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Applied Biotechnology, Bioengineering, Ophthalmology, Research, Science, Technology

New retinal implant could restore sight

New retinal implant could restore sight

2618400441_c19946dff4_zIf your car battery runs out of juice, the car won’t run, but that doesn’t mean it’s time to scrap the car. Similarly (at least slightly), if your photoreceptors are worn out due to a disease such as retinitis pigmentosa or macular degeneration, then you might not be able to see, but your eyes still have a lot of functioning parts.

That’s the principle behind a new retinal implant developed by team of Stanford-led researchers. Unlike previous devices, which require wires and unwieldy surgeries, the new implant is wireless and needs only a minimally invasive surgery to inject a small, photovoltaic chip inside the eye. The team published their results in Nature Medicine.

That chip capitalizes on the remaining capabilities of existing retinal cells known as bipolar and ganglion cells and produces more refined images than existing devices. The chip responds to signals from special glasses worn by the recipient.

“The performance we’re observing at the moment is very encouraging,” Georges Goetz, a lead author of the paper and graduate student in electrical engineering at Stanford, said in our press release. “Based on our current results, we hope that human recipients of this implant will be able to recognize objects and move about.”

The implant has only been used in animal studies, but a clinical trial is planned next year in France.

“Eventually, we hope this technology will restore vision of 20/120,” co-senior author Daniel Palanker, PhD, told me. “And if it works that well, it will become relevant to patients with age-related macular degeneration.”

Previously: Stanford researchers develop solar powered wireless retinal implant, Factors driving prescription decisions for macular degeneration complex — and costly and Tiny size, big impact: Ultrasound powers miniature medical implant 
Photo by Ali T

Behavioral Science, Mental Health, Research

Type of verbal therapy could reduce PTSD risk among trauma victims

Type of verbal therapy could reduce PTSD risk among trauma victims

217849066_f011b26437_zTurning on the bedroom light can knock the teeth out of all kinds of terrors. This same concept – seeing things as they are, not as we fear them to be – also forms the basis for many therapies used to treat the estimated 5.2 million people living in the U.S. with post-traumatic stress disorder (PTSD). Now, research shows that treating a victim of trauma with a certain type of therapy within six hours of the event – when most memories are formed – can reduce his or her risk of developing PTSD.

In the study, researchers from King’s College London and the University of Oxford investigated the effect of two treatments: “updating” therapy, where the patient talks about traumatic memories to update them with more factual information, and “exposure” therapy where the patient revisits the source of fear to decrease its emotional effect. These two techniques were applied to 115 participants after they watched six film clips containing real-life footage of humans and animals in distress.

The researchers found giving the participants “information about the fate of the films’ protagonists” (i.e., using the updating technique) significantly reduced the occurrence of fearful feelings, and it reduced these intrusive thoughts better than the exposure treatment and no treatment at all.

As psychologist and lead author Victoria Pile, PhD, explains in a press release, this study is important because there are currently no established therapies to help victims of trauma fend off PTSD. And, she said, “this research implies that finding out what actually happened as soon as possible after the trauma might change the way the memory is stored and so limit the devastating effects of PTSD.”

The researchers note that these findings could be especially helpful for people who are routinely exposed to traumatic situations, such as emergency service workers, military personnel and people working in conflict zones.

Previously: Study shows benefits of breathing meditation among veterans with PTSDExamining the scientific evidence behind experimental treatments for PTSDUsing mindfulness therapies to treat veterans’ PTSD and In animal study, sleep deprivation after traumatic events lowers risk of PTSD symptoms
Image by Capture Queen

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

Cancer, Neuroscience, Pediatrics, Research, Stanford News, Videos

Brain tumor growth driven by neuronal activity, Stanford-led study finds

Brain tumor growth driven by neuronal activity, Stanford-led study finds

Nerve activity in the cerebral cortex can drive the growth of deadly brain tumors called high-grade gliomas, new research has found. The finding, from a study of mice with human brain tumors, provides a surprising example of an organ’s function driving the growth of tumors within it, according to Michelle Monje, MD, PhD, the Stanford neuroscientist who led the work. The work appears online today in Cell.

High-grade gliomas include tumors that affect children, teens and adults. They are the most lethal of all brain tumors, and their survival rates have scarcely improved in 30 years. Monje’s team and others around the world are trying to learn how the tumors arise and grow, with the hope that this understanding will enable development of new drugs that specifically attack the tumors’ vulnerabilities.

From our press release about the research:

Monje’s team identified a specific protein, called neuroligin-3, which is largely responsible for the increase in tumor growth associated with neuronal activity in the cerebral cortex. Neuroligin-3 had similar effects across the different types of high-grade gliomas, in spite of the fact that the four cancers have different molecular and genetic characteristics.

“To see a microenvironmental factor that affects all of these very distinct classes of high-grade gliomas was a big surprise,” Monje said.

The identity of the factor was also unexpected. In healthy tissue, neuroligin-3 helps to direct the formation and activity of synapses, playing an important role in the brain’s ability to remodel itself. The new study showed that a secreted form of neuroligin-3 promotes tumor growth.

“This group of tumors hijacks a basic mechanism of neuroplasticity,” Monje said.

Blocking the tumor-stimulating effects of neuroligin-3 might be an effective treatment for high-grade gliomas, Monje added.

In the video above, Monje describes some of the earlier work that led her team to ask whether nerve activity could drive tumor growth. In the healthy brain, it’s important for neuronal activity to be able to modify how the brain grows and develops, she explains – this is how experience changes our brains. But: “The growth-inducing effects of neuronal activity are very robust and it made me wonder if a similar physiology was being hijacked by glioma cells,” she says in the video.

