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Global Health, Health Policy, Nutrition, Public Health, Research, Stanford News, Videos

A team approach to international health

A team approach to international health

When it comes to issues in international public health, the challenge is more than just one of medicine. Solutions require people from multiple disciplines to work together, along with governmental ministries and often non-profit organizations.

Grant Miller, PhD, an associate professor of medicine, has been working on one such challenge – that of micronutrient deficiency in the Indian state of Tamil Nadu.

“There are at least three ministries that have key responsibility over this area,” Miller says. “We then have to work with an NGO partner, and we have to go out and collect our own data and evaluate how this intervention works.”

Miller works with both the Freeman Spogli Institute for International Studies and the Stanford Institute for Economic Policy Research, and he says the institutes play an important role in supporting interdisciplinary collaborations like this one.

“Stanford makes it very easy to do interdisciplinary research,” he says. “I think the pay off is huge, but it’s not an easy thing to do.”

More faculty talk about the value of collaboration in their work as part of the new Stanford Interdisciplinary website.

Previously: New website chronicles tales of collaborative research and Stanford journalist returns to old post in India – and finds health care still lagging
Video by Worldview Stanford

Research, Science

The 10 biggest pitfalls in scientific presentations and how to avoid them

The 10 biggest pitfalls in scientific presentations and how to avoid them

14037224149_65205456a9_zOne of the most valuable things I got out of graduate school was this bit of career advice: “There’s no shortage of scientists. What we’re lacking — and what we need — are people who can actually explain this stuff and do it well.”

At first, I thought this meant we need more science writers. But really, the advice is intended for everyone. We all need to do a better job of communicating our work — it could be the key to a job, a valuable collaboration or more money and resources for your work.

So how can you communicate better? One way is to watch out for the “10 biggest pitfalls” as laid out by David Rubenson, the associate director of administration and strategic planning at Stanford’s Cancer Institute. In a recent post on the Naturejobs blog, he cites common traps such as not rehearsing your presentation and rushing through your slides.

And the number one mistake?

Thinking a collection of slides is enough

Your 50 slides may allow you to talk for 50 minutes, but that doesn’t mean you have anything to say. Always have an overarching scientific question and narrative. Slides fragment even the most coherent story, so make sure each slide supports the narrative.

Previously: Making science accessible to scientistsFree, online Stanford course on science writing opens this week and A call to fix the “crisis of communication” in science
Photo by Stanford University

Addiction, Neuroscience, Research, Stanford News

Stanford scientists uncover new approach to reduce opiate withdrawal

Stanford scientists uncover new approach to reduce opiate withdrawal

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Opiates produce a sense of euphoria that is highly addictive. If addicts stop taking the drugs, they are faced with opiate withdrawal, which can feel like the worst imaginable stomach flu with symptoms that include muscle aches, sweating, nausea, vomiting, diarrhea and a runny nose.

Stanford researchers have identified and suppressed the neural pathway responsible for these withdrawal symptoms in opiate-addicted mice, as reported in Nature.

Xiaoke Chen, PhD, the lead investigator and an assistant professor of biology, explains in a recent news release:

Most research that studies drug addiction is focused on the reward pathway because that is the reason you start to take drugs, but people who really get addicted also take drugs to get rid of the withdrawal effect. This is especially important in opiate addiction.

Chen’s team studied the nucleus accumbens, a group of neurons that plays a key role in addiction through its response to rewarding and aversive stimuli. They used fluorescent proteins to identify a clear link between the nucleus accumbens and another brain center associated with drug-seeking behavior called the paraventricular nucleus of the thalamus (PVT).

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Autoimmune Disease, Biomed Bites, Immunology, Research, Videos

Calcium channel plays integral role in immune response

Calcium channel plays integral role in immune response

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

The immune system’s main players — the B cells and T cells, as well as others — are credited for helping the body ward off invaders. And rightly so. But to work their magic, they rely on under-recognized calcium channels, gates in the cell surface that, among other actions, switch the immune cells into “action” mode.

