Following the people and events that make up the research community at Duke

Category: Genetics/Genomics Page 1 of 9

Trust-Building, Re-Visited History, and Time Pertinent to Achieve Health Equity for Black Americans

Along with being a beautiful person and leading a productive life, Henrietta Lacks is the mother of modern medicine. Her scientific child was born without Henrietta’s consent through the clinical breakthroughs and medical miracles achieved with the help of her cervical cells – HeLa cells – stolen without her knowledge when she sought healthcare. Ironically, the same treatments developed from the cells of this Black woman are inaccessible for many Black Americans contemporarily. Though Ms. Lacks passed away from cervical cancer at the premature age of 31, her unique cells have become immortal. Her story lives on as a pertinent reminder of the importance of building trust between medicine and the Black community. In honor of her birthday, expert panelists met to both celebrate Ms. Lacks and discuss the path forward in trust-building, equity, and reckoning with our history to change the narrative of healthcare for Black Americans.

The panel honored Henrietta Lacks through discussion of the path forward for biomedical research and Black communities. The panel was hosted in August in remembrance of Ms. Lacks’ birthday on August 1st.

The panel, which took place on Tuesday, August 31, began as a conversation between Nadine Barrett (Ph.D.), Robert A. Winn (M.D.) and Vanessa B. Sheppard (Ph.D.). Among their many other titles and positions, Barrett is Director, Center for Equity in Research, Dukev CTSI and Associate Director of Equity, Community and Stakeholder Strategy, Duke Cancer Institute, Dr. Winn is the Director of the Virginia Commonwealth University (VCU) Massey Cancer Center, and Sheppard is the Associate Director of Community Outreach Engagement and Health Disparities at VCU Massey Cancer Center. The trio were joined by Reuben Warren (D.D.S., M.P.H., Dr. P.H., M.DIV.), Director of Tuskegee University’s Bioethics Center, along with a handful of other contributors including Veronica Robinson – Henrietta Lacks’ great-granddaughter and a registered nurse who represents the Lacks family on the NIH panel that reviews applications to conduct research using the HeLa genome.

A screenshot of panelists who took part in Tuesday’s conversation.

Winn began by referencing the U.S. 1932 public health service study that took place in Tuskegee, Alabama. The experiment exploited Black men in Tuskegee when an effective form of treatment for syphilis was discovered 15 years into the study but withheld from participants “to track the disease’s full progression.” In 1972, 40 years after the study began, it was the associated press, not the scientific community that finally led to the experiment’s demise and the issue of an apology from the U.S. President.

As Warren pointed out, the issue with the study was less about the treatment and more about the dishonesty, the falsifying information, and lies. “Stop calling them poor, stop calling them all sharecroppers,” Warren said of the Black men who participated in the study, “They were far more than that.” “[The study] was an issue of trust, not an issue of ignorance,” he continued. Unfortunately, when talking about this story, Winn said that Black Americans “don’t always talk about the power of us standing up and saying not again.

Bioethics violations have been a continuous part of the biomedical research enterprise in the U.S., and race and racism have been part of scientific inquiry, which continues to be of great concern, Warren said. Often, rather than putting preventative protections in place, bioethics regulations have come as a reaction to extreme violations of justice. Thus, Warren laid out a central theme of the panel that “You build trust by making yourself trustworthy and that takes time.” Rather than initiating transactional research with Black communities when the scientific and medical community needs something, Warren offered that they should start when they want to help with something.

Dr. Rueben Warren presenting examples of bioethics violations in the history of biomedical research, with most examples stemming from the United States

As Sheppard said, “[Black people] have earned a mistrust” for medical communities. This is largely hinged on Barrett’s argument that the American systems from health to education to criminal justice “are working as they were designed” – to ensure that the very inequalities that exist today came to be. Using the analogy of a marathon, Barrett said while white men in the U.S. started the race 450 years ago, Black men and women only began running this race hundreds of years later. “Those who start the race are going to…ensure that they thrive,” Barrett said. This has led to Black people dying disproportionately from often treatable diseases, Sheppard said, continuing to add that these sorts of disparities were front and center for the world to see during the COVID-19 pandemic.

In the creation of our structural inequalities, the system created “two bookends: Black and white.” But there has to be a narrative that keeps this story alive. “In order to create the change, we have got to do the work to change the narrative,” said Barrett.

Nadine Barrett (Ph.D.), Director of Health Equity and Disparities at Duke Cancer Institute

Robinson pointed to the importance of history, paralleling Warren’s comments that in focusing on health equities we are fully focusing on the future in a way that ignores the past and does not deal with “what really brought us into health disparities” in the first place. Robinson said that we “can no longer sweep [conversations on the historical injustices of medical racism] under the rug.” She continued to say that the reason why Tuesday’s conversation and the ongoing dialogue that is sure to follow is so powerful is because “we are no longer victims in our own legacies” by taking over conversations at the table rather than being the topics of discussion at the table.

Mistrust in the Black community for systems of medicine and healthcare are based on hundreds of years of action. Hesitancy – from Covid-19 vaccinations to participation in clinical trials for cancer research – amongst Black Americans “aren’t us saying no,” said Robinson, “We’re saying something happened.” Sharon Ribera Sanchez, Founder-Director of Saving Pennies 4 A Cure, is a cancer survivor and advocate for people of color to engage in clinical trials because of the difference they can make in medical developments that draw on more diverse and robust data.

But there is a bigger conversation than just having more Black folks take place in research and clinical trials, Winn said. “How are you going to look at my biology without looking at my history?” he asked, referencing the genetic implications of environmental conditions and stressors from socially constructed race that impact DNA.

An image of HeLa cells

The dialogue, which was opened and closed with a prayer, also spoke to the importance of establishing regular, ongoing, transparent relationships between the Black faith community and the medical community. This should happen, not just in times of crisis, because “mass hysteria is prime for miscommunication,” Ralph Hodge, pastor of the Second Baptist Church in South Richmond, Virginia, said.

