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Events, Research, Science, Stanford News

Live tweeting from Association of Health Care Journalists conference

Live tweeting from Association of Health Care Journalists conference

10948923353_90e2273cdc_zStarting tomorrow morning, we’ll be live tweeting from the Association of Health Care Journalists 2015 conference, which is being held in Santa Clara, Calif. and is co-hosted by Stanford Medicine.

The conference brings together hundreds of the top journalists who cover health care and, thanks to its proximity to our campus, also includes numerous top Stanford medical experts.

We’ll start our tweeting efforts on Friday morning at 9 a.m. Pacific time with “Ebola and Ebolanoia: Covering outbreaks responsibly,” a panel discussion that includes Michele Barry, MD, director of the Stanford Center for Innovation in Global Health. At 10:40 a.m., Henry Lee, MD, assistant professor of pediatrics, and Amen Ness, MD, associate professor of obstetrics and gynecology, will participate in a discussion on “High-risk obstetrics: Challenges of very preterm births.”And later in the day, at 4:20 p.m., we’ll be there as Michael Snyder, PhD, chair of the Department of Genetics, discusses “How big data might revolutionize medical research and treatment.”

Early Saturday, we’ll dive into the brain with Amit Etkin, MD, PhD, and Michael Greicius, MD, MPH. Their session, “Inside the living brain: What have we learned, and what’s next?”, begins at 9 a.m. Next, at 10:40 a.m., George Sledge, Jr., MD, will discuss “Cancer as a chronic condition.” Finally, at 3 p.m., Dean Lloyd Minor, MD, will join a panel discussion on “The shifting demands in health provider education.”

We’ll be using the hashtag #AHCJ15 and tweeting from @StanfordMed. And we’ll be featuring blog posts on the conference – including one on a kickoff talk by physician-author Abraham Verghese, MD, – here on Scope.

Photo by Esther Vargas

Biomed Bites, Imaging, Neuroscience, Research, Science, Videos

Vrrrooom, vrrrooom vesicles: A Stanford researcher’s work on neurotransmission

Vrrrooom, vrrrooom vesicles: A Stanford researcher's work on neurotransmission

Welcome to Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers.

When one neuron wants to communicate with another neuron, it doesn’t talk, make gestures, or perform an interpretive dance. Instead, it ejects a vesicle filled with chemical information. That vesicle travels like an interstellar ship to the next neuron, which sucks it up, receiving the message.

And this isn’t a slow, hmm, maybe-I-should-send-this-out-sometime-today kind of message.

“The process of effusion of synaptic vesicles is very fast,” says Axel Brunger, PhD, in the video above. “It occurs on the order of a millisecond. It’s one of the fastest known biological processes, so we’re trying to understand this process at a molecular level and how it actually works is a big mystery at the moment.”

Brunger, the chair of the Department of Molecular and Cellular Physiology, and his team use a variety of optical imaging methods and high-resolution structural methods to examine the transmission of synaptic vesicles:

We’re now using our [in vitro] system to study the effect of a number of factors, including factors involved in a number of diseases.

What we are hoping from these studies is to obtain a better understanding of how these factors and then secondly and importantly, to develop new strategies or therapeutics to combat these diseases.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: New insights into how the brain stays bright, Revealed: The likely role of Parkinson’s protein in the healthy brain and Examining the potential of creating new synapses in old or damaged brains 

Events, Medicine and Society, otolaryngology, Science, Stanford News

A lesson in voice and anatomy from an opera singer

A lesson in voice and anatomy from an opera singer

IMG_0766This past Thursday, I watched an opera singer’s throat as he sung. Not the bulging Adam’s apple above his shirt collar, but the shiny lumps and taut cartilage of his larynx, the mucus on his vocal folds, all healthy pink and slick and breathing.

It was a curious combination, opera and anatomy, and I didn’t know what to expect from this World Voice Day event – “Anatomy of An Opera Singer” – which was offered as a collaboration between the Stanford Medicine Music Network (part of Medicine and the Muse), Stanford Live, and the Department of Otolaryngology: Head & Neck Surgery. Surrounded by community members of various ages and people in scrubs, I entered Berg Hall to the sound of Cake’s “Opera Singer”: I am an Opera Singer, I stand on painted tape; It tells me where I’m going, and where to throw my cape. 

