senior authors of the letter, Sean Wu, MD, PhD, explains:

By eliminating federal funding for all aspects of this research, the NIH casts a shadow of negativity toward all experiments involving chimera studies regardless of whether human cells are involved. The current NIH restriction serves as a significant impediment to major scientific progress in the fields of stem cell and developmental biology and regenerative medicine and should be lifted as soon as possible.

Science recently published a great background article describing the ban, and its effect on researchers like Sean Wu and geneticist and stem cell researcher Hiromitsu Nakauchi, MD, PhD, who also signed the letter. Other signees include Joseph Wu, MD, PhD, professor of medicine and director of Stanford Cardiovascular Institute; Christopher Scott, PhD, director of Stanford’s Program on Stem Cells and Society; and Vittorio Sebastiano, PhD, assistant professor of obstetrics and gynecology and director of Stanford’s Human Pluripotent Stem Cells Core Facility.

Previously: NIH intramural human embryonic stem cell research haltedSupreme Court decision on human embryonic stem cell case ends research uncertaintyUsing organic chemistry to decipher embryogenesis and The best toxicology lab: a mouse with a human liver
Photo by Fimb

In the News, Research, Science, Stanford News, Videos

Brain cell spheres offer new tool to study disease

Brain cell spheres offer new tool to study disease

Earlier this year my colleague reported on some pretty neat work from the labs of psychiatrist Sergiu Pasca, MD, and neurobiologist Ben Barres, MD, PhD. Researchers there figured out how to create spheres of neuronal cells resembling the cerebral cortex, making functional human brain tissue available for the first time to study neuropsychiatric diseases such as autism and schizophrenia. In an article today the Associated Press highlighted this work, with Malcolm Ritter writing:

It’s part of a larger movement over the past few years to create “organoids,” miniature versions of the body’s organs or key parts of organs. Goals include studying disease, testing possible treatments and perhaps supplying replacements for transplants. Scientists have made organoids representing the intestine, prostate, kidney, thyroid, retina and liver.

This overall organoid approach “is a major change in the paradigm in terms of doing research with human tissues rather than animal tissues that are substitutes. … It’s truly spectacular,” says Arnold Kriegstein, who studies the brain at the University of California, San Francisco.

Pasca talks more about the work in the AP video above; Stanford ethicist Hank GreelyJD, also weighs in.

Previously: Brain cell spheres in a lab dish mimic human cortex, Stanford study says

Chronic Disease, Dermatology, Immunology, Pain, Research, Science, Stanford News

Stanford researchers investigate source of scarring

Stanford researchers investigate source of scarring

2570500512_22e7fdcd48_zIf you’ve ever had a piercing that you’ve let grow closed, you’ll know that the healing process isn’t perfect. There’s almost always a little dimple to remind you of that perhaps questionable choice you may (or may not) have made during early adulthood.

Now former Stanford pediatric dermatologist Thomas Leung, MD, PhD, and developmental biologist Seung Kim, MD, PhD, have published some interesting research in Genes and Development regarding the healing and scarring process. Their findings may one day lead to advances in regenerative medicine.

As Leung, who is now an assistant professor at the University of Pennsylvania’s Perelman School of Medicine explained in an email to me:

One of the great mysteries in biology is how salamanders and worms regenerate lost body parts following trauma. In contrast to wound healing, tissue regeneration restores tissue to their original architecture and function, without a scar.  Although less dramatic, a few examples of mammalian tissue regeneration exist, including liver and digit tip regeneration.  These examples suggest that the underlying mechanisms driving tissue regeneration may still be intact in humans and perhaps we may use them for regenerative medicine.

The researchers studied how the ears of mice heal from a hole punched through the thin tissue (much like  ear piercing in humans). In many strains of mice, the holes partially fill but remain visible. In a few others, the holes heal with little perceptible scarring. Leung and Kim found that the strains of mice that heal well lack production of a protein that normally recruits white blood cells to the injury; blocking the ability of the protein, called Sdf1, to signal to the white blood cells resulted in enhanced tissue regeneration and less scarring in mice that would normally have been unable to close the hole.

Because the drug used to block Sdf1 signalling is already used clinically in humans for another purpose, Leung is hopeful that it can quickly be tested in humans struggling to heal  chronic or slow-healing wounds. He is currently designing a clinical trial to test the drug, called AMD3100.

The implications of improved wound healing with less scarring stand to benefit many more people than just those wishing away the physical evidence of a hasty cosmetic decision. Tens of millions of surgical incisions are made every year, and not all heal well. Scar tissue is less flexible than normal skin and can significantly interfere with function. In addition, people with certain medical conditions such as diabetes or poor circulation can face ongoing disability or amputation when wounds don’t heal. But the group that inspired Leung to conduct the research is especially poignant.