“Today was a big way of us looking back at the past, looking at where we are at now, and moving forward to the solutions,” said Barrett. This comes by letting communities know that we care, said Winn, along with “doing things with our communities, not through them.”

A key factor in deconstructing this issue and achieving health equity is time. Time to reflect on the past in order to avoid reliving it; time to generate innovative solutions to the problems at hand; and time to invest in Black communities – to learn from them, support them, and earn their trust not because they can offer science something, but because science has something to offer them.

Post by Cydney Livingston

In Drawers of Old Bones, New Clues to the Genomes of Lost Giants

DNA extracted from a 1,475-year-old jawbone reveals genetic blueprint for one of the largest lemurs ever.

By teasing trace amounts of DNA from this partially fossilized jawbone, nearly 1,500 years after the creature’s death, scientists have managed to reconstruct the first giant lemur genome. Credit: University of Antananarivo and George Perry, Penn State

If you’ve been to the Duke Lemur Center, perhaps you’ve seen these cute mouse- to cat-sized primates leaping through the trees. Now imagine a lemur as big as a gorilla, lumbering its way through the forest as it munches on leaves.

It may sound like a scene from a science fiction thriller, but from skeletal remains we know that at least 17 supersized lemurs once roamed the African island of Madagascar. All of them were two to 20 times heftier than the average lemur living today, some weighing up to 350 pounds.

Then, sometime after humans arrived on the island, these creatures started disappearing.

The reasons for their extinction remain a mystery, but by 500 years ago all of them had vanished.

Coaxing molecular clues to their lives from the bones and teeth they left behind has proved a struggle, because after all this time their DNA is so degraded.

But now, thanks to advances in our ability to read ancient DNA, a giant lemur that may have fallen into a cave or sinkhole near the island’s southern coast nearly 1,500 years ago has had much of its DNA pieced together again. Researchers believe it was a slow-moving 200-pound vegetarian with a pig-like snout, long arms, and powerful grasping feet for hanging upside down from branches.

A single jawbone, stored at Madagascar’s University of Antananarivo, was all the researchers had. But that contained enough traces of DNA for a team led by George Perry and Stephanie Marciniak at Penn State to reconstruct the nuclear genome for one of the largest giant lemurs, Megaladapis edwardsi, a koala lemur from Madagascar.

Ancient DNA can tell stories about species that have long since vanished, such as how they lived and what they were related to. But sequencing DNA from partially fossilized remains is no small feat, because DNA breaks down over time. And because the DNA is no longer intact, researchers have to take these fragments and figure out their correct order, like the pieces of a mystery jigsaw puzzle with no image on the box.

Bones like these are all that’s left of Madagascar’s giant lemurs, the largest of which weighed in at 350 pounds — 20 times heftier than lemurs living today. Credit: Matt Borths, Curator of the Division of Fossil Primates at the Duke Lemur Center

Hard-won history lessons

The first genetic study of M. edwardsi, published in 2005 by Duke’s Anne Yoder, was based on DNA stored not in the nucleus — which houses most of our genes — but in another cellular compartment called the mitochondria that has its own genetic material. Mitochondria are plentiful in animal cells, which makes it easier to find their DNA.

At the time, ancient DNA researchers considered themselves lucky to get just a few hundred letters of an extinct animal’s genetic code. In the latest study they managed to tease out and reconstruct some one million of them.

“I never even dreamed that the day would come that we could produce whole genomes,” said Yoder, who has been studying ancient DNA in extinct lemurs for over 20 years and is a co-author of the current paper.

For the latest study, the researchers tried to extract DNA from hundreds of giant lemur specimens, but only one yielded enough useful material to reconstitute the whole genome.

Once the creature’s genome was sequenced, the team was able to compare it to the genomes of 47 other living vertebrate species, including five modern lemurs, to identify its closest living relatives. Its genetic similarities with other herbivores suggest it was well adapted for grazing on leaves.

Despite their nickname, koala lemurs weren’t even remotely related to koalas. Their DNA confirms that they belonged to the same evolutionary lineage as lemurs living today.

To Yoder it’s another piece of evidence that the ancestors of today’s lemurs colonized Madagascar in a single wave.

Since the first ancient DNA studies were published, in the 1980s, scientists have unveiled complete nuclear genomes for other long-lost species, including the woolly mammoth, the passenger pigeon, and even extinct human relatives such as Neanderthals.

Most of these species lived in cooler, drier climates where ancient DNA is better preserved. But this study extends the possibilities of ancient DNA research for our distant primate relatives that lived in the tropics, where exposure to heat, sunlight and humidity can cause DNA to break down faster.

“Tropical conditions are death to DNA,” Yoder said. “It’s so exciting to get a deeper glimpse into what these animals were doing and have that validated and verified.”

See them for yourself

Assembled in drawers and cabinets cases in the Duke Lemur Center’s Division of Fossil Primates on Broad St. are the remains of at least eight species of giant lemurs that you can no longer find in the wild. If you live in Durham, you may drive by them every day and have no idea. It’s the world’s largest collection.

In one case are partially fossilized bits of jaws, skulls and leg bones from Madagascar’s extinct koala lemurs. Nearby are the remains of the monkey-like Archaeolemur edwardsi, which was once widespread across the island. There’s even a complete skeleton of a sloth lemur that would have weighed in at nearly 80 pounds, Palaeopropithecus kelyus, hanging upside down from a branch.

Most of these specimens were collected over 25 years between 1983 and 2008, when Duke Lemur Center teams went to Madagascar to collect fossils from caves and ancient swamps across the island.

“What is really exciting about getting better and better genetic data from the subfossils, is we may discover more genetically distinct species than only the fossil record can reveal,” said Duke paleontologist Matt Borths, who curates the collection. “That in turn may help us better understand how many species were lost in the recent past.”

They plan to return in 2022. “Hopefully there is more Megaladapis to discover,” Borths said.