Many unknowns remain about how these cells function, but Richard Lewis, PhD, professor of molecular and cellular physiology, is working to close the gaps in knowledge. He explains in the video above:

We’re mostly interested in two things related to these channels: First, we would like to understand how these channels work. How is it that contact with the antigen-presenting cell turns these cells on to admit calcium into the T cell?

A second area of interest is to understand what happens when the calcium comes into the cell.

Malfunctions in these channels can lead to severe immunodeficiencies or other problems, Lewis says:

We may be able to design better drugs in the future that target these channels to either inhibit them, which would be useful therapy for treating autoimmune disorders like arthritis, multiple sclerosis and lupus, or to potentiate the activity of these channels, which would be a useful way of boosting the immune response in patients with immunosuppressed conditions.

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

Previously: ‘Pacemaker’ channels in hair stem cells offer clues to tissue regeneration, say Stanford experts, Found: A molecule mediating memory meltdown in aging immune systems and Women and men’s immune system genes operate differently, Stanford study shows

Cancer, Immunology, Research, Stem Cells

How cancer stem cells dodge the immune system

How cancer stem cells dodge the immune system

Hidden cat

Cancer stem cells are tricky beasts. They are often resistant to common treatments and can hide out in the body long after the bulk of tumor cells have been eliminated. Over time, they’re thought to contribute to the recurrence of disease in seemingly successfully treated people.

Stanford head and neck surgeon John Sunwoo, MD, and graduate student Yunqin Lee have been investigating how stem cells in head and neck cancers manage to evade the body’s immune system. Although it’s been known that a type of head and neck cancer cells — CD44+ cells — are particularly resilient to treatment, it’s not been known exactly how they accomplish this feat.

Now, Sunwoo and Lee published today in Clinical Cancer Research a study that sheds some light on the issue. They found that a protein called PD-L1 is expressed at higher levels on the surface membrane of CD44+ cells than on other cancer cells. PD-L1  is believed to play a role in suppressing the immune system during pregnancy and in diseases like hepatitis. It does so by binding to a protein called PD-1 on a subset of immune cells (T cells) and dampening their response to signals calling for growth and activation.

As Sunwoo described to me in an email:

We believe that our work provides very important insight into how cancer stem cells, in general, contribute to tumor cell dormancy and minimally residual disease that may recur years later. Our findings also provide rationale for targeting the PD-1 pathway in the adjuvant therapy setting of head and neck cancer following surgical resection.

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Global Health, Infectious Disease, Microbiology, Research, Stanford News

If you gum up a malaria parasite’s protein-chewing machine, it can’t do the things it used to do

If you gum up a malaria parasite's protein-chewing machine, it can't do the things it used to do

chewing gum“Life in the tropics” evokes images of rain forests, palm trees, tamarinds and toucans. It also has a downside. To wit: One-third of the Earth’s population – 2.3 billion people – is at risk for infection with the mosquito-borne parasite that causes malaria.

Thankfully, mortality rates are dropping because of large-scale global intervention efforts. But malaria remains stubbornly prevalent in sub-Saharan Africa and Southeast Asia, where hundreds of millions of people become infected each year and more than 400,000 of them – mostly children younger than 5 – still die from it.

The parasite has the knack of evolving rapidly to develop resistance to each new generation of drugs used to fend it off. Lately, resistance to the current front-line antimalarial drug, artemisinin, is spreading and has now been spotted in a half-dozen Southeast Asian countries.

So it’s encouraging to learn that Stanford drug-development pioneer Matt Bogyo, PhD, and his colleagues have designed a new compound that can effectively kill artemisinin-resistant malaria parasites. Better, exposure to low doses of this substances re-sensitizes them to artemisinin.

By exploiting tiny structural differences between the parasitic and human versions of an intercellular protein-recycling machine called the proteasome, the compound Bogyo’s team has created attacks the malaria parasite while sparing human cells.

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Neuroscience, Research

Successful replacement of eye cells hints at future glaucoma treatment

Successful replacement of eye cells hints at future glaucoma treatment

2553516471_2dbf6fbb2f_oFor the first time, a team has successfully transplanted retinal ganglion cells into living animals. The new cells mimicked existing cells in the eye and responded to light.

