Developing “guided missiles” to attack cancer: A podcast featuring a Stanford bioengineer

Posted March 16, 2018 by Jennifer Huber
Categories: Health, biology

Tags: ,

Photo by Allocer

Chemotherapy attacks cancer by killing cells that are rapidly dividing. But this leads to serious side effects, like intestinal upset and hair fallout, because these normal cells grow quickly.

So researchers like Jennifer Cochran, PhD, a professor and the chair of bioengineering at Stanford, are developing more targeted cancer therapies, dubbed “guided missiles.” She recently described her work to professor and radio show Russ Altman, MD, PhD, on an episode of the Sirius radio show The Future of Everything.

“We, and others, have developed novel proteins that can selectively target cancer cells and then we can attach cargo to them — this is where the missile analogy comes in,” Cochran told Altman. “The cargo that we attach, things like chemotherapy, can then be selectively targeted to the tumor.” The idea is to precisely deliver to the tumor a more poisonous dose than you could deliver systemically, she said.

One way to do this is to bioengineer antibodies, which are molecules that recognize and help neutralize foreign substances like bacteria. However, Cochran’s lab took a slightly different approach. She explained to Altman:

“As amazing as antibodies are, they can have some limitations in that they are very large in terms of molecular size so they have trouble wiggling into a tumor. So we’ve created smaller versions of tumor-targeting proteins that can hopefully penetrate into tumors better. And we’ve then chemically attached chemotherapy molecules to deliver a punch to the cancer cells.”

In order to develop these proteins, her team is expediting protein evolution in a test tube — making favorable properties that would normally evolve over millions of years happen in just a few weeks. To do this, the team uses genetic manipulation to create millions of slightly different protein variants, tests them with high-throughput screening in just a few hours, identifies the ones most desirable for a certain task, and then determines these variants’ DNA sequences.

For example, they used this evolutionary process on a peptide, a small fragment of protein, from the seeds of a plant known as a squirting cucumber to turn the molecule into a favorable drug scaffold. “We ran the protein through this evolution process to create a tumor-targeting protein that we then hooked the chemotherapy agents on to,” said Cochran.

Cochran’s group is also investigating immunotherapy applications for her proteins. She is teaming up with Dane Wittrup, PhD, a professor in chemical engineering and biological engineering at Massachusetts Institute of Technology, who has developed new ways to use the immune system. By combining Cochran’s tumor-targeting technology with Wittrup’s insights into immunotherapy, they are able to give a “one-two punch” and activate multiple factors of the immune system to more effectively attack cancer, she said.

Her research team is also interested in applying their work to other diseases. She explained to Altman:

“We’ve been applying them for cancer, but you can use the same approach to deliver therapies to other types of disease tissue. We have really only just scratched the surface of what we can do. A big driver of this has been the interdisciplinary culture of collaborative research at Stanford. We’ve been working together with physicians, clinicians, scientists, engineers and physicists to tackle really challenging problems.”

Cochran’s bioengineered proteins are not yet available to patients. However, some tumor-targeting molecules are already approved by the U.S. Food and Drug Administration and many more are in the pipeline. “There are a number of molecules that are FDA approved and you might have heard commercials for them,” she told Altman. “But they only work for a subset of patients. So the question is: how do we make them work better for a larger subset of patients?”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


BrainPost: Neuroscience summarized and delivered to your inbox

Posted March 14, 2018 by Jennifer Huber
Categories: Health

Image by Laszlo Ilyes

Like most busy professionals, neuroscientists have trouble keeping up with everything that’s going on in their field. They just don’t have enough time to read all the papers being published.

Neuroscientists Kasey Hemington and Leigh Christopher, PhD, a Stanford postdoctoral researcher, want to help. They created a new weekly e-newsletter, called BrainPost, that sends easy-to-read summaries of the latest neuroscience publications into their readers’ inbox. To learn more, I spoke with Christopher recently.

What inspired you to create BrainPost?

“Throughout my PhD and during my postdoc, I noticed two trends. First, when I talked to other neuroscientists, they were often unaware of research going on in closely related fields. I know that science is specialized, but it dawned on me that if scientists themselves are unable to keep up with other research, there was no way that members of the general public could even begin to stay on top of the latest advances. The second trend is one of too much data. I think with big data comes big confusion. We have too much to consume and therefore we often choose not to consume at all, because it’s overwhelming.