A fossil site in Madagascar. Courtesy of Matt Borths, Duke Lemur Center Division of Fossil Primates

CITATION: “Evolutionary and Phylogenetic Insights From a Nuclear Genome Sequence of the Extinct, Giant, ‘Subfossil’ Koala Lemur Megaladapis Edwardsi,” Stephanie Marciniak, Mehreen R. Mughal, Laurie R. Godfrey, Richard J. Bankoff, Heritiana Randrianatoandro, Brooke E. Crowley, Christina M. Bergey, Kathleen M. Muldoon, Jeannot Randrianasy, Brigitte M. Raharivololona, Stephan C. Schuster, Ripan S. Malhi, Anne D. Yoder, Edward E. Louis Jr, Logan Kistler, and George H. Perry. PNAS, June 29, 2021. DOI: 10.1073/pnas.2022117118.

Duke Researcher Busts Metabolism Myths in New Book

Herman Pontzer explains where our calories really go, and what studying humanity’s past can teach us about staying healthy today.

Photo by Elena Georgiou, My City /EEA

Duke professor Herman Pontzer has spent his career counting calories. Not because he’s watching his waistline, exactly. But because, as he sees it, “in the economics of life, calories are the currency.” Every minute, everything the body does — growing, moving, fighting infection, even just existing — “all of it takes energy,” Pontzer says.

In his new book, “Burn,” the evolutionary anthropologist recounts the 10-plus years he and his colleagues have spent measuring the metabolisms of people ranging from ultra-athletes to office workers, as well as those of our closest animal relatives, and some of the surprising insights the research has revealed along the way.

Much of his work takes him to Tanzania, where members of the Hadza tribe still get their food the way our ancestors did — by hunting and gathering. By setting out on foot each day to hunt zebra and antelope or forage for berries and tubers, without guns or electricity or domesticated animals to lighten the load, the Hadza get more physical activity each day than most Westerners get in a week.

So they must burn more calories, right? Wrong.

Herman Pontzer
Herman Pontzer, associate professor of evolutionary anthropology at Duke

Pontzer and his colleagues have found that, despite their high activity levels, the Hadza don’t burn more energy per day than sedentary people in the U.S. and Europe.

These and other recent findings are changing the way we understand the links between energy expenditure, exercise and diet. For example, we’ve all been told that if we want to burn more calories and fight fat, we need to work out to boost our metabolism. But Pontzer says it’s not so simple.

“Our metabolic engines were not crafted by millions of years of evolution to guarantee a beach-ready bikini body,” Pontzer says. But rather, our metabolism has been primed “to pack on more fat than any other ape.” What’s more, our metabolism responds to changes in exercise and diet in ways that thwart our efforts to shed pounds.

What this means, Pontzer says, is you can walk 16,000 steps each day like the Hadza and you won’t lose weight. Sure, if you run a marathon tomorrow you’ll burn more energy than you did today. But over time, metabolism responds to changes in activity to keep the total energy you spend in check.

Pontzer’s book is more than a romp through the Krebs cycle. For anyone suffering pandemic-induced pangs of frustrated wanderlust, it’s also filled with adventure. He takes readers on an hours-long trek to watch a Hadza man track a wounded giraffe across the savannah, to the rainforests of Uganda to study climbing chimpanzees, and to the foothills of the Caucasus Mountains to unearth the 1.8 million-year-old remains of some of the first people who trekked out of Africa.

His humor shines through along the way. Even when awoken by a chorus of 300-pound lions just a few hundred yards from his tent, he stops to ponder whether his own stench gives him away, and what he might do if they come for his “soft American carcass, the  warm triple crème brie of human flesh.”

Pontzer spoke via email with Duke Today about his book:

Q: What’s the lesson the Hadza and other hunter-gatherers teach us about managing weight and staying healthy?

A: The Hadza stay incredibly fit and healthy throughout their lives, even into their older ages (60’s, 70’s, even 80’s). They don’t develop heart disease, diabetes, obesity, or the other diseases that we in the industrialized world are most likely to suffer from. They also have an incredibly active lifestyle, getting more physical activity in a typical day than most Americans get in a week.

My work with the Hadza showed that, surprisingly, even though they are so physically active, Hadza men and women burn the same number of calories each day as men and women in the U.S. and other industrialized countries. Instead of increasing the calories burned per day, the Hadza physical activity was changing the way they spend their calories — more on activity, less on other, unseen tasks in the body.

The takeaway for us here in the industrialized world is that we need to stay active to stay healthy, but we can’t count on exercise to increase our daily calorie burn. Our bodies adjust, keeping energy expenditure in a narrow range regardless of lifestyle. And that means that we need to focus on diet and the calories we consume in order to manage our weight. At the end of the day, our weight is a matter of calories eaten versus calories burned — and it’s really hard to change the calories we burn!

Q: You’re saying that exercise doesn’t matter? What’s the point, if we can’t eat that donut?

A: All those adjustments our bodies make responding to exercise are really important for our health! When we burn more calories on exercise, our bodies spend less energy on inflammation, stress reactivity (like cortisol), and other things that make us sick.

Q: What’s the biggest misunderstanding about human metabolism?

A: We’re told — through fitness magazines, diet fads, online calorie counters — that the energy we burn each day is under our control: if we exercise more, we’ll burn more calories and burn off fat. It’s not that simple! Your body is a clever, dynamic product of evolution, shifting and adapting to changes in our lifestyle.

Q: In your book you say we’re driven to magical thinking when it comes to calories. What do you mean by that?

A: Because our body is so clever and dynamic, and because humans are just bad at keeping track of what we eat, it’s awfully hard to keep track of the calories we consume and burn each day. That, along with the proliferation of fad diets and get-thin-quick schemes, has led to this idea that “calories don’t matter.” That’s magical thinking. Every ounce of your body — including every calorie of fat you carry — is food you consumed and didn’t burn off. If we want to lose weight, we must eat fewer calories than we burn. It really comes down to that.