The work, which was co-led by Jeffrey Goldberg, MD, PhD, professor and chair of ophthalmology at Stanford, is an effort to improve therapies for retinal and optic nerve diseases including glaucoma, which is the leading cause of irreversible blindness. Glaucoma is caused by a variety of conditions, but it leads to the loss of retinal ganglion cells, nerve cells that transmit information from photoreceptors in the eye to the visual centers in the brain.

“These data provide a hint that replacing these cells and restoring these connections is one step closer to possible,” Goldberg told me.

The team, including first author Praseeda Venugopalan, PhD, a former graduate student in neuroscience at the University of Miami, injected labeled retinal ganglion cells into 152 adult rats. Although the new cells integrated into only about one of six animals, that success rate was surprisingly high, Goldberg said.

Goldberg said they are not sure why their procedure worked when other attempts have failed. They used fully differentiated retinal ganglion cells, rather than undifferentiated stem cells, which could be an important factor, he said.

In this study, the team implanted the cells in healthy eyes, but they’re planning future studies to determine if the procedure is equally successful in eyes already suffering from glaucoma, Goldberg said.

The study appeared recently in Nature Communications. Kenneth Muller, PhD, professor of neuroscience at the University of Miami, is also a senior author.

Previously: Stanford-developed eye implant could work with smartphone to improve glaucoma treatments, What I did this summer: Stanford medical student investigates early detection methods for glaucoma and The retina: One researcher’s window into the brain
Photo by Rachel Collins

HIV/AIDS, Infectious Disease, Research, Science, Stanford News

“Unprecedented” approach for attempting to create an HIV vaccine

"Unprecedented" approach for attempting to create an HIV vaccine

Stanford’s 588732155_c05dda114e_zPeter S. Kim, PhD, was recently elected to the National Academy of Engineering, making him one of only 20 people who are members of all three National Academies (the other two are Medicine and Science). Stephen Quake, PhD, a bioengineer here, is also a member of all three academies.

This honor is particularly fitting for Kim, who joined Stanford in 2014 to be part of the new interdisciplinary institute Stanford ChEM-H, which bridges the schools of medicine, engineering and humanities & sciences for research in human health. Kim had spent a decade as president of Merck Research Laboratories and hopes that in his return to academic research his group will be able to help create a vaccine for HIV.

I talked to Kim recently about why he thinks he’ll succeed where so many have failed in their efforts to develop an HIV vaccine, and the importance of working across disciplines:

How is your approach to creating an HIV vaccine different from ones that haven’t been successful?

In over 30 years of intense work by many people to try and come up with a vaccine, none has succeeded. That’s in large part because the virus can mutate very quickly. It can change and therefore escape an antibody. The approach that we’re taking is to target a part of HIV that is normally buried but becomes exposed during the infection process. This region is highly conserved – it is 90 percent identical between all HIV strains.

If this region doesn’t mutate often why haven’t other people tried to target it?

It is unprecedented to make a vaccine against a region of a protein that is only exposed briefly. People are skeptical because the vaccine has to be there right at the moment that the virus is infecting the cell.

What gives you confidence the approach will work?

There’s an FDA-approved drug, called Fuzeon, that binds this same region and has been shown to be effective in people. That drug isn’t widely used because it has to be injected, but it validates our idea that targeting this transiently exposed part of the protein can be effective at fighting the virus in humans.

How far along are you?

We’ve shown that we can elicit antibodies in animals that are capable of inhibiting HIV in a lab dish. Thus, we know that our vaccine candidates can generate antibodies against the virus, and that those antibodies recognize and fight the virus. But, we still need to generate a much stronger inhibitory response before we test it in people.

You’re now a member of the three academies that also represent the academic interests of ChEM-H, which brought you to Stanford. Do you think spanning disciplines helps in your work?

The research that we do is greatly enhanced by having the proximity of engineering, medicine and science at Stanford. We study things as basic as the molecular structures of viral proteins. Ultimately, we need to understand how the human immune system creates antibodies against these proteins. This work is greatly facilitated by engineering methods to determine the DNA sequence of single immune cells. In the future, we would also love to see what is occurring at a single molecule level when a virus infects a cell. To do that will require bringing together world class engineering, science and medicine.