Stanford’s C. Kwang Sung, MD, MS, who has a professional background in both singing and otolaryngology, started the evening by performing a song honoring his parents’ inspirational role in his life – after which he introduced his parents sitting in the front row! After giving us a basic introduction to throat anatomy, he introduced internationally acclaimed opera singer Eugene Brancoveanu, who performed a song from “The Rape of Lucretia,” accompanied by Stanford pianist Laura Dahl. Brancoveanu’s beautiful voice and elaborate variety of facial expressions was stirring.

What followed elicited gasps and laughter from the audience – the view from a laryngoscopic camera in Brancoveanu’s throat was projected on big screens while Sung and Elizabeth DiRenzo, PhD, vocal fold biologist and assistant professor of otolaryngology, explained what we were seeing. The video tour had been recorded prior, and throughout the evening new twists and turns were revealed. Sung and DiRenzo had recorded Brancoveanu while he sang, while he played with falsetto and passaggio and while he varied the vowel sounds, and they walked us through this intimate demonstration of living vocal anatomy.

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Evolution, Genetics, Microbiology, Pregnancy, Research, Science, Stanford News, Stem Cells

My baby, my… virus? Stanford researchers find viral proteins in human embryonic cells

My baby, my... virus? Stanford researchers find viral proteins in human embryonic cells

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One thing I really enjoy about my job is the opportunity to constantly be learning something new. For example, I hadn’t realized that about eight percent of human DNA is actually left-behind detritus from ancient viral infections. I knew they were there, but eight percent? That’s a lot of genetic baggage.

These sequences are often inactive in mature cells, but recent research has shown they can become activated in some tumor cells or in human embryonic stem cells. Now developmental biologist Joanna Wysocka, PhD, and graduate student Edward Grow, have shown that some of these viral bits and pieces spring back to life in early human embryos and may even affect their development.

Their research was published today in Nature. As I describe in our press release:

Retroviruses are a class of virus that insert their DNA into the genome of the host cell for later reactivation. In this stealth mode, the virus bides its time, taking advantage of cellular DNA replication to spread to each of an infected cell’s progeny every time the cell divides. HIV is one well-known example of a retrovirus that infects humans.

When a retrovirus infects a germ cell, which makes sperm and eggs, or infects a very early-stage embryo before the germ cells have arisen, the viral DNA is passed along to future generations. Over evolutionary time, however, these viral genomes often become mutated and inactivated. About 8 percent of the human genome is made up of viral sequences left behind during past infections. One retrovirus, HERVK, however, infected humans repeatedly relatively recently — within about 200,000 years. Much of HERVK’s genome is still snuggled, intact, in each of our cells.

Wysocka and Grow found that human embryonic cells begin making viral proteins from these HERVK sequences within just a few days after conception. What’s more, the non-human proteins have a noticeable effect on the cells, increasing the expression of a cell surface protein that makes them less susceptible to subsequent viral infection and also modulating human gene expression.

More from our release:

But it’s not clear whether this sequence of events is the result of thousands of years of co-existence, a kind of evolutionary symbiosis, or if it represents an ongoing battle between humans and viruses.

“Does the virus selfishly benefit by switching itself on in these early embryonic cells?” said Grow. “Or is the embryo instead commandeering the viral proteins to protect itself? Can they both benefit? That’s possible, but we don’t really know.”

Wysocka describes the findings as “fascinating, but a little creepy.” I agree. But I can’t wait to hear what they discover next.

Previously: Viruses can cause warts on your DNA, Stanford researcher wins Vilcek Prize for Creative Promise in Biomedical Science and Species-specific differences among placentas due to long-ago viral infection, say Stanford researchers
Photo of Joanna Wysocka by Steve Fisch

Cancer, Genetics, Patient Care, Research, Science, Stanford News

Identifying relapse in lymphoma patients with circulating tumor DNA

Identifying relapse in lymphoma patients with circulating tumor DNA

3505577004_6fc17ba8c2_zCancer patients in remission often live on a knife’s edge, wondering if their disease will recur. This possibility is more likely in some types of cancers than in others. One of these is diffuse large B-cell lymphoma, which is the most common blood cancer in this country. It’s often successfully treated, but a significant minority of patients will relapse. Detecting these relapses early is critical, but difficult.