Q: Some people say that if the cavemen didn’t eat it, we shouldn’t either. What does research show about what foods are “natural” for humans to eat?

A: There’s no singular, natural human diet. Hunter-gatherers like the Hadza eat a diverse mix of plant and animal foods that varies day to day, month to month, and year to year. There’s even more dietary diversity when we look across populations. Humans are built to thrive on a wide variety of diets — just about everything is on the menu.

That said, the ultra-processed foods we’re inundated with in our modern industrialized world really are unnatural. There are no Twinkies to forage in the wild. Those foods are literally engineered to be overconsumed, with a mix of flavors that overwhelm our brain’s ability to regulate our appetites. Now, it is still possible to lose weight on a Twinkie diet (I’m not recommending it!), if you’re very strict about the calories eaten per day. But we need to be really careful about how we incorporate ultra-processed foods into our daily diets, because they are calorie bombs that drive us to overconsume.

Q: If we could time travel, what would our hunter-gatherer ancestors make of our industrialized diet today?

A: We don’t even need to imagine — We are those hunter-gatherers! Biologically, genetically, we are the same species that we were a hundred thousand years ago, when hunting and gathering were the only game in town. When we’re confronted with modern ultra-processed foods, we struggle. They are engineered to be delicious, and we tend to overconsume.

Q: Has the COVID-19 pandemic brought any of these lessons home for you? What can we do to keep active and watch what we eat, even while working from home?

The pandemic has been a tragedy on so many levels — the loss of life, those suffering with long-term effects, the social and economic impacts. The impact on diet and exercise have been bad as well, for many of us. Stress eating is a real phenomenon, and the stress and emotional toll of the pandemic — along with having easy access to the snacks in our kitchen — have led many to gain weight. Physical activity seems to have declined for many. There aren’t easy answers, but we should try to make a point to get active every day. And we can help ourselves make better decisions about food by keeping ultra-processed foods out of our houses. You can’t plow through a bag of chips if you don’t have chips in your cupboard.

Q: You’ve measured the energy costs of activities ranging from taking a breath to doing an Ironman. What is one of the more extreme or surprising calorie-burning activities that you’ve measured, or would like to measure, in humans or some other animal?

A: With colleagues from Japan, I measured the energy cost of a heartbeat – a tricky bit of metabolic measurement! Turns out each beat of your heart burns about 1/300th of a kilocalorie! Amazing how efficient our bodies can be.

Q: What is something people have questions about that we just don’t know the answer to yet? What would it take to find out?

A: Right now we’re excited about measuring the adjustments our bodies make when we increase our exercise: how exactly does burning more energy on physical activity impact our immune system, our stress response, our reproductive system? It will take a long-term study of exercise to see how these systems change over time.

Robin Smith - University Communications
Robin Smith – University Communications

A Computer Scientist Investigating the Source Code of Life

We are all born with defining physical characteristics. Whether it be piercing blue eyes or jet black hair, these traits distinguish us throughout our entire lives. However, there is something that all of our attributes have in common, a shared origin: genes.

Beyond dictating our individual features, genes instruct cells to create proteins that are essential for a variety of processes, from controlling muscle function to managing digestive systems. Despite their importance in the workings of our body, genes can also code for detrimental diseases, such as Huntington’s disease or Duchenne muscular dystrophy.

Raluca Gordân, Ph.D.

These types of diseases are exactly what Raluca Gordân, Ph.D. is battling through her research. She and her group are trying to figure out how to decode the non-coding genome, the DNA apart from protein-coding genes. They are deepening their understanding of the role non-coding areas of the genome play in the expression of the coding genes and the production of proteins.

Gordân, an associate professor in biostatistics and bioinformatics at Duke, said a majority of disease-causing genetic mutations derive from the genome outside of genes.

“That is a huge search space,” she says, chuckling. “Genes only make up about 2% of the genome. If we don’t understand what those non-coding regions are doing, it’s hard to make predictions about what the mutation in those regions would be doing and how to connect that to the development of a disease.”

Gordân recently published a paper, entitled “DNA mismatches reveal conformational penalties in protein–DNA recognition,” which focuses on transcription factors and their exceptional ability to bind to mispaired DNA, misspellings that occur as DNA is copied. During regular replication, nucleotide bases (the building blocks of our DNA) are paired correctly, where adenine pairs with thymine and cytosine goes with guanine. However, when an error occurs during replication, mispairs start to appear, as adenine may pair with guanine instead.

“Normally, those are mistakes that get repaired by specific mismatch repair pathways but that repair might not happen if one of these transcription factors sits on the replication error and doesn’t allow the repair mechanism to see it,” Gordân explains. “Normally, one would expect the transcription factors not to bind to those errors. But we found that they can bind way better than their actual genomic targets.”

Modeling of the binding between mismatched DNA and transcription factors.

To expand on her computational discovery, Gordân is now following up with a study of transcription factor binding to mismatches in living cells, observing whether they adopt their usual role of regulating gene expression or contribute to the development of mutations.

Gordân’s research is a product of her passion and desire to make change. It also can be attributed to a series of realizations she made during college and inspirational mentors who guided her along the way.

While pursuing her undergraduate degree, Gordân was a purely computer science major, concentrating on cryptography. However, as she was nearing the end of her four years of college, she soon found herself yearning for the opportunity to do more. She began looking into machine learning applications and enrolled in a course based around genetic algorithms which she credits for launching her career path.

At that point, she attained what she describes as her “first taste of genetics” and her interest in bioinformatics was irrevocably piqued. Thereafter, Gordân applied for a PhD at Duke, where she worked with advisor Alex Hartemink investigating transcription factor proteins in regulatory genomics. At Duke, her work was primarily computational.  But with her postdoctoral advisor Martha Bulyk of Harvard Medical School, Gordan was exposed to the more experimental aspects of biology.

Today, she recognizes these experiences as integral to her ongoing research, which requires her to frequently iterate between observational approaches and computational work.