We wanted to simplify the process of consuming neuroscience, which is constantly changing. We also wanted to make the information easily accessible when open access to the original scientific publications is not an option. Hopefully, BrainPost can help make neuroscience convenient, fun and digestible.”

Who is your primary target audience?

“BrainPost summaries provide a little more information than traditional science journalism aimed at the general public. We primarily want to improve awareness about new neuroscience research within the science community. This means anyone who is engaging with neuroscience: a researcher, graduate student, undergraduate student, biotech employee, policy maker, clinician, psychologist, science journalist or science enthusiast. We want to encourage cross-discipline communication and collaboration.”

What is your selection and writing process?

“We choose recently published online articles from reputable journals that we feel are high quality and move neuroscience forward. We would love to cover more, but for now, we are limited by time as only myself and Kasey are working on the newsletter. In the future, we want to bring on more writers.

We send out all of our summaries to authors before publishing the e-newsletter. We’re able to incorporate their edits and comments to ensure our summaries are accurate and don’t sensationalize the findings or misguide the reader.

We hope to eventually cover most of the latest neuroscience publications on our website, acting as a continuously updated resource for neuroscience. Our ultimate goal is to expand and have customized newsletters on topics of interest, as well as a repository of summaries on our website.”

Why do you encourage readers to connect directly with the study authors?

Kasey had this great idea to engage scientists by asking them to comment and to respond on social media. Social media can have a positive impact on the way we communicate about science. We want readers to start discussions with study authors to help create a more cohesive community amongst people engaging with neuroscience. When scientists are more social and vocal about their work, it helps to get the word out and for them to be better understood.

All of the scientists who we’ve reached out to on Twitter so far have been very enthusiastic and responsive. I think they’re excited to have their work recognized, since the academic world does not always offer enough of this recognition. BrainPost will hopefully help with that.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


On writing about female physicians and the Grand Canyon: A Q&A

Posted March 12, 2018 by Jennifer Huber
Categories: Science Education

Tags: ,

Photo by DomCarver

As a voracious reader, I particularly enjoy mystery novels featuring a female detective or medical examiner. And as physicians know so well, medical mysteries can be just as gripping, and surprising, as crimes. So I was eager to read the novel, Only Rock is Real, about a female doctor with a family practice at the Grand Canyon. I spoke recently with the book’s author, Sandra Miller, MD, who is a writer and retired family physician.

What motivated you to write novels?

I have always written poetry and essays, but crafting a novel pushes my writing to another level. The process of weaving a plot — while creating compelling and authentic characters, developing their growth and showing their stumbles — is riveting to me. The greatest compliment is when readers tell me they feel like they know my characters personally and care about them.

I’m also on a mission to promote family medicine and women physicians through fiction. I really want to encourage physicians to write, and especially to write fiction. There is little medical fiction being written currently, with the exception of the crime scene/thriller genre. I would love to see more fiction about everyday physicians and their trials and joys. And I welcome with any medical writers who want to brainstorm, share or seek feedback about their work.

How did you develop the main character, Dr. Abby Wilmore?

Like most fictional characters, Abby is partly a conglomerate of people I have known and partly made up. Every physician wants to be highly competent and strives for excellence, but there are many potholes along that path. Perfectionism and anxiety are common in doctors; finding your peace with an ever changing and critical career like medicine is no small task. I wanted to show how her confidence builds and then derails — the ups and downs of successes and errors, real or perceived, in both her professional and personal life. I wanted to show how very human physicians are.

How did you select which patient cases to include?

I tried to use a mix of cases representing a typical day: some common and some less common, some routine prevention and occasionally a very difficult case. I also wanted to include a mix of physical and mental health issues. I guess the teacher in me is always lurking, because I also selected cases where readers can learn about topics like diabetes, the morning after pill and contraception, heat injury and flu vaccines.

I keep them as realistic as I can. Sometimes you know the diagnosis immediately and other times it takes detective work. Sometimes you’re wrong because people aren’t textbooks and they don’t always follow the rules. I’ve put much effort into making all the science — medicine, geology and astronomy — as accurate as I can.