Previously: Emmy nod for film about Stanford brain tumor research — and the little boy who made it possible, Big advance against a vicious pediatric brain tumor and New Stanford trial targets rare brain tumor

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 

Big data, Chronic Disease, Public Health, Research

Finding asthma outbreaks using Twitter: How social media can improve disease detection

Finding asthma outbreaks using Twitter: How social media can improve disease detection

Asthma_inhaler_useWant to know if bad air has sparked an asthma epidemic in your neighborhood? Well, you’ll have to wait several weeks using traditional epidemiologic methods, a time lag that makes prompt response efforts quite tricky.

Or, perhaps you can just check out your Twitter feed.

A team led by Sudha Ram, PhD, at the University of Arizona found that a model that aggregates Twitter data, Google searches, air quality data and asthma-related emergency room visits can predict outbreaks with 70 percent precision. It’s big data in action.

As Ram comments in a press release:

The CDC gets reports of emergency department visits several weeks after the fact, and then they put out surveillance maps. With our new model, we can now do this in almost real time, so that’s an important public health surveillance implication.

With that information, hospitals could beef up their staff and health care workers could reach out to at-risk populations.

In the future, Ram said she plans to examine diseases with greater geographic and temporal variability such as chronic obstructive pulmonary disease (COPD) and diabetes. Her research was published in a special issue of the Institute of Electrical and Electronics Engineers Journal of Biomedical and Health Informatics.

Previously: Advice for young doctors: Embrace Twitter, Mining Twitter to identify cases of foodborne illness and Text messages about asthma could help children breathe easier 
Via MedCity News
Photo by Wikimedia

Aging, Pain, Palliative Care, Research, Stanford News

How would you like to die? Tell your doctor in a letter

How would you like to die? Tell your doctor in a letter

writing a letterAsking patients how they would like to die is not a question that comes easy to most doctors. Not surprisingly, most of us – doctors and patients alike – prefer to avoid the topic completely. That’s not good, says VJ Periyakoil, MD, director of palliative care education and training at Stanford.

As I wrote in an Inside Stanford Medicine article on Periyakoil’s new study on end-of-life conversations:

End-of-life conversations help clarify for doctors what matters most to patients in their waning days of life… “What are their hopes, wants, needs and fears? Do they want to die at the hospital on a machine? Do they want to die at home? We can’t know unless we have a conversation,” she said.

Her study, published today in PLOS One, surveyed more than 1,000 medical residents and found that most balk at talking with seriously ill patients about what’s important to them in their final days, especially if the patient’s ethnicity is different than their own. Of those surveyed, 99.99 percent reported barriers, with 86 percent rating them as very challenging.

The upshot for Periyakoil, as she explains in a New York Times column published today, is that if we want to have a say in how we die, we should start that conversation ourselves.

To get these conversations started far and wide, she has launched the Stanford Letter Project – a campaign to empower all adults to take the initiative to talk to their doctor about what matters most to them at life’s end. The project’s website hosts templates for a letter about this to your doctor to get the conversation rolling. The templates are in Mandarin, Spanish and Tagalog as well as English – and Periyakoil says translations in additional languages will be available soon.

Previously: In honor of National Healthcare Decisions Day: A reminder for patients to address end-of-life issues, Study: Doctors would choose less aggressive end-of-life care for themselvesAsking the hardest questions: Talking with doctors while terminally ill, On a mission to transform end-of-life care and The importance of patient/doctor end-of-life discussions
Photo by Gioia De Antoniis

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

Wysocka - 560

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

Ebola, Global Health, Infectious Disease, Microbiology, Research

Can a single drug outsmart many kinds of viral invaders?

Can a single drug outsmart many kinds of viral invaders?

blue virus

We’ve got plenty of effective antibiotics – maybe even too many- to knock off bacteria we don’t like. But when it comes to viruses, it’s a different story, Stanford infectious-disease specialist Shirit Einav, MD, and postdoc Elena Bekerman, PhD, write in a recently published perspective piece in Science.

“Although hundreds of viruses are known to cause human disease, antiviral therapies are approved for fewer than 10,” the authors write, before going on:

[Antiviral drugs that interfere with crucial viral enzymes] have shown considerable success in the treatment of HIV and hepatitis C virus… infections. However, this approach does not scale easily and is limited particularly with respect to emerging viruses against which no vaccines or antiviral therapies are approved.

Which is too bad, because viruses can be nasty. Not to mention creepy: They’re master puppeteers when it comes to manipulating us into submission. They can’t even replicate on their own. The little body-snatchers need our own cells, which they break into, bamboozle, and bully into producing copies of themselves and then squirting them out so they can infect other cells and, with luck, other people.

A partial list of merging and re-emerging viruses for which there are no decent treatments includes dengue, estimated to infect 400 million people each year; SARS and MERS, responsible for outbreaks of severe acute respiratory syndromes; and Ebola, which, as everybody now knows, caused an ongoing epidemic in Africa.

Developing antiviral drugs is a huge challenge. It takes, on average, more than $2 billion and about a decade, plus or minus a couple of years, to develop a new drug targeting just one single type of virus, Bekerman and Einav write. To make things worse, these nano-villains evolve even faster than bacteria do.

Einav’s research has been taking a different tack. She’s working on drugs that, instead of gumming up this or that viral enzyme (at least until it mutates into a form the drug can’t gum up), interfere with the activity of components in our cells that the viruses absolutely depend on for their own survival and replication. There are already drugs, many of them already approved for far different indications such as cancer, that can do just that – without, however, disabling our own cells so much that the cure becomes worse than the disease.

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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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