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Neuroscience, Research, Science, Stanford News

Building for collaboration spurs innovative science

Building for collaboration spurs innovative science

clarkWhen Stanford’s original main quad was built 125 years ago, it was with the intent of bringing faculty together in its outdoor spaces and walkways. From its inception, the university was a place where faculty were encouraged to collaborate across disciplines.

Nothing has done more to extend that original idea than the James H. Clark Center, which opened in 2003 at the intersection of the Schools of Medicine, Engineering and Humanities and Sciences. It was built as a home for Stanford Bio-X, which brings faculty together from across disciplines to solve problems in the life sciences.

As people around the world began seeing the kind of science that came out of the interdisciplinary mix in the Clark Center, that style building has begun springing up world-wide. In fact, in 2014, the National Academies specifically pointed to the Clark Center as one way of encouraging what they call “convergence” science.

Stanford has since constructed another building to encourage collaboration (the Jerry Yang and Akiko Yamazaki Environment and Energy Building) and just broke ground on a research facility to house the two newest interdisciplinary institutes: Stanford ChEM-H and the Stanford Neurosciences Institute.

In my story about this building trend, Ann Arvin, MD, Stanford’s dean of research and vice provost, comments, “This building is a physical manifestation of Stanford’s commitment to breaking down barriers between disciplines.”

Arvin went on to say that she thinks disciplines still need to be strong, but that the really innovative research is taking place at the intersections between those disciplines. The new research facility will be across the street from the Clark Center, perfectly poised to continue bringing disciplines together around problems in neuroscience and human health.

Previously: They said “Yes”: The attitude that defines Stanford Bio-X and Stanford’s Clark Center, home to Bio-X, turns 10
Image from Stanford Office of Development

Aging, Big data, Genetics, Research, Science, Stanford News

Genetic links to healthy aging explored by Stanford researchers

Genetic links to healthy aging explored by Stanford researchers

Old man with babyIs the secret to a long life written in your genes? Or will your annual merry-go-rides around the sun be cut short by disease or poor health? The question is intriguing, but difficult to answer. But that hasn’t stopped researchers from looking for genes or biological traits that may explain why some people live to be very old while others sicken and die at relatively young ages.

Today, developmental biologist Stuart Kim, PhD, published some very interesting research in PLoS Genetics about regions of the human genome that appear to be associated with extreme longevity  (think upper 90s to over 100 years old).

One, a gene called APOE, is associated with the development of Alzheimer’s disease. It’s been previously been implicated in longevity. However, the other four regions identified by the study are new. They are involved in biological processes such as cellular senescence or aging, autoimmune disease and signaling among cells.

As explained in the journal’s press release:

Previous work indicated that centenarians have health and diet habits similar to normal people, suggesting that factors in their genetic make-up could contribute to successful aging. However, prior genetic studies had identified only a single gene (APOE, known to be involved in Alzheimer’s disease) that was different in centenarians versus normal agers.

As we’ve explained here before, studying the very old is difficult, in part because there are so few of them. That makes it hard to come up with statistically significant results when comparing them to others. For this study, Kim and his colleagues devised a new technique to identify regions of the genome associated with longevity by linking it to the likelihood of developing other common diseases or disease-related traits, including type 2 diabetes, bone density, blood pressure and coronary artery disease.

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Bioengineering, Evolution, Research, Science, Stanford News, Technology

Fast-forwarding evolution to select suitable proteins

Fast-forwarding evolution to select suitable proteins

4286076672_2763323a1e_zNature churns out new versions of proteins in response to environment changes or random mutations. Sometimes the new versions work better than old. Other times, not.

But now, Stanford researchers have developed a super speedy technique to test millions of versions of a certain protein to see which one works best.

A Stanford news release explains:

The researchers call their tool µSCALE, or Single Cell Analysis and Laser Extraction.

The “µ” stands for the microcapillary glass slide that holds the protein samples. The slide is roughly the size and thickness of a penny, yet in that space a million capillary tubes are arrayed like straws, open on the top and bottom.

The microcapillary glass slide, roughly the size and thickness of a penny, holds the protein samples.

The power of µSCALE is how it enables researchers to build upon current biochemical techniques to run a million protein experiments simultaneously, then extract and further analyze the most promising results.

The research was led by Jennifer Cochran, PhD, associate professor of bioengineering and Thomas Baer, PhD, executive director of the Stanford Photonics Research Center.

The system is easy to use with numerous applications, Baer said.

“Evolution, the survival of the fittest, takes place over a span of thousands of years, but we can now direct proteins to evolve in hours or days,” Cochran said in the release.