Gordân is acclimating to the newly quarantined world. While she strives to continue her research, in the pandemic, it has changed her routine.

“I think what was affected a lot since the pandemic started is the fact that we don’t meet in person,” she says. “A lot of the quick progress was being made when we were in the same physical space and were able to get feedback immediately, with students learning about each other’s results in the lab, in real time. That was replaced with Zoom meetings, where students get to see the other students’ results mainly at lab meetings, weeks or months later. Those continuous discussions that were going on in the lab all the time. We’re missing that.”

Gordân offered some thoughtful parting advice to aspiring computational biologists, like me.

“I was trained as a computer scientist, so I wasn’t really sure about experimental work. But after actually doing the experimental work, I realized how much value there is in doing both,” she said. “You have to pick what you’re strongest at, either the computational or experimental part, but you should not be afraid of the other side.”

Guest Post by Akshra Paimagam, Class of 2021, NC School of Science and Math

Claire Engstrom, a Student Researcher Working to Treat Duchenne’s Muscular Dystrophy by Optimizing CRISPr-cas9

Meet Claire Engstrom, a Senior from Pasadena California. Claire is a Biology major who works in the Gersbach Lab at Duke. 

Claire first got involved with on-campus research through her pre-orientation program, PSearch that introduces incoming first-years to undergraduate research. Following her experience in PSearch, Claire got her first work-study research position in the Tung Lab where she worked closely with Jenny Tung, an Associate Professor in the Departments of Evolutionary Anthropology and Biology at Duke and a Faculty Associate of the Duke University Population Research Institute. 

In the Tung Lab, Claire’s research focused on how DNA methylation is passed through generations. Essentially looking at the inheritance of DNA whose methylation was impacted by environmental factors and how that affects future generations. 

Duke has research opportunities available in all disciplines as well as across departments. Approximately 53% of undergraduates graduate with research experience. Not only can students participate in groundbreaking research, but they can receive funding from the university as well to support the work they are doing.

Within the Biology department, there is a fellowship called B-SURF, the Biological Sciences Undergraduate Research Fellowship, an 8-week summer research program for rising sophomores. Claire applied for and was accepted to the fellowship and placed in one of Duke’s biomedical science laboratories. She also received a $4,000 stipend for her summer research.

Claire was placed in Charles Gersbach’s Lab focused on researching Genome Editing for Gene and Cell Therapy. Dr, Gersbach is a Rooney Family Associate Professor of Biomedical Engineering and has conducted groundbreaking work in genome editing.

Members of the Gersbach Lab in Fall 2019

Gersbach is doing research in several different domains of biomedical engineering. Claire’s project focuses on using CRISPR-Cas9, a technology that allows scientists to change an organism’s DNA using clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. faster, cheaper, more accurate, and more efficient than other existing genome editing methods. 

Prior to joining his lab, Claire had already heard a lot about Gersbach in her course Biology 201 as well as through reading his papers. The project she would spend the next two and a half years working on focused on using and optimizing CRISPR-Cas9 to treat Duchenne’s Muscular Dystrophy and lessen the severity of the symptoms. 

Duchenne’s Muscular Dystrophy is a muscle wasting disease that affects one in every five thousand male births.

“People are diagnosed when they are around five and then they lose the ability to walk and their heart can’t pump blood because of the lack of muscles.” Claire explained.  

“CRISPR-based genome editing restores dystrophin expression in mouse models of Duchenne muscular dystrophy. Cross-sections of muscle tissue where the dystrophin protein has been labeled green, including normal, healthy tissue (left), tissue from a mouse model of Duchenne muscular dystrophy (middle), and tissue from the same mouse model that has been treated with the CRISPR gene editing system (right). Nelson et al., Science (2016)”

Thus, those affected often die in early adulthood despite current advances in cardiovascular and respiratory treatments. Duchenne’s Muscular Dystrophy generally occurs as a result of a frameshift mutation of the dystrophin gene. As a result, one’s muscles can no longer connect to anything making it nearly impossible to contract and function properly. In the Gersbach lab they are trying to treat the mutation by using CRISPR-Cas9 to remove an exon or coding region of the gene in order to shift the reading frame back into its normal place. 

This shift produces a less severe phenotype that lessens the effects of Duchenne’s Muscular Dystrophy. The result will significantly improve the quality of life and life spans for affected patients. 

Claire will be continuing her work in the Gersbach lab full time in Spring 2021 as she graduated early, with distinction in the Fall. Her thesis on the work she did in the Gersbach lab was recently approved and her results will be published in a larger paper in the future. After this year she plans to take a gap year an then return to California to hopefully attend grad school and pursue a Ph.D. in Biology.

By Anna Gotskind

Dealing With Lead for Life

Though lead has been widely eliminated from use in products due to proven health risks, the lifelong consequences of childhood lead exposure for children born in the era of lead use in gasoline are still unknown.

Aaron Reuben, fifth-year Ph.D. candidate in clinical psychology at Duke, spoke about the long-term implications of childhood lead exposure Friday, September 18th through the Nicholas School’s Environmental Health and Toxicology Seminar series. He conducts research as a member of the Moffitt and Caspi Lab, studying genes, environment, health, and behavior.

Aaron Reuben

Reuben started with a brief history of lead exposure. After the United States’ initial use of lead in gasoline in 1923, the practice became widespread with the U.S. Public Health Services approval for expansion. Five decades later, in the mid-1970s, the Environmental Protection Agency issued the first restrictions on lead use in gasoline products. Simultaneously, surveillance of population-level blood-lead levels indicated cause for concern. Though lead was phased of out of gas completely by 1995, the peak led exposures in the 70s were on average three to four times higher than current levels that demand clinical attention. Despite lead regulations, the impacts of exposure did not miraculously cease as well.

Lead use in gasoline quickly increased after its initial introduction.