Why did you set your books in national parks?

For the last thirty years of my career in academic medicine, I helped train family medicine residents who often did a rotation at the Grand Canyon clinic. And I have friends who worked there for years. I know their stories, the human dynamics in such unusual places. Only a few national parks actually support a physician.

In addition, I have always felt a deep connection to the natural world. We’re all constructed of the same molecules; all follow the same rules of development and decay. The wonders around us are simply stunning and worth celebrating.

How do you describe your books?

I’m calling my books ‘evidence-based medical adventures.’ There is romance and a bit of a thriller plot, but the books are also filled with tons of real medicine, science and the quandaries physicians face every day. And the poetry of the night sky and the rock under our feet, not to mention the value of humor.

Are there similarities between writing and being a family physician?

I think it helps for both to know you can never know everything. And that much of life comes at us in tones of gray. Being a family physician certainly gives you a broad view of the world and the vagaries of the human mind. You need to know as much as you possibly can and you need to know what you don’t know. You keep trying your best. I think this experience helped me as a writer.

Photo by DomCarver

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


Use your range hood for a healthier home, advises indoor air quality expert Brett Singer

Posted March 9, 2018 by Jennifer Huber
Categories: Health

Tags: ,

Photo courtesy of Brett Singer.

Most Americans don’t realize cooking can be a major source of indoor air pollutants, unless they’ve recently burned something on the stove. But studies have shown that cooking-related contaminants can cause health problems such as respiratory illness and asthma attacks.

To learn more, I spoke with Brett Singer, PhD, a scientist at Berkeley Lab who investigates indoor air quality. Recently, he measured the levels of pollutants emitted from gas cooking burners and ovens in several Bay Area homes. I asked him about this study and for advice on how to reduce cooking pollutants.

Are harmful pollutants emitted when cooking?

“A gas burner almost always produces significant quantities of nitrogen dioxide, which is a respiratory irritant. Depending on the burner configuration, it can also produce carbon monoxide, which is regulated by the Environmental Protection Agency. In general, newer cooktop burners don’t produce much carbon monoxide because of design improvements. Finally, the gas produces ultrafine particles, smaller than 100 nanometers, which are dangerous because they can move around your body in ways that larger particles can’t.

Electric burners don’t produce carbon monoxide and produce only small amounts of nitrogen dioxide. But an electrical coil burner can produce ultrafine particles, particularly when you first turn it on.

Cooking food on either type of burner also produces fine particles and some organic chemicals, including acrolein and polynuclear aromatic hydrocarbons that are known to be hazardous. Frying, broiling and other cooking at high temperatures generally produces more pollutants.

However, these pollutants can be easily addressed with good kitchen ventilation, which is especially important if you live in a small home.”

What did your in-home study find?

“We went into moderately sized homes — eight 1,400 to 2,500-square-foot homes and one small apartment — with common, well-functioning equipment that had been in use for a few years. We measured the concentrations of pollutants in the kitchen and elsewhere as we boiled and steamed water on the cooktop and/or oven, with and without ventilation. We found issues in half of these homes and that’s not good. In four of the homes, we showed that the gas-cooking burners emitted enough nitrogen dioxide to exceed the health standards for outdoor air.”

What are your tips to minimize these cooking pollutants?

“The first tip is to ventilate when you cook, and to ventilate more the more you cook. Range hoods are the most effective way to do this, if your range hood actually moves air out of the kitchen. If you have a range hood that just recirculates air back into the kitchen, you need to use another exhaust fan — for example, from a nearby bathroom — or open windows.

You also need to use your hood or exhaust fan regularly. Based on several surveys, many people only occasionally use them. People report not using them because they’re noisy, because people forget to turn them on or because they aren’t needed unless removing smoke, odors and moisture — like when frying something stinky. Those are good reasons to use ventilation, but people can’t sense pollutants, so they may not be ventilating sometimes when it’s really needed.

If you’re buying a new range hood, buy a quiet one that you like. If it isn’t quite as efficient but you’re happy with it and you’ll use it, then great. To improve on that, a range hood needs to have higher flow rates and cover the front burners.

Beyond that, almost any range hood works better if you cook on the back burners. If you put it on a low speed and cook on a single back burner, then you’ll typically capture 50 to 70 percent of the pollutants.”

