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.”
You might have thought this was Lincoln’s birthday, or just Presidents’ Day weekend, but today is also the 207th anniversary of Charles Darwin’s birthday, otherwise known as Darwin Day.
I called Paul Norman, PhD — a senior research scientist who studies genetic variation, especially in human immune cells — and asked him how the theory of evolution has influenced his work. In a charming academic parry and thrust, he immediately pointed out to me that Darwin didn’t come up with the theory of evolution.
The idea that living organisms can change, or evolve, over time had been around for a long time. Even the related idea that all organisms are related through “common descent” from a single ancient ancestor wasn’t entirely new.
What Darwin did was come up with was a mechanism — natural selection — that could explain how evolution could happen. And Darwin was able to persuade people that evolution is happening all around us and how it works. He left an indelible stamp on all of biology.
It turns out that Norman has a special connection to Darwin: The two scientists were born and raised just a mile apart in the same medieval town of Shrewsbury, where Darwin famously hiked, hunted and collected beetles.
Evolution informs the work that Norman does every day, as well as that of most people in the biological science, he says. “It’s rare that one person has such a long lasting influence.”
It’s frightening to think that coronary artery disease is the most common cause of death globally. And it’s scarier to think that few people likely know much about it. Who’s at risk? How do you prevent it? How do you treat it? In a recent BeWell@Stanford interview, Themistocles Assimes, MD, PhD, answered some of these questions and more:
Risk factors for the development of CAD include older age, male sex, smoking, elevated blood pressure, diabetes, physical inactivity, and elevated bad cholesterol in the blood stream…
The most dreaded complication of CAD is a myocardial infarction, or “heart attack” — which occurs when the lining of a plaque inside the vessel breaks open and spills the contents of the plaque into the blood stream.
Fortunately, CAD is not a death sentence and can be treated. In the piece, Assimes explains the importance of helpful medications: blood thinners such as aspirin, which prevent clots from forming, drugs that lower blood pressure, and drugs that lower bad cholesterol. But more importantly:
The good news is that everyone can reduce his or her risk of CAD by maintaining a healthy weight and through regular aerobic exercise. These two lifestyle factors have beneficial effects on multiple risk factors. A diet that is low in saturated fats appears to decrease the risk of CAD, not only by making it easier to maintain a healthy weight, but also by reducing bad cholesterol levels in the blood stream.
Read the full Q&A for more helpful information on CAD.
One 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.
When Carla Shatz, PhD, was an undergraduate at Radcliffe College, her grandmother suffered a stroke that left her partially paralyzed and unable to speak. Shatz was devastated.
“My grandmother was the first person in our family to go to college, and she was an unbelievable athlete and a brilliant woman,” she told a Stanford audience during a recent Personal Perspectives lecture hosted by the Translational Research and Applied Medicine (TRAM) program in the Department of Medicine.
“After the stroke, my grandmother was miserable. All of these diagnosticians could say exactly where the stroke was, but there weren’t many treatment options.” The experience unexpectedly sparked Shatz’s curiosity – and got her thinking about neuroscience and the brain.
Today, Shatz, the director of Stanford Bio-X, is widely considered a leader in neuroscience. She has spent the last 40 years studying the brain and has made significant discoveries about its development and plasticity. She has authored over 120 publications, received countless awards and nurtured the careers of many young academics.
She’s also blazed trails for women in science. She was the first woman to receive a PhD in neurobiology from Harvard and later became the first female chair of the same program. She was also the first woman to receive tenure in the basic sciences at Stanford.
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.
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).
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.
The Zika virus has been reported in 23 countries and territories in the Americas. Brazil is the hardest hit nation so far with more than 1 million infections. In the continental U.S. the 35 known cases of Zika have been the result of people who have traveled to infected areas and returned to the U.S. No local mosquito-borne transmission has been reported.
Globalization has changed the rapid nature in which viruses spread. To that end, broad calls for action have been engaged. The World Health Organization has declared Zika an international health crisis, and the U.S. Centers for Disease Control and Prevention declared it a Level 1 alert – the highest activation. Earlier this week, President Obama asked Congress to allocate $1.8 billion in emergency finding to vaccine research, surveillance and rapid response programs. The request also includes foreign aid to countries most impacted by Zika.
While the virus is not known to be deadly and most people who contact it will have no symptoms at all, pregnant women are most at risk. To protect their babies, the CDC is warning pregnant women not to travel to areas affected by the virus. There is no vaccine to prevent the disease.
The New York Times yesterday provided an interesting detailed history of the virus’ path since its discovery in 1947, and new information about the virus is emerging every day. Just yesterday, CDC Director Thomas Frieden told the House Foreign Affairs Committee that the CDC has uncovered new evidence supporting the link between Zika and microcephaly, a birth defect in which infants are born with unusually small heads and incomplete brain development.
In this new 1:2:1 podcast I spoke with Stanford infectious disease expert Yvonne Maldonado, MD, about Zika and the latest on the virus. She’s a professor of pediatrics at the school of medicine and the chief of pediatric infectious disease at Stanford Children’s Health.
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.
“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.