Hematologist and oncologists Ash Alizadeh, MD, PhD, and David Kurtz, MD, and former postdoctoral scholar Michael Green, PhD, wanted to find a better way to track disease progression in these patients. They’ve developed a new technique, published Friday in the journal Blood, that is more accurate and can detect relapses earlier than conventional methods.

“As a clinician, I care for many of these patients,” Alizadeh explained to me. “Detecting relapse can be very difficult. It would be a major step forward to develop a way to identify these patients before they become sick again.”

Detecting relapse can be very difficult. It would be a major step forward to develop a way to identify these patients before they become sick again.

The researchers turned to what’s known as circulating tumor DNA in the blood. The approach, which was pioneered by Stanford bioengineer Stephen Quake, PhD, relies on the idea that when the cells in our body die, they rupture and release their contents, including their DNA, into our bloodstream. Tracking the rise and fall of the levels of these tiny snippets of genetic information can give insight into what is happening throughout the body.

When a B cell becomes cancerous, it begins to divide uncontrollably. Each of these cancer cells shares the DNA sequence of the original cell; as the cells multiply, so does the overall amount of that DNA sequence in the body. Alizadeh and his colleagues wondered whether tracking the levels of cancer-specific DNA in a patient’s blood could help them identify those patients in the early stages of relapse.

Currently patients in remission are monitored for relapse with regular physical exams and blood tests. Imaging techniques such as PET or CT scans can be used to look for residual disease, but they don’t detect every case, and often deliver false positive results. They are also costly and expose the patient to DNA-damaging radiation that could potentially cause secondary cancers years later.

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Research, Science, Stanford News, Surgery

Will scars become a thing of the past? Stanford scientists identify cellular culprit

Will scars become a thing of the past? Stanford scientists identify cellular culprit

346801775_c5a1e37a6d_zI have a scar on my chin from a fall I took while rollerskating when I was about 12. One minute I was blithely zooming along to Bob Seger’s hit Against the Wind (earworm alert!), reveling in my new ability to skillfully cross one foot in front of the other and thinking about that cute boy by the snack counter, and the next I was chin down skidding across the flat, grey and (I then realized) very hard floor to come to rest against the wooden wall in an ignominious heap.

Although the experience left an impression on my psyche, as well as my skin, I can’t claim any long-lasting problem from the thin line on my chin. After all, nearly all of us have something similar. But scars can also be debilitating and even dangerous.

Now plastic and reconstructive surgeon Michael Longaker, MD, and pathologist and stem cell expert Irving Weissman, MD, have identified the cell type in mice that is responsible for much of the development of a scar. They’ve shown that blocking this cell’s activity with a small molecule can reduce the degree of scarring. Because a similar drug molecule is already approved for use in humans to treat Type 2 diabetes, the researchers are hopeful that they can begin clinical trials in humans soon. The research was published today in Science.

As Longaker explained in our release on the study:

The biomedical burden of scarring is enormous. About 80 million incisions a year in this country heal with a scar, and that’s just on the skin alone. Internal scarring is responsible for many medical conditions, including liver cirrhosis, pulmonary fibrosis, intestinal adhesions and even the damage left behind after a heart attack.

Longaker and his colleagues found that a subset of a skin cell called a fibroblast is responsible for much of the collagen deposition that leads to scarring. Inhibiting the activity of a protein on the surface of the cells significantly reduced the amount of scarring during wound healing in laboratory mice – from about 30 percent of the original wound area down to about 5 percent -the researchers found. Furthermore, they showed the cells are also involved in the thickening and darkening of skin exposed to radiation therapy for cancer, as well as the spread of melanoma cancer cells in the animals.

Longaker’s been interested in how the skin heals for decades–ever since he learned as a student that, prior to the third trimester, human fetuses heal from trauma or surgery without any scarring. Now he’s excited to learn whether there’s a way to recapture that long-lost ability as adults and at least reduce the degree of scarring during skin repair.

“I’ve been obsessed with scarring for 25 years,” Longaker told me. “Now we’re bringing together the fields of wound healing and tumor development in remarkable new ways. It’s incredibly exciting.”

Longaker and Weissman are both also members of the Stanford Cancer Institute.

Previously: New medicine? A look at advances in wound healing, Stanford-developed device shown to reduce the size of existing scars in clinical trial and Mast cells not required for wound healing, according to Stanford study
Photo by Paulo Alegria

Biomed Bites, Immunology, Research, Science, Technology, Videos

Not immune from the charms of the immune system

Not immune from the charms of the immune system

Welcome to Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers.