As Leung explained:

 The inspiration for this work was driven by our clinical experience.  At Stanford, I co-directed the Epidermolysis Bullosa (EB) clinic.  EB is a rare genetic skin disease (about eight babies are affected per million births in this country), where affected patients lack a protein that binds the skin together, resulting in fragile skin. Incidental trauma like rubbing of skin against clothing tears the skin and leaves a scar.  This endless cycle of trauma and scarring and fibrosis inevitably leads to decreased joint function and complete loss of hand function by teenage years.

My recent article for Stanford Medicine magazine and the accompanying video shed light on this devastating condition. Even a small improvement in the pain these children suffer would be a tremendous step forward. And, although Kim emphasizes that greater feats in regenerative medicine (limb regeneration, anyone?) are still years of research away, this finding shows that we’re making progress.

Previously: Limb regeneration mysteries revealed in Stanford studyTo boldly go into a scar-free future: Stanford researchers tackle wound healing and Life with epidermolysis bullosa: “Pain is my reality, pain is my normal”
Photo by The Guy with the Yellow Bike

Events, Neuroscience, Science, Stanford News, Stem Cells

Stanford Neuroscience Institute’s annual symposium captured on Storify

Stanford Neuroscience Institute's annual symposium captured on Storify

IMG_0246When I talked to William Newsome, MD, PhD, director of the Stanford Neurosciences Institute, about its annual symposium last week, he told me one of the pleasures of directing the institute is getting to pick speakers whose science he really likes.

We captured tweets, images and videos from those speakers on our Storify page, and they make it clear that Newsome has very diverse tastes. Topics ranged from aging and mental health policy to virtual reality for mice.

From Stanford, geneticist Anne Brunet, PhD, discussed her work on aging, particularly how stem cells in the brain change with age. Engineer Krishna Shenoy, PhD, described how his lab was reading signals from the brains of paralyzed people and using those to drive computer cursors or prosthetic limbs. Others discussed machine learning, new technologies for imaging the brain, the genetics of mental health disorders, and insights into how smells illicit behaviors in flies.

It’s worth a look at the Storify page to get a sense of the breadth of work encompassed under the banner of neuroscience.

Previously: “Are we there yet?” Exploring the promise, and the hype, of longevity researchMy funny Valentine – or, how a tiny fish will change the world of aging research and Stanford researchers provide insights into how human neurons control muscle movement
Photo of Krishna Shenoy by Matt Beardsley

Research, Science, Stanford News

How Bio-X is fueling the #NextGreatDiscovery

How Bio-X is fueling the #NextGreatDiscovery


The videos, images and stories of #NextGreatDiscovery share two things in common: 1) They reveal the lives and motivations of amazing scientists carrying out basic research, and 2) All the scientists are affiliated with Stanford’s pioneering interdisciplinary institute Bio-X.

Almost 15 years ago, Stanford Bio-X was founded to support biomedical research with an interdisciplinary blend of X, which is to say all the fields across the street from Stanford University School of Medicine – engineering, chemistry, physics, biology, math and statistics as well as the professional schools of business, law and education. Bio-X later came to be housed in the Clark Center, located with crosswalks linking those schools and departments.

Two of the scientists featured in #NextGreatDiscovery recently won Nobel prizes in chemistry, and both discuss the importance of Stanford’s collaborative spirit in their research.

From Michael Levitt, PhD:

The university has the medical school and other departments very close to each other. This means that you can mix together all the sciences whether it is engineering and medicine, mathematics and medicine, statistics and medicine. All of these things are really close together so people are able to interact, groups are able to mix. I think it really is a remarkable environment.

From W.E. Moerner, PhD:

One aspect of research today is that our science has become more and more multidisciplinary. Exciting science occurs at the boundaries between conventional disciplines. Here at Stanford we have a spectacular environment for multidisciplinary work. That’s because in a very close proximity we have all of the humanities and sciences departments, the medical school departments and the engineering departments all close together, essentially across the street from one another right here close to my office.

In the series, scientists discuss the importance of funding for the basic sciences, as federal sources become more scarce. Both Levitt and Moerner have received Seed funding through Bio-X, which support new collaborations between scientists bridging disciplines. These grants are critical for promoting interdisciplinary research through funding at a time when federal resources for early stage collaborations are hard to come by, even for scientists whose research receives a nod from Stockholm.