Previously: Proteins from pond scum revolutionize neuroscience, Study shows toothed whales have persisted millions of years without two common antiviral proteins and Computing our evolution
Photo by Alexander Boden

Events, Genetics, Research, Science, Stanford News

Personalised Health Conference explores paradigm shift from treating disease to maintaining wellness

Personalised Health Conference explores paradigm shift from treating disease to maintaining wellness

Lars Steinmetz talkingWhat does it mean to be healthy? This is an important question for the numerous laboratories and hospitals worldwide who dedicate their livelihoods to defeating disease. Thanks to breakthroughs in biotechnology, researchers are starting to develop a more thorough profile of health – and to realize how different it can be from person to person. “We should all go get our ‘healthy’ profiles now before we get sick,” insists Michael Snyder, PhD, professor and chair of Stanford’s Department of Genetics.

Understanding what health means at an individual, molecular, and systematic level was the focus of the recent Personalised Health Conference at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany. Notably, the conference served as the kickoff event for the EMBL-Stanford Life Science Alliance and was the first of many anticipated joint conferences. In a preview of the interdisciplinary collaborations the alliance will enable, the four-day conference brought together international experts in genomics, healthcare, bioethics, bioinformatics, cancer, and more.

“The technologies now at our disposal are ushering in a change in the state of medicine, from reactive to proactive, from treating disease to maintaining health,” said Lars Steinmetz, PhD, the conference’s main organizer, in his opening remarks. Steinmetz is spearheading the EMBL-Stanford Life Science Alliance, inspired by his dual affiliation: At Stanford, he is co-director of the Stanford Genome Technology Center (SGTC); at EMBL, he is associate head of the Genome Biology Unit.

The conference was kicked off with a keynote lecture from Leroy Hood, MD, PhD, president and co-founder of the Institute for Systems Biology, who is widely known as the father of personalized medicine. In addition to his vision for systems medicine, Hood presented the 100K Wellness Project, a longitudinal, multiparametric study that generates “dynamical data clouds” for 100,000 healthy individuals.

“By studying the earliest wellness to disease transitions, we aim to enable the earliest reversal of disease back to wellness,” said Hood. “Understanding wellness will allow individuals to reach their full health potential. I predict that a major scientific wellness industry will emerge to play a dominant role in the democratization of health care.”

Hood’s vision was supported by several research efforts presented at the conference. Snyder’s integrative personal omics profiling (iPOP) protocol here at Stanford now measures billions of molecular parameters in several individuals over time, in efforts to develop predictive models of disease that integrate genomic, molecular, environmental, and physiological datasets. Genomics England’s Tim Hubbard, PhD, presented the United Kingdom’s 100,000 Genomes Project, which aims to leverage genome sequence data in the treatment of 100,000 people in the national healthcare system with unmet clinical needs. As the largest national project of its kind, it will help to establish principles and frameworks for incorporating genomics into standard clinical care.

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Podcasts, Research, Science

On communicating science and uncertainty: A podcast with John Ioannidis

On communicating science and uncertainty: A podcast with John Ioannidis

If you listen to one podcast this week, pick this one. It’s a crisp, thought-provoking exchange between health journalism critic Gary Schwitzer, publisher of HealthNewsReview.org, and epidemiologist John Ioannidis, MD, DSc, recorded at the recent METRICS (Meta-Research Innovation Center at Stanford) conference. They tackle the state of health journalism and the problems plaguing science, all in just 7 minutes and 49 seconds.

(Quick background: Ioannidis is well-known for his blockbuster 2005 paper, “Why most published research findings are false” – and the first METRICS conference brought together researchers from a variety of fields to examine ways to improve the quality of science.)

Schwitzer points out that from the public’s point of view, there’s a fine line between critiquing science and declaring the entire scientific enterprise rubbish.

Ioannidis responds:

Science is the best thing that has happened to human beings. One key reason for that is that it helps people think carefully about the world surrounding them and about themselves and their knowledge base…

The way to educate the public is really to offer them science as it is, not in any way that would be more dogmatic than it should be and then have to fight against other types of dogmas. I think we need to tell people that this is why science is important, that it does have that threshold of uncertainly that dogma doesn’t have.

Previously: A conversation with John Ioannidis, “the superhero poised to save” medical research, Shake up research rewards to improve accuracy, says Stanford’s John Ioannidis and John Ioannidis discusses the popularity of his paper examining the reliability of scientific research 

 

Science, Science Policy, Stanford News

At Stanford, Rep. Jerry McNerney discusses life in Congress, science funding and the value of squash

At Stanford, Rep. Jerry McNerney discusses life in Congress, science funding and the value of squash

McNerny on campusFor many of us who work in or around science, it can be baffling to watch some of the decisions made by politicians. Some neuroscience faculty, staff and students got a look behind the scenes of what it’s like to be a scientist in government on Friday from congressman Jerry McNerney, PhD, who represents California’s 9th district. (His degree is in math). McNerney was at Stanford touring neuroscience labs at the VA and on campus, hosted by the Stanford Neurosciences Institute, and he took a pause at lunch for a town hall to answer questions about science, policy, and life in government.