The research Reuben covered in his talk centers on the Dunedin Study. This study of 1,037 people born between April 1972 and March 1973 in Dunedin, New Zealand is an ongoing longitudinal research project comprised of over 30 years of data. The cohort of participants provide a unique chance for research in which social and economic factors do not have to be detangled from findings as they represent the full range of socioeconomic statuses in their city.

Reuben’s first question was about the impact of lead exposure on psychiatric and personality differences in adulthood. Study members were asked about symptoms such as substance dependence, depression, fears and phobias, or mania. These reports were transformed into a continuous measure of general psychopathology, which indicated that children with high lead levels experienced more psychiatric problems across adulthood. Though the developmental differences were modest, the associations between lead and psychopathological issues are of a similar magnitude to other known risk factors like childhood maltreatment and family history of mental illness. Yet, unlike the latter two risk factors, Reuben said, “Lead exposure is not preordained – it’s modifiable.”

The research team also measured participant personality using the Big Five Inventory and found that individuals with high-blood level levels as children exhibited more difficult personality styles as adults. The biggest difference between groups with high and low childhood blood-lead level was the trait of conscientiousness, which has impacts on goal obtainment within one’s education and occupation, as well as overall satisfaction with relationships.

Findings from the Big Five Inventory of Dunedin participants.

The next question of the presentation centered on differences in adulthood cognitive ability. At midlife, defined as age 38 for this question, children with higher blood-lead levels had lower cognitive ability, experiencing a deficit of two IQ points per five microgram per deciliter increase of blood-lead level. Once again, though these findings were relatively modest, the loss of IQ points was accompanied by downward social mobility compared to participants’ parents. Further, when evaluations that took place at age 45 were included in the data, researchers saw even larger declines in IQ points between exposure-level groups, which Reuben predicts may even represent a trend of acceleration. He believes that as the study continues with the participants, they will find rapid decline around age 65, with higher levels of dementia symptoms among participants compared to same-aged peers.

The last question evaluated the structural integrity of the brain at midlife. The team found that children with higher lead exposure had lower gray-matter integrity, lower white-matter integrity, and older estimated brain age at age 45. Estimated brain age was predicted by an algorithm based on MRI scans, as brains look physically different as they age and gray- and white-matter integrity refers to the conditions of physical structures in the brain. These findings suggest that childhood led exposure may result in an overall lowered brain integrity at midlife, as well as accelerated brain aging.

Reuben’s take-away findings from his presentation.

Reuben’s work is important for understanding how childhood exposure to this neurotoxin has the ability to influence continued development, behavior, emotion, and life outcomes decades later. It is crucial to evaluate long-term ramifications of childhood lead exposure – a phenomena experience by hundreds of millions of people across the globe during the era of lead in gasoline who are likely unknowingly dealing with impacts now.

Post by Cydney Livingston

Duke Scientists Studying the Shape of COVID Things to Come

The novel coronavirus pandemic has now resulted in more than 3 million confirmed cases globally and is pushing scientists to share ideas quickly and figure out the best ways to collaborate and contribute to solutions.

SARS-CoV-2 surface proteins illustrated by We Are Covert, via Wikimedia Commons

Recently, Duke researchers across the School of Medicine came together for an online symposium consisting of several short presentations to summarize the latest of what is known about the novel coronavirus, SARS-CoV-2.

This daylong event was organized by faculty in the Department of Molecular Genetics and Microbiology and researchers from different fields to share what they know about the virus and immunity to guide vaccine design. This conference highlighted the myriad new research pathways that Duke researchers are launching to better understand this pandemic virus.

One neat area of research is understanding viral processes within cells to identify steps at which antivirals may block the virus. Stacy Horner’s Laboratory studies how RNA viruses replicate inside human cells. By figuring out how viruses and cells interact at the molecular level, Horner can inform development of antivirals and strategies to block viral replication. Antivirals stop infections by preventing the virus from generating more of copies of itself and spreading to other cells. This controls damage to our cells and allows the immune system to catch up and clear the infection.

At the symposium, Horner explained how the SARS-CoV viral genome consists of 29,891 ribonucleotides, which are the building blocks of the RNA strand. The viral genome contains 14 areas where the RNA code can be transcribed into shorter RNA sequences for viral protein production. Though each RNA transcript generally contains the code for a single protein, this virus is intriguing in that it uses RNA tricks to code for up to 27 proteins. Horner highlighted two interesting ways that SARS-CoV packs in additional proteins to produce all the necessary components for its replication and assembly into new viral progeny.

The first way is through slippery sequences on the RNA genome of the virus. A ribosome is a machine inside the cell that runs along a string of RNA to translate its code into proteins that have various functions. Each set of 3 ribonucleotides forms one amino acid, a building block of proteins. In turn, a string of amino acids assembles into a distinct structure that gives rise to a functional protein.

One way that SARS-CoV-2 packs in additional proteins is with regions of its RNA genome that make the ribosome machinery slip back by one ribonucleotide. Once the ribosome gets offset it reads a new grouping of 3 ribonucleotides and creates a different amino acid for the same RNA sequence. In this way, SARS-CoV-2 makes multiple proteins from the same piece of RNA and maximizes space on its genome for additional viral proteins.

An example of an RNA ‘hairpin’ structure, which might fool a ribosome to jump across the sequence rather than reading around the little cul de sac. (Ben Moore, via Wikimedia Commons)

Secondly, the RNA genome of SARS-CoV-2 has regions where the single strand of RNA twists over itself and connects with another segment of RNA farther along the code to form a new protein. These folds create structures that look like diverse trees made of repetitive hairpin-like shapes. If the ribosome runs into a fold, it can hop from one spot in the RNA to another disjoint piece and attach a new string of amino acids instead of the ones directly ahead of it on the linear RNA sequence. This is another way the SARS-CoV-2 packs in extra proteins with the same piece of RNA.

Horner said a step-by-step understanding of what the virus needs to survive at each step of its replication cycle will allow us to design molecules that are able to block these crucial steps.