Once upon a time, a researcher named Holden Maecker, PhD, met flow cytometry, a technique used to examine cells by suspending them in fluid and then passing them by an electronic detector.

A match that could only be made in a science lab, Maecker was hooked. Maecker tells the tale in the video above:

Flow cytometry is a great technique for looking at the immune system and it’s also a little bit of an art, which also attracted me. It’s something that not everybody can do perfectly well and I got a little bit good at it and decided it was a fun thing to do and a good way to look at the immune system.

Maecker and flow cytometry haven’t parted, yet he’s broadened his mastery of a variety of other techniques to study the immune system as the director of Stanford’s Human Immune Monitoring Center.

“It’s a very interesting position because it allows me to collaberate with a lot of different peopel doing projects that have to do wiht human immune responses — everything from sleep apnea and wound healing to flu vaccines and HIV infections,” Maecker said. “It’s amazing the breadth we have here [at Stanford].”

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: Knight in lab: In days of yore, postdoc armed with quaint research tools found immunology’s Holy Grail, Immunology meets infotech and Stanford Medicine magazine traverses the immune system

Evolution, In the News, Research, Science

Chins make us human; new study examines why

Chins make us human; new study examines why

il-150226-ts-08When we think of what makes us human, it’s common to think of something like language or tool-making. Something that likely doesn’t pop into mind is the chin – but humans are the only species to have one! The bony prominence is missing from the skulls of Neanderthals, archaic humans, primates, and indeed all other animals. (In the photo, the skull on the left is human, and the one on the right is Neanderthal).

Scientists have puzzled for more than a century over why chins developed, and the dominant theory has been that they resulted from mechanical forces like chewing. Bones under pressure sustain tiny tears that then enable new bone to grow, much like weight lifting does to muscles. But a new study conducted by University of Iowa researchers suggests that mechanical forces have nothing to do with it: It’s more likely that chins resulted from shifting social dynamics.

The study, published in the Journal of Anatomy, capitalized on the fact that children don’t have chins either – the bone underneath their lower lip is smooth, and the prominence develops with age. The study examined nearly 40 people ranging from 3-20 years old, correlating their chin development with various forces exerted by their cranio-facial anatomy (during chewing, for example), and concluded that mechanical forces don’t play a role in chin development. In fact, those with the most mechanical force had the smallest chins.

Nathan Colton, PhD, professor of orthodontics at the UI College of Dentistry and lead author of the study, is quoted in a UI press release:

In short, we do not find any evidence that chins are tied to mechanical function and in some cases we find that chins are worse at resisting mechanical forces as we grow. Overall, this suggests that chins are unlikely related to the need to dissipate stresses and strains and that other explanations are more likely to be correct.

Instead, the researchers think that the chin results from the facial structure being rearranged as faces got smaller – human faces are 15 percent smaller than those of Neanderthals. This reduction resulted from a decrease in testosterone levels, which happened as males of the species benefitted more from interacting socially with other groups rather than fighting other males.

Robert Franciscus, PhD, professor of anthropology at UI and a contributing author on the study, also comments:

What we’re arguing is that modern humans had an advantage at some point to have a well-connected social network, they can exchange information, and mates, more readily, there’s innovation. And for that to happen, males have to tolerate each other. There had to be more curiosity and inquisitiveness than aggression, and the evidence of that lies in facial architecture.

Previously: Humans share history – and a fair amount of genetic material – with Neanderthals
Photo by Tim Schoon, University of Iowa

In the News, Media, Science

Science enthusiasts flock to #IAmAScientistBecause and #BeyondMarieCurie on Twitter

Science enthusiasts flock to #IAmAScientistBecause and #BeyondMarieCurie on Twitter

iamascientistbecause tweet - smallRecently, a friend of mine commented that scientists “don’t use Twitter much.” The statement may have been true in the past, but as evidenced by #IAmAScientistBecause and #BeyondMarieCurie, scientists and science enthusiasts are now driving some trending topics on Twitter.

Yesterday, a story on Nature.com explained how these two popular hashtags have encouraged scientists to speak out. The first was created by the NatureCareers team in summer 2014, and the hashtag’s popularity suddenly increased earlier this week after Jon Tennant (@Protohedgehog), a graduate student studying paleontology at Imperial College London, shared the hashtag with his 6,000 some followers on Twitter. By Tuesday, the hashtag was trending on Twitter.