McNerney talked about the challenges of explaining science to his colleagues and advocating for science-based policy on issues relating to energy and the environment as well as funding for biomedical research. He said one of his greatest tools is athletics. If he plays squash with someone he disagrees with, it’s easier to have calm conversations about policy. “If you communicate in an aggressive way you make it worse,” he said. “But you have to work at it.”

He encouraged scientists in the audience to talk with those they disagree with because their voices need to be heard. “To be a great country and a leader we need great research,” he said. Ensuring funding for that research is going to require scientists to be actively involved in explaining the value of their work.

McNerney was particularly interested in research related to traumatic brain injury, which is a critical problem for veterans returning from duty. He visited the lab of bioengineer David Camarillo, PhD, who is developing better ways of measuring head impacts and the damage they cause.

“We want to do the best we can to help these folks,” McNerney said.

Image of Rep. McNerney learning about concussion prevention by Tanya Raschke

Aging, Evolution, Genetics, Research, Science, Stem Cells

The war within: In our aging bodies, the “fittest” stem cells may not be the ones that ensure our survival

The war within: In our aging bodies, the "fittest" stem cells may not be the ones that ensure our survival

ageAnti-aging research has been in the news lately: for instance, here, here and (less recently and less frivolously) here.

Albert Einstein College of Medicine researcher Nir Barzilai, MD, who’s spearheading the groundbreaking anti-aging trials referred to in these articles, is far from frivolous. I remember really liking a talk he gave at Stanford a few years ago about his ongoing study of super-old Ashkenazis, at a symposium sponsored by Stanford’s Glenn Laboratories for the Biology of Aging.

Now, Tom Rando, MD, PhD, the director of Glenn Labs at Stanford, has co-authored a thought-provoking review in Science that advances a theory of why we age.

It’s not the only theory. Judy Campisi of the Buck Institute for Research on Aging, for example, has explored the detrimental activities of differentiated cells gone wrong within our tissues. The older the tissue, the wronger the cells in it go.

Rando and his co-author, Baylor College of Medicine regenerative-medicine expert Margaret Goodell, PhD, come at aging from the opposite end of the spectrum: stem cells, the least-differentiated cells in the body. In particular, Rando and Goodell target the aging-associated actions of so-called somatic stem cells, which reside in virtually all (and, probably, actually all) of our tissues and whose fates are restricted to spawning only cell types that belong in those tissues. While we’re growing up, those somatic stem cells are the reason why: They divide to generate the differentiated cells that bulk us up. Once we’ve matured, they mostly hang back, springing into action to replace tissue lost to injury or to wear and tear.

Radiation, noxious foreign substances, and plain old existence wreaks sporadic damage on somatic stem cells by triggering genetic mutations or by altering the cells’ epigenetic settings, the patterns of chemical stop-and-go signs that variously switch the 20,000-odd genes in each cell’s genome on or off. These insults pile up as life’s pages turn. Eventually, Rando and Goodell write, a curious, Darwin-like natural selection occurs among our tissue-resident stem cells.

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Cancer, Neuroscience, Research, Science, Stanford News

“Chemobrain” studied by researchers at Stanford, MD Anderson

"Chemobrain" studied by researchers at Stanford, MD Anderson

5490361039_7af0ae216b_zIt’s an unfortunate fact that even successful cancer treatment can leave lasting scars. Surgeries are sometimes needed to remove tumors, skin can be permanently damaged from radiation therapy and powerful chemotherapy drugs can wreak havoc throughout the body.

One of the least understood lasting effects, however, is a cognitive deficit that some survivors describe as “chemobrain.” The difficulties they experience in focusing and remembering are attributed to the neurotoxic effects of chemotherapy. But it’s not been clear whether some drugs are worse than others in this regard.

Now Stanford oncologist Douglas Blayney, MD, and former Stanford faculty member Shelli Kesler, PhD, have published a study in JAMA Oncology assessing cognitive defects in a group of 62 breast cancer patients treated between 2008 and 2014. About one-third of the patients had received a class of chemotherapy drugs that are anthracycline-based, like doxorubicin; one-third received other chemotherapy drugs that were non-anthracycline-based; and the remainder received no chemotherapy at all.

As Blayney explained in an email to me:

Chemotherapy for breast cancer is often associated with cognitive problems in patients. However, it is unclear whether certain treatment regimens are associated with greater cognitive difficulties than others. In a small study, we showed that women treated with anthracycline-based chemotherapy had lower verbal memory, including immediate recall and delayed recall, compared with non-anthracycline chemotherapy treated breast cancer patients, and breast cancer patients not treated with chemotherapy.