Indeed, shapes of molecules can determine their function inside the cell. Three Duke teams are pursuing detailed investigation of SARS-CoV-2 protein structures that might guide development of complementarily shaped molecules that can serve as drugs by interfering with viral processes inside cells.

Some Duke faculty who participated in the virtual viral conference. (L-R from, top) Stacy Horner, Nick Heaton, Micah Luftig, Sallie Permar, Ed Miao and Georgia Tomaras. (image: Tulika Singh)

For example the laboratory of Hashim Al-Hashimi, develops computational models to predict the diversity of structures produced by these tree-like RNA folds to identify possible targets for new therapeutics. Currently, the Laboratories of Nicholas Heaton and Claire Smith are teaming up to identify novel restriction factors inside cells that can stop SARS-CoV-2.

However, it is not just the structures of viral components expressed inside the cells that matter, but also those on the outside of a virus particle. In Latin, corona means a crown or garland, and coronaviruses have been named for their distinctive crown-like spikes that envelop each virus particle. The viral protein that forms this corona is aptly named the “Spike” protein.

This Spike protein on the viral surface connects with a human cell surface protein (Angiotensin-converting enzyme 2, abbreviated as ACE2) to allow the virus to enter our cells and cause an infection. Heaton proposed that molecules designed to block this contact, by blocking either the human cell surface protein or the viral Spike protein, should also be tested as possible therapies.

One promising type of molecule to block this interaction is an antibody. Antibodies are “Y” shaped molecules that are developed as part of the immune response in the body by the second week of coronavirus infection. These molecules can detect viral proteins, bind with them, and prevent viruses from entering cells. Unlike several other components on our immune defense, antibodies are shaped to specifically latch on to one type of virus. Teams of scientists at Duke led by Dr. Sallie Permar, Dr. Georgia Tomaras, and Dr. Genevieve Fouda are working to characterize this antibody response to SARS-CoV-2 infection and identify the types of antibodies that confer protection.

Infectious disease specialist Dr. Chris Woods is leading an effort to test whether plasma with antibodies from people who have recovered can prevent severe coronavirus disease in acutely infected patients.

Indeed, there are several intriguing research questions to resolve in the months ahead. Duke scientists are forging new plans for research and actively launching new projects to unravel the mysteries of SARS-CoV-2. With Duke laboratory scientists rolling up their sleeves and gowning up to conduct research on the novel coronavirus, there will be soon be many more vaccine and therapeutic interventions to test.

Guest post by Tulika Singh, MPH, PhD Candidate in the Department of Molecular Genetics and Microbiology (T: @Singh_Tulika)

Duke’s Fundamental Research Can Turn Viruses Into Marvels

The COVID-19 epidemic has impacted the Duke research enterprise in profound ways. Nearly all laboratory-based research has been temporarily halted, except for research directly connected to the fight against COVID-19. It will take much time to return to normal, and that process of renewal will be gradual and will be implemented carefully.

Trying to put this situation into a broader perspective, I thought of the 1939 essay by Abraham Flexner published in Harper’s magazine, entitled “The Usefulness of Useless Knowledge.” Flexner was the founding Director of the Institute for Advanced Study at Princeton, and in that essay, he ruminated on much of the type of knowledge acquired at research universities —  knowledge motivated by no objective other than the basic human desire to understand. As Flexner said, the pursuit of this type of knowledge sometimes leads to surprises that transform the way we see that which was previously taken for granted, or for which we had previously given up hope. Such knowledge is sometimes very useful, in highly unintended ways.

Gregory Gray, MD MPH
Gregory Gray, MD MPH

The 1918 influenza pandemic led to 500 million confirmed cases, and 50 million deaths. In the Century since, consider how far we have come in our understanding of epidemics, and how that knowledge has impacted our ability to respond. People like Greg Gray, a professor of medicine and member of the Duke Global Health Institute (DGHI), have been quietly studying viruses for many years, including how viruses at domestic animal farms and food markets can leap from animals to humans. Many believe the COVID-19 virus started from a bat and was transferred to a human. Dr. Gray has been a global leader in studying this mechanism of a potential viral pandemic, doing much of his work in Asia, and that experience makes him uniquely positioned to provide understanding of our current predicament.

From the health-policy perspective, Mark McClellan, Director of the Duke Margolis Center for Health Policy, has been a leading voice in understanding viruses and the best policy responses to an epidemic. As a former FDA director, he has experience bringing policy to life, and his voice carries weight in the halls of Washington. Drawing on faculty from across Duke and its extensive applied policy research capacity, the Margolis Center has been at the forefront in guiding policymakers in responding to COVID-19.

Through knowledge accrued by academic leaders like Drs. Gray and McClellan, one notes with awe the difference in how the world has responded to a viral threat today, relative to 100 years ago. While there has been significant turmoil in many people’s lives today, as well as significant hardship, the number of global deaths caused by COVID-19 has been reduced substantially relative to 1918.

One of the seemingly unusual aspects of COVID-19 is that a substantial fraction of the population infected by the virus has no symptoms. However, those asymptomatic individuals shed the virus and infect others. While most people have no or mild symptoms, other people have very adverse effects to COVID-19, some dying quickly.

This heterogeneous response to COVID-19 is a characteristic of viruses studied by Chris Woods, a professor medicine in infectious diseases. Dr. Woods, and his colleagues in the Schools of Medicine and Engineering, have investigated this phenomenon for years, long before the current crisis, focusing their studies on the genomic response of the human host to a virus. This knowledge of viruses has made Dr. Woods and his colleagues leading voices in understanding COVID-19, and guiding the clinical response.

A team led by Greg Sempowski, a professor of pathology in the Human Vaccine Institute is working to isolate protective antibodies from SARS-CoV-2-infected individuals to see if they may be used as drugs to prevent or treat COVID-19. They’re seeking antibodies that can neutralize or kill the virus, which are called neutralizing antibodies.