Previously: Research investment needed now, say top scientists and Stanford ChEM-H bridges chemistry, engineering and medicine
Image of an HIV particle by AJ Cann

History, Research, Surgery

Ancient surgical technique still used to rebuild noses today

Ancient surgical technique still used to rebuild noses today

When facial surgeon Sam Most, MD, first contacted me about doing a story on one of his favorite procedures called the “forehead flap,” which he uses for major nose reconstructions, he sent along photos of what a patient looks like prior to surgery.

The photos make it clear real fast how unfortunate it is to lose your nose. The nose is the focal point of the face. It’s what people notice first. The numbers of people losing their noses due to skin cancer is on the rise, and many, are left wearing uncomfortable, unflattering prostheses for years.

Enter surgeons like Most, part artist, part scientist — a sculptor of noses. According to Most, it’s the most difficult facial plastic surgery procedure. And key among the many necessary tools needed to succeed is the “forehead flap” — a procedure that originated with cobblers in ancient India. My article tells the story of this fascinating surgery, which was first introduced into Western medicine in 1794:

Most is quick to recount the historical significance of the forehead flap, Most is quick to recount the historical significance of the forehead flap technique, which originated in India probably before the birth of Christ but wasn’t widely known to Western medicine until 1794 with the publication of a letter to the editor in Gentlemen’s Magazine of London. The letter provided the first account in English literature of the procedure.

At the time, India was a colony of the British. A sultan, angry at the occupation, offered bounties for the amputated ears, noses and hands of British sympathizers. The letter describes the nasal reconstruction of an Indian bullock driver who, having been imprisoned by the sultan, had his nose and one of his hands cut off for delivering supplies to British troops. It goes into detail how the driver’s nose was rebuilt 12 months later, after he joined the Bombay Army of the East India Company.

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Research, Science, Sleep, Stanford News

Flashing light at night could help beat jet lag, Stanford study says

Flashing light at night could help beat jet lag, Stanford study says

plane in sunsetThe body will eventually adjust to jet lag, it’s just that it takes time — about an hour a day to be precise. And anyone who has suffered the unpleasant side effects of jet lag – brain fog, body achiness, an overwhelming need for endless pots coffee — might have an interest in speeding the process up.

A new Stanford study suggests that exposing travelers to short bursts of flashing lights the night before a trip while asleep could help speed up the process significantly. In a press release I wrote on the study, which was published today in the Journal of Clinical Investigation, researchers explained how this works at a biological level:

The transfer of light through the eyes to the brain does more than provide sight; it also changes the biological clock. A person’s brain can be tricked into adjusting more quickly to disturbances in sleep cycles by increasing how long he or she is exposed to light prior to traveling to a new time zone.

Light therapy is designed to speed up the brain’s adjustment to time changes. By conducting light therapy at night, the brain’s biological clock gets tricked into adjusting to an awake cycle even when asleep. It’s a kind of “biological hacking” that fools the brain into thinking the day is longer while you get to sleep.

 To determine whether continuous or flashing lights would provide the fastest method of sleep cycle adjustment, researchers had 39 study participants sleep in a lab, exposing some to continuous light for an hour, and others to flashing light for an hour. They found that the flashing light —which most could sleep through just fine— elicited about a two-hour delay in the onset of sleepiness, while those exposed to continuous light, the delay was only 36 minutes.

Jamie Zeitzer, PhD, the senior author of the study, described how flashing-light therapy could be used to adapt to traveling from California to the East Coast: “If you are flying to New York tomorrow, tonight you use the light therapy. If you normally wake up at 8 a.m., you set the flashing light to go off at 5 a.m. When you get to New York, your biological system is already in the process of shifting to East Coast time.”

“This could be a new way of adjusting much more quickly to time changes than other methods in use today,” he told me.

Previously: Cheating jet lag: Stanford researchers develop methods to treat sleep disturbances, Why sleeping in on the weekends may not be beneficial to your health, How sleep acts as a cleaning system for the brain, Study shows altered circadian rhythms in the brains of depressed people, Jet-lag drug is a no go and Jet-lagged hamsters flunk IQ test
Photo by Eric Prado

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