What is the ultimate goal of your research?

“The goal of our work on kitchen ventilation is to help people cook all they want  — with gas or electric — without exposing themselves to harmful air pollutants. This is an important part of our broader work on high performance homes that use very little energy and provide a healthier environment for their occupants. We try to provide the science to inform builders, retrofit contractors and the general public.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


Tackling the “childcare-conference conundrum”

Posted March 6, 2018 by Jennifer Huber
Categories: Other

Tags: , ,

Attending conferences is a critical part of professional development, particularly for early-stage academic researchers. At these meetings, scientists further their careers by presenting their research discoveries and networking with potential collaborators, employers and funding agencies.

However, many early-stage researchers are moms who are primary caretakers of their children, which makes it difficult to attend conferences that lack childcare accommodations. Recently, a group of women scientists came together to address this “childcare-conference conundrum.”

The group, called a Working Group of Mothers in Science, was spearheaded by Rebecca Calisi, PhD, an assistant professor at the University of California, Davis. Last fall, she reached out to other women scientists after attending a large neuroscience conference — including Stanford’s Erin Gibson, PhD, a research scientist in neurology, and Lauren O’Connell, PhD, an assistant professor of biology — and this led to the formation of the group of almost 50 women last December.

The working group wants to help conferences establish safe and effective childcare options for all working parents with young children. They argue that solving the childcare-conference conundrum will help primary caretakers, foster scientific advancements and innovation by allowing a population of scientists to remain engaged, and benefit the conferences themselves and businesses associated with them.

“While childcare disproportionately affects women and their career mobility especially in the sciences, we want to bring attention to this problem as it can impact all parents from breast-feeding mothers to fathers who are the primary caretakers,” explained Gibson. “Relatively simple changes could dramatically affect the lives of primary caregivers at these conferences. And the more well-trained scientists we can keep in science by not leaving them out due to childcare restrictions, the more the entire scientific community benefits.”

In an editorial published this week in the Proceedings of the National Academy of Sciences, the group outlined four concrete recommendations for organizations:

  • Provide financial support for individually arranged childcare for smaller conferences and onsite childcare for larger ones.
  • Select family-friendly dates, venues and daily schedules.
  • Provide adequate facilities and equipment, including lactation areas with storage lockers for breast pumps and refrigeration for expressed milk; baby-changing facilities in all bathrooms and dedicated playroom space.
  • Establish a conference-specific parent social network.

The authors wrote that the adoption of these practices will send a strong and positive message, as well as support an inclusive family-friendly environment.

“I have never had a positive experience attending a conference after having children,  whether I was nursing either of my two daughters or just wanting them to attend,” Gibson told me. “We hope this op-ed can help guide future conferences to provide resources for working parents. I hope within the next year to attend conferences where all scientists feel included, especially those with children.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


“Slow and steady wins this race”: Stanford pain specialist studies opioid tapering

Posted February 20, 2018 by Jennifer Huber
Categories: Health

Tags: , ,

Image of Beth Darnall courtesy of Stanford Pain Medicine

Given America’s opioid epidemic, reducing opioid use has become a national priority. But for patients with chronic pain, successfully lowering their long-term dose can prove quite challenging.

A new Stanford study suggests that a patient-centered tapering program may be the solution for many opioid users with chronic pain. The researchers conducted a voluntary opioid reduction study focused on helping patients feel in control. This differed from traditional programs with forced, more aggressive dose tapering.

“Slow and steady wins this race. In most cases there is no urgency so we took several months to help patients make the transition comfortably,” said first author Beth Darnall, PhD, a Stanford clinical associate professor of anesthesiology, perioperative and pain medicine.

Another key aspect of their tapering program was the cultivation of a trusting patient-physician bond. “Many patients are fearful about reducing opioids. Our study methods focused on providing education to help allay their fears, as well as strengthening that bond to help patients succeed and achieve best outcomes,” Darnall explained.

Specifically, the team studied patients with non-cancer chronic pain who were being treated with long-term opioids through a community pain clinic in Colorado. Of the 110 patients invited to participate, 68 volunteered to reduce their opioids and 51 completed the study.