Previously: #NextGreatDiscovery: Exploring the important work of basic scientists, The value of exploring jellyfish eyes: Scientist-penned book supports “curiosity-driven” research, Basic research underlies effort to thwart “greatest threat to face humanity”For third year in row, a Stanford faculty member wins the Nobel Prize in Chemistry and Stanford’s Michael Levitt wins 2013 Nobel Prize in Chemistry
Photo by Peter van Agtmael/Magnum Photos

Research, Science, Stanford News

#NextGreatDiscovery: Exploring the important work of basic scientists

#NextGreatDiscovery: Exploring the important work of basic scientists

Today, Stanford is launching a digital series, called #NextGreatDiscovery, to share the stories of some of the scientists doing groundbreaking basic research here. Through photographs and short videos, followers will get a taste of the work of these grad students, postdocs and professors – in fields ranging from computational structural biology to genetics to immunology – and hear about how important it is that this work continues. After all, basic science not only advances knowledge but has the potential to lead to great biomedical innovations.

Our series comes at a time where national funding for research is critically low, and some investigators are opting to leave academia in favor of industry positions that may not support fundamental research. What would we lose if more of these great minds chose different paths? What would go undiscovered? It’s something to keep in mind as you read this feature story, view our photos on Instagram, and follow #NextGreatDiscovery on Twitter.

Previously: The value of exploring jellyfish eyes: Scientist-penned book supports “curiosity-driven” research, Basic research underlies effort to thwart “greatest threat to face humanity” and Funding basic science leads to clinical discoveries, eventually
Photo by Peter van Agtmael/Magnum Photos

Cancer, Genetics, Research, Science, Stanford News

Combination therapy could fight pancreatic cancer, say Stanford researchers

Combination therapy could fight pancreatic cancer, say Stanford researchers

I’ve mentioned here before my personal connection to pancreatic cancer, which claimed the life of my grandmother. So I was excited to hear from Stanford cancer researcher Julien Sage, PhD, about some developments on the research front. Sage and postdoctoral scholar Pawal Mazur, PhD, collaborated with Alexander Herner, MD and Jens Svieke, MD, at the Technical University Munich to conduct the work, which was published today in Nature Medicine.

In our release on the study, which was done in animal models, Sage explained:

Pancreatic cancer is one of the most deadly of all human cancers, and its incidence is increasing. Nearly always the cause of the disease seems to be a mutation in a gene called KRAS, which makes a protein that is essential for many cellular functions. Although this protein, and others that work with it in the Ras pathway, would appear to be a perfect target for therapy, drugs that block their effect often have severe side effects that limit their effectiveness. So we decided to investigate drugs that affect the DNA rather than the proteins.

Mazur and Herner worked together to test whether drugs that affect the epigenetic status of a cancer cell (that is, the dynamic arrangement of chemical tags on the DNA and its associated proteins that control how and when genes are expressed) could rein in its growth without serious side effects. Many of these tags are what’s called acetyl groups, and they are added to protein complexes called histones that keep the DNA tightly wound in the cell’s nucleus. As I explained in our release:

They started by investigating the effect of a small molecule they called JQ1 on the growth of human pancreatic tumor cells in a laboratory dish. JQ1 inhibits a family of proteins responsible for sensing acetyl groups on histones. The researchers found that the cells treated with JQ1 grew more slowly and displayed fewer cancerous traits. The molecule was also able to significantly shrink established pancreatic tumors in mice with the disease. However, it did not significantly affect the animals’ overall likelihood of survival.

Mazur, who began the work in Siveke’s lab and continued it when he moved to Sage’s lab, next tested whether using JQ1 in combination with any other medications could be more effective:

“It happened that the drug that worked best was another epigenetic drug called vorinostat,” said Sage. “On its own, vorinostat didn’t work very well, but when combined with JQ1 it showed a very strong synergistic effect in both the laboratory mice with pancreatic cancer and in pancreatic cancer cells from people with the disease.”

Vorinostat works by inhibiting a family of proteins that remove the acetyl groups from histones. It has been approved by the FDA for use in people with recurrent or difficult-to-treat cutaneous T cell lymphoma. When human pancreatic cancer cells were treated simultaneously with JQ1 and vorinostat, the cells grew more slowly and were more likely to die.

Mice with established pancreatic cancers treated with both of the drugs showed a marked reduction in tumor size and a significant increase in overall survival time. Their tumors showed no signs of developing a resistance to the treatment, and the mice did not develop any noticeable side effects.