Kesler, who has published before on chemobrain in breast cancer patients, is now at MD Anderson Cancer Center in Texas.

Although their results are intriguing, Blayney cautions that the study was relatively small and it’s too soon to start ruling out one type of chemotherapy over another. But it’s important to begin these types of analyses. He writes:

Patient-reported outcomes of cognitive dysfunction and psychological distress were elevated in both groups of women treated with chemotherapy compared with patients treated without chemotherapy.  Our study is hypothesis generating, involves small numbers of patients, there is no dose-response information available, and it is way too soon to abandon doxorubicin adjuvant treatment, which remains a valuable chemotherapeutic agent.  We are currently enrolling in a larger, longitudinal study of women measuring cognitive functioning before any treatment, after completion of systemic treatment, and one year later.

Previously: Wellness after cancer: Stanford opens clinic to address survivors’ needs,  A look at stem cells and “chemobrain” and Stanford study shows effects of chemotherapy and breast cancer on brain function
Image by Steve Snodgrass

Aging, Genetics, Research, Science, Stanford News

A tiny fish helps solve how genes influence longevity

A tiny fish helps solve how genes influence longevity

Nothobranchius_furzeri_GRZ_thumb_wikimedia_UgauA tiny, short-lived fish may help solve one of the largest mysteries: how do genes influence longevity?

The African turquoise killifish has evolved as the shortest-lived known vertebrate — driven by its survival in the hot climate of Mozambique and Zimbabwe in seasonal ponds that only exist for a few months during the wet season. This compressed life span makes the killifish an ideal organism for genetic studies on aging and longevity.

To help researchers study this intriguing animal model, Stanford geneticist Anne Brunet, PhD, and her colleagues have now fully mapped the genome of the African turquoise killifish. Their initial insights into the genetic determinants of the killifish’s life span were published today in Cell.

Brunet’s team sequenced short segments of the killifish DNA and then assembled them using specialized software to create a complete map of the turquoise killifish genome.

Brunet explains in a news release:

The range of life spans seen in nature is truly astonishing, and really we have very little insight into how this has evolved or how this works. By having the genome of this fish and comparing it to other species, we start seeing differences that could underlie life span differences both between species and also within a species.

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Big data, Events, Science

At TEDMED 2015: Using data to maximize human potential

This year’s TEDMED was held Nov. 18-20 in Palm Springs, Calif. Stanford Medicine is a medical research institution partner of TEDMED, and a group of MD and PhD students who represented Stanford at the conference will be sharing their experiences here. 

A tall, striking woman walked out onto the TEDMED stage. Energetically and confidently, Vivienne Ming, PhD, a theoretical neuroscientist and entrepreneur, went on to tell us about her passion for optimizing human potential utilizing big data.

There are many examples where Ming has used data for social good, such as matching refugees to their families with image-recognition software, but here at TEDMED she discussed personalized education. By looking for trends and patterns in classroom data, she has built an educational tool that predicts a child’s grade trajectory in the class and then chooses the highest impact personalized intervention for each individual student. Using data-science techniques to study society and education, Ming dazzles us with the possibilities of data in improving our capacity to reach our individual potentials.

Ming completely upended my view on data science in social issues

As a graduate student applying these same techniques to the field of genomics, I was intrigued. My understanding of data science applied to the social sciences, such as in the field of economics, was that the modeling remained fairly straightforward and simple: Understandable models were very important for the social sciences, and complex data-science models were not very interpretable. As a medical student, I found this frustrating – my interests lay both in cutting-edge computational advances as well as empathy for human suffering, and I couldn’t figure out how to apply my data-science skills beyond the world of science to answer questions of social and health inequalities.

Ming completely upended my view on data science in social issues. I was fortunate enough to have the chance to chat with her the next day, and I asked her about the computational work, as I was curious how complex her models really could be. She displayed a wonderful technical capacity and a deep understanding of how to choose the right algorithms for the social problems at hand. Granted, it’s still not common to find such imaginative interdisciplinary work combining cutting-edge computer science work and social science work. But Ming showed me a world of possibility around bringing data skills into improving everything from hiring to education to gender equality. I came away impressed, inspired, and excited about the possibilities of utilizing my own skills in the world beyond genomics.

Working at the intersection of two fields can be extremely challenging to impossible. And it’s particularly tricky to apply the latest data-science methods to societal questions. As such, to be able to intelligently and thoughtfully do the two together is an art – and Ming is a master of the important intersection where computation meets humanity.

Daniel Kim is a fifth-year MD/PhD student at Stanford. He studies biomedical informatics and genomics and is interested in all things data-related.

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