Participating patients were given a self-help book on reducing opioids and an individual plan to slowly taper their dose. They also completed a survey on their demographics, drug use, pain levels and psychosocial measures — both at the beginning of the study and 4 months later.

Physicians lowered each patient’s dose as much as possible over one year, pausing or stopping as needed, Darnall explained. Many patients reduced their dose by over 50 percent.

Darnall summarized their findings:

“We found many patients were interested in joining a voluntary opioid taper program if recommended to them by their doctor. And those who engaged in the opioid taper substantially reduced their opioid dose over 4 months without experiencing increased pain — even for those on high-dose opioids who had been taking them for years. Our pilot data suggest that many patients are open to a tapering pathway, if it is presented to them compassionately and in a patient-centered way.”

The team is now testing their voluntary tapering program in a large, multi-site study on almost 900 patients taking long-term opioids — using voluntary tapering alone or combined with behavioral pain treatment.

“We recognize that it’s not enough to just reduce patient risks with opioid reduction; we also need to help patients with chronic pain learn the tools to best help themselves,” said Darnall. “We hypothesize that patients will have better opioid and pain reduction when they learn to self-manage their pain and symptoms through one of these two group behavioral treatment classes.”

This is a reposting of my Scope blog post, courtesy of Stanford School of Medicine.


Gene Enhancers Are Important Despite Apparent Redundancy

Posted January 31, 2018 by Jennifer Huber
Categories: biology, Health

Tags: ,

Cell activity patterns of two gene enhancers (red and green cells). Cells in which both enhancers are active appear yellow. (Credit: Marco Osterwalder).

Every cell in the body has the same DNA and genes, so a cell’s properties and functions are determined by which genes are turned on. That’s why it is critical to understand enhancers, short sections of non-coding DNA that regulate the expression of specific genes.

An enhancer doesn’t have a one-to-one relationship with the gene it controls. Instead, there are many more enhancers than genes and their relationship is unclear. Do many enhancers regulate a given gene’s expression in a given tissue, providing redundancy? Researchers at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) investigated this question, and the overall importance of enhancers to development, in two recent studies.

The researchers answered a long-standing question about the role of enhancers. And by better linking the genomic complement of an organism with its expressed characteristics, their work offers new insights that further the growing field of systems biology, which seeks to gain a predictive understanding of living systems.

Perfect Conservation

In their new study published in Cell, the team investigated enhancers containing “ultraconserved elements,” which are at least 200 base pairs in length and are 100 percent identical in the genomes of humans, mice and rats. Ultraconserved elements have been perfectly conserved for over 80 million years since these mammals shared a common ancestor.

Previously, the group individually deleted four ultraconserved brain enhancers in the mouse genome. All four mouse lines were viable and fertile, which shocked the genomics and evolutionary biology research communities who thought these enhancers were critical for life since they have been so perfectly conserved.

“In our follow-up study, we wanted to dig deeper to test two possible explanations,” said Diane Dickel, a research scientist at Berkeley Lab’s Environmental Genomics and Systems Biology Division. “First, maybe there is some redundancy between these enhancer sequences, and losing two of them will cause the mice to be nonviable or infertile. Second, maybe the mice do have something wrong with them, but it’s more subtle.”

In the new study, the team used the gene-editing tool CRISPR-CAS9 to further investigate enhancers near the Arx gene that, when defective, cause neurological and sexual-development disorders in mice and humans. “We focused on Arx because it has an unusually large number of very long ultraconserved sites nearby,” said Dickel who co-led the studies with Len Pennacchio and Axel Visel, both senior scientists in the same division.

Specifically, they knocked out four of Arx’s brain enhancers, which are active in pairs in either the top or bottom of the forebrain. When these enhancers were individually deleted, all the mice were viable and fertile — confirming that ultraconserved enhancers aren’t essential to life within a given generation. When they were deleted in pairs with similar activity, the mice were still viable and fertile — ruling out redundancy as the primary explanation for the absence of major defects upon knockout of individual ultraconserved enhancers.

But were there more subtle brain defects? To answer this question, the researchers teamed up with John Rubenstein, a neurobiologist at UC San Francisco, who provided in-depth neurological phenotyping.

In three of the four cases with only one enhancer deletion, they found abnormalities —either in overall growth or brain development. In one case, the mice had a severe structural defect in the hippocampus. In another case, the mice had fewer cholinergic neurons.