The resulting flood of tweets rallied scientists like epidemiologist Chelsea Polis, PhD, (@cbpolis) who told Nature.com she spent a day following the IAmAScientistBecause Twitter campaign online. “Despite all of the negatives, there’s so much that’s beautiful about science,” Polis said.

Meanwhile, a separate empowering conversation began when science editor Melissa Vaught (@biochembelle) tweeted about Rachel Swaby’s (@rachelswaby) Wired.com story on scientific achievements made by women. In her story, Swaby states that one woman tends to dominate conversations of female scientists and that we need to open our eyes to the many contributions other female scientists have made, and are making, to science:

Today if you ask someone to name a woman scientist, the first and only name they’ll offer is Marie Curie. It’s one of the biggest obstacles to better representation of women in science and technology, and it’s time to cut it out. Stop talking about Marie Curie; she wouldn’t have wanted things this way.

Vaught told Nature.com that she created #BeyondMarieCurie as a response to Swaby’s article because “we need diverse stories of women in science.”

As I scrolled through the hundreds of Tweets aggregated by the two hashtags one post in particular stood out. As shown above, chemist Carina Jensen, PhD, (@Chem_Monkey) tweeted, “IAmAScientistBecause a professor said women don’t do well in Chemistry. I proved him wrong.” For me, this unites the sentiments of the two hashtags beautifully.

Previously: The power of social media: How one man uses it to help amputees get prostheticsA day in the lab: Stanford scientists share their stories, what fuels their workChipping away at stereotypes about older women and science, one story at a timeWhat’s holding women in the sciences back? and Women in science: A rare breed

In the News, Medicine and Literature, NIH, Research, Science

The value of exploring jellyfish eyes: Scientist-penned book supports “curiosity-driven” research

The value of exploring jellyfish eyes: Scientist-penned book supports "curiosity-driven" research

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As an academic, I often encounter variations of the question “And so… what are you going to do with that?” In other words, why should anyone care about insights, experiments, and questions that serve no obvious functional purpose?

A PNAS release published earlier this week spotlights a novel that tackles just this issue. Joram Piatigorsky, PhD, a retired scientist from the NIH’s National Eye Institute who now devotes his time to his passion for art and literature, went through the arduous process of writing and publishing a novel because he sees literature as an important way to make statements about society. And the statement that he wants to get across loud and clear is that basic research matters, and needs to be funded.

The book, called Jellyfish Have Eyes, is set in the near future and follows a scientist who gets into serious legal and professional trouble because he departs from research that is clearly related to a human disease in favor of researching jellyfish, and in a mix-up uses government funding to do so. Piatigorsky laments how in today’s tight funding environment, students who would otherwise pursue basic questions – such as whether jellyfish have eyes – are forced to do more routine, translational research that doesn’t make use of their creativity.

And when creativity gets stymied, important breakthroughs are simply missed. The release quotes the book’s main character, who is modeled after Piatigorsky:

I justify my research on delving into the mysteries of Nature because generally the experiments yield new insights that benefit people. There’s penicillin, recombinant DNA, genetic engineering… Bacteria provided the first models for gene regulation, which set the stage for gene therapy. Sea slugs—snails without shells—revealed mysteries of memory. Birds have taught us that it’s possible to rest half the brain at a time. Think how useful it would be if we could be asleep and active at the same time.

Piatigorsky worries about the current research climate, where “anti-science politicians” force cuts to basic research and pundits and the public insist on knowing what “cure” a research project aims to find, says the release. But Piatigorsky is optimistic about the power of storytelling: “I have a very strong feeling that science is not a collection of facts. You have to make the facts into a story of communication… The narrative aspect of science is very compelling.”

And, in case you were wondering, jellyfish do have eyes – “magnificent eyes. It depends on the species. They have lenses, corneas, retinas,” says Piatigorsky in the release. No one knows what they can see or how vision might affect their behavior, but such impractical questions might lead to the next breakthrough. In the meantime, they promote curiosity and wonder about our world.

Previously: Research in medical school: the need to align incentives with value, Can science journals have beautiful prose? and Science is like an ongoing mystery novel, says Stanford neurobiologist Carla Shatz
Photo by Lassi Kurkijarvi

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