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Cardiovascular Medicine, Chronic Disease, Science, Stanford News, Stem Cells

Patching broken hearts: Stanford researchers regrow lost cells

Patching broken hearts: Stanford researchers regrow lost cells

Design 1_2Most heart attack survivors face a long and progressive course of heart failure due to damage done to the heart muscle. Now, in a study published in the journal Nature, researchers are reporting a method of delivering a missing protein to the lining of the damaged heart that regenerates heart muscle cells — cardiomyocytes — killed off during a heart attack.

The study, which was conducted in animal models, offers hope for future treatments in humans, according to the senior author of the study. “This finding opens the door to a completely revolutionary treatment,” Pilar Ruiz-Lozano, PhD, told me. “There is currently no effective [way] to reverse the scarring in the heart after heart attacks.”

The delivery system that researchers used in this study is a biodesigned tissue-like patch that gets stitched directly onto the damaged portion of the heart. The protein Fstl1 is mixed into the ingredients of the patch, and the patch, made of an acellular collagen, eventually gets absorbed into the heart leaving the protein behind. Our press release explains how the patch came to be:

The researchers discovered that a particular protein, Fstl1, plays a key role in regenerating cardiomyocytes. The protein is normally found in the epicardium — the outermost layer of cells surrounding the heart — but it disappears from there after a heart attack. They next asked what would happen if they were to add Fstl1 back to the heart. To do this, they sutured a collagen patch that mimicked the epicardium to the damaged muscle. When the patch was loaded with Fstl1, it caused new cardiomyocytes to regenerate in the damaged tissue.

In reading over the study, I was particularly interested in what an engineered tissue-like patch applied to a living heart looked like – and how exactly the patch got made. I called one of the study’s first authors and went to see him in his lab.

Vahid Serpooshan, PhD, a postdoctoral scholar in cardiology at Stanford, told me he can make a patch in about 20 minutes. It’s a bit like making Jell-O, he said; collagen and other ingredients get mixed together then poured into a mold. Serpooshan uses molds of various sizes depending on what kind of a heart the patch will be surgically stitched onto.

“The damaged heart tissue has no mechanical integrity,” Serpooshan said. “Adding the patch is like fixing a tire… Once the patch is stitched onto the heart tissue, the cardiac cells start migrating to the patch. They just love the patch area…”

Previously: Stanford physician provides insight on use of aspirin to help keep heart attacks and cancer away, Collagen patch speeds healing after heart attacks in mice and Big data approach identifies new stent drug that could help prevent heart attacks
Image, of a patch stitched to the right side of the heart, by Vahid Serpooshan

Mental Health, Research, Science

Optimizing work breaks for health, job satisfaction and productivity

5187630414_6102463a6c_zThink about the breaks you take during the day. Perhaps you hit pause midday to grab lunch and to run errands. Or maybe you step away from your desk frequently to briefly socialize with co-workers, get coffee or satisfy a sugar craving. Have you ever wondered what might be the optimal length and type of break?

Researchers at Baylor University asked themselves that question and discovered new insights into what constitutes a “better break.” In a study involving employees ages 22 to 67, researchers asked participants to document their breaks from work and analyzed their responses. Psych Central reports that study results suggest not all breaks are created equal, and that the type of breaks we take could potentially affect our health and job satisfaction.

Findings showed a mid-morning break can help boost your concentration, motivation and energy and that doing things you either choose or like to do during a break can help aid in recovery from stress or fatigue. According to the story:

People who take “better breaks” experience better health and increased job satisfaction.

The employee surveys showed that recovery of resources — energy, concentration, and motivation — following a “better break” (earlier in the day, doing things they preferred) led workers to experience less somatic symptoms, including headache, eyestrain, and lower back pain after the break.

These employees also experienced increased job satisfaction and organizational citizenship behavior as well as a decrease in emotional exhaustion (burnout), the study shows.

Longer breaks are good, but it’s beneficial to take frequent short breaks.

While the study was unable to pinpoint an exact length of time for a better workday break (15 minutes, 30 minutes, etc.), the research found that more short breaks were associated with higher resources, suggesting that employees should be encouraged to take more frequent short breaks to facilitate recovery.

Researchers believe breaks are an essential intervention to help a person stay sharp and energized.

“Unlike your cellphone, which popular wisdom tells us should be depleted to zero percent before you charge it fully to 100 percent, people instead need to charge more frequently throughout the day,” [said Emily Hunter, PhD, associate professor of management in Baylor University’s Hankamer School of Business.]

Previously: No time for a vacation? Take a break without leaving the officeHow Stanford and Silicon Valley companies are fostering “work-life integration”, Workplace stress and how it influences health and Stanford class teaches students how to live a happier, healthier life,
Photo by Daniil Kalinin

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