“The changes to the brain in these mice are reminiscent of those seen in humans with seizure disorders or dementia,” Dickel said. “While we don’t know yet if these mice are affected by such problems, it’s likely that the physiological changes we found are selected against in the wild, and that’s why you maintain a high level of conservation at these sites.”

Pictures of a normal part of the mouse forebrain (left) compared with a mouse missing one ultraconserved enhancer (right). (Credit: Athena Ypsilanti /UCSF)

Protective redundancy

While there are only a few hundred ultraconserved sites in the human and mouse genomes, there are also approximately 100,000 other, less well-conserved enhancers. The defects observed upon deletion of individual ultraconserved enhancers raise the question if deletion of less well-conserved enhancers generally causes similar problems. Are defects the exception or the rule? This question was investigated in a second study, led by postdoctoral researcher Marco Osterwalder, which focused on enhancers for limbs. Limb enhancers were targeted because limbs are easy to assess, unlike neurological phenotyping.

As reported today in Nature, the team deleted ten limb enhancers near genes essential for limb development. They expected to see some anomalies but all ten mouse lines had perfectly normal-looking limbs.

However, the team also observed some genes with two enhancers that appeared to be active at the same time during limb development. When the team knocked out such pairs of limb enhancers with similar activity, they saw characteristics like extra digits or differences in bone length — indicating that these enhancers functioned redundantly. “It’s like the pilot and copilot having redundant control sticks in the cockpit,” explained Visel. “Either one can control the plane, but you’re in trouble if you get rid of both control sticks.”

To determine whether or not it’s common to have such a regulatory back-up system, the team computationally analyzed genomic datasets from many different tissues. They determined that genes that control central processes in embryonic development are commonly equipped with sets of enhancers that are likely redundant. In more than 1000 extreme cases, they found sets of five or more enhancers with similar activity patterns controlling the same gene.

Despite the redundancy, these enhancers are evolutionarily conserved, which leads the scientists to surmise that disrupting these enhancers may cause some sort of decrease in fitness in the wild, even if it is so small it can’t be readily detected in the lab.

“We’re not saying these enhancers are perfectly redundant in that one or the other isn’t important, but rather there is a mechanism of protecting against deleterious effects on the order of a given generation,” Pennacchio summarized. “Selection happens over many generations.”

Taken together, these studies demonstrate a varied importance of enhancer redundancy. “The genome is a big place,” Dickel said. “It’s hard to fit every single locus in the genome into one specific model of gene regulation. Some loci have more redundancy than others.”

Broader implications

Complex questions such as these are addressed by biological systems science, where these results can be used to understand the effects of genetic perturbations on inherited and expressed characteristics in a larger context.

Ultimately, the team is interested in whether enhancer mutations contribute to human disease. “With whole human genome sequencing now a reality, we are focusing on studying how human mutations impact health and development in vivo,” Pennacchio said.

The research, funded by the National Institutes of Health, was performed at Berkeley Lab and is a natural evolution of the work that was begun by the DOE and became the Human Genome Project.

The following Berkeley Lab researchers also contributed to the studies: Iros Barozzi, Yoko Fukuda-Yuzawa, Brandon Mannion, Sarah Afzal, Elizabeth Lee, Yiwen Zhu, Ingrid Plajzer-Frick, Catherine Pickle, Momoe Kato, Tyler Garvin, Quan Pham, Anne Harrington, Jennifer Akiyama and Veena Afzal. Also participating in the research were scientists from the University of California San Francisco, University of Basel, and the Centro Andaluz de Biología del Desarrollo.


Lawrence Berkeley National Laboratory addresses the world’s most urgent scientific challenges by advancing sustainable energy, protecting human health, creating new materials, and revealing the origin and fate of the universe. Founded in 1931, Berkeley Lab’s scientific expertise has been recognized with 13 Nobel Prizes. The University of California manages Berkeley Lab for the U.S. Department of Energy’s Office of Science. For more, visit

DOE’s Office of Science is the single largest supporter of basic research in the physical sciences in the United States, and is working to address some of the most pressing challenges of our time. For more information, please visit

This is a reposting of my news release, courtesy of Berkeley Lab.


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