Barton Haynes,MD
Barton Haynes, MD

Many believe that only a vaccine for COVID-19 can truly return life to normal. Human Vaccine Institute Director Barton Haynes, and his colleagues are at the forefront of developing that vaccine to provide human resistance to COVID-19. Dr. Haynes has been focusing on vaccine research for numerous years, and now that work is at the forefront in the fight against COVID-19.

Engineering and materials science have also advanced significantly since 1918. Ken Gall, a professor of mechanical engineering and materials science has led Duke’s novel application of 3D printing to develop methods for creatively designing personal protective equipment (PPE). These PPE are being used in the Duke hospital, and throughout the world to protect healthcare providers in the fight against COVID-19.

Much of the work discussed above, in addition to being motivated by the desire to understand and adapt to viruses, is motivated from the perspective that viruses must be fought to extend human life.

In contrast, several years ago Jennifer Doudna and Emmanuelle Charpentier, academics at Berkeley and the Max Planck Institute, respectively, asked a seemingly useless question. They wanted to understand how bacteria defended themselves against a virus. What may have made this work seem even more useless is that the specific class of viruses (called phage) that infect bacteria do not cause human disease. Useless stuff! The kind of work that can only take place at a university. That basic research led to the discovery of clustered regularly interspaced short palindromic repeats (CRISPR), a bacterial defense system against viruses, as a tool for manipulating genome sequences. Unexpectedly, CRISPR manifested an almost unbelievable ability to edit the genome, with the potential to cure previously incurable genetic diseases.

Charles Gersbach, a professor of Biomedical Engineering, and his colleagues at Duke are at the forefront of CRISPR research for gene and cell therapy. In fact, he is working with Duke surgery professor and gene therapy expert Aravind Asokan to engineer another class of viruses, recently approved by the FDA for other gene therapies, to deliver CRISPR to diseased tissues. Far from a killer, the modified virus is essential to getting CRISPR to the right tissues to perform gene editing in a manner that was previously thought impossible. There is hope that CRISPR technology can lead to cures for sickle cell and other genetic blood disorders. It is also being used to fight cancer and muscular dystrophy, among many other diseases and it is being used at Duke by Dr. Gersbach in the fight against COVID-19. 

David Ashley, Ph.D.
David Ashley, Ph.D.

In another seemingly bizarre use of a virus, a modified form of the polio virus is being used at Duke to fight glioblastoma, a brain tumor. That work is being pursued within the Preston Robert Tisch Brain Tumor Center, for which David Ashley is the Director. The use of modified polio virus excites the innate human immune system to fight glioblastoma, and extends life in ways that were previously unimaginable. But there are still many basic-science questions that must be overcome. The remarkable extension of life with polio-based immunotherapy occurs for only 20% of glioblastoma patients. Why? Recall from the work of Dr. Woods discussed above, and from our own observation of COVID-19, not all people respond to viruses in the same way. Could this explain the mixed effectiveness of immunotherapy for glioblastoma? It is not known at this time, although Dr. Ashley feels it is likely to be a key factor. Much research is required, to better understand the diversity in the host response to viruses, and to further improve immunotherapy.

The COVID-19 pandemic is a challenge that is disrupting all aspects of life. Through fundamental research being done at Duke, our understanding of such a pandemic has advanced markedly, speeding and improving our capacity to respond. By innovative partnerships between Duke engineers and clinicians, novel methods are being developed to protect frontline medical professionals. Further, via innovative technologies like CRISPR and immunotherapy — that could only seem like science fiction in 1918 (and as recently as 2010!) — viruses are being used to save lives for previously intractable diseases.

Viruses can be killers, but they are also scientific marvels. This is the promise of fundamental research; this is the impact of Duke research.

“We shall not cease from exploration
And the end of all our exploring
Will be to arrive where we started
And know the place for the first time.”

T.S. Eliot, Four Quartets

Post by Lawrence Carin, Vice President for Research

The evolution of a tumor

The results of evolution are often awe-inspiring — from the long neck of the giraffe to the majestic colors of a peacock — but evolution does not always create structures of function and beauty.

In the case of cancer, the growth of a population of malignant cells from a single cell reflects a process of evolution too, but with much more harrowing results.

Johannes Reiter uses mathematical models to understand the evolution of cancer

Researchers like Johannes Reiter, PhD, of Stanford University’s Translational Cancer Evolution Laboratory, are examining the path of cancer from a single sell to many metastatic tumors. By using this perspective and simple mathematical models, Reiter interrogates the current practices in cancer treatment. He spoke at Duke’s mathematical biology seminar on Jan. 17.

 The evolutionary process of cancer begins with a single cell. At each division, a cell acquires a few mutations to its genetic code, most of which are inconsequential. However, if the mutations occur in certain genes called driver genes, the cell lineage can follow a different path of rapid growth. If these mutations can survive, cells continue to divide at a rate faster than normal, and the result is a tumor.

As cells divide, they acquire mutations that can drive abnormal growth and form tumors. Tumors and their metastases can consist of diverse cell populations, complicating treatment plans out patient outcomes. Image courtesy of Reiter Lab

With each additional division, the cell continues to acquire mutations. The result is that a single tumor can consist of a variety of unique cell populations; this diversity is called intratumoral heterogeneity (ITH). As tumors metastasize, or spread to other locations throughout the body, the possibility for diversity grows.

Intratumoral heterogeneity can exist within primary tumors, within metastases, or between metastases. Vogelstein et al., Science, 2013

Reiter describes three flavors of ITH. Intra-primary heterogeneity describes the diversity of cell types within the initial tumor. Intrametastatic heterogeneity describes the diversity of cell types within a single metastasis. Finally, inter-metastatic heterogeneity describes diversity between metastases from the same primary tumor.

For Reiter, inter-metastatic heterogeneity presents a particularly compelling problem. If treatment plans are made based on biopsy of the primary tumor but the metastases differ from each other and from the primary tumor, the efficacy of treatment will be greatly limited.

With this in mind, Reiter developed a mathematical model to predict whether a cell sample collected by biopsy of just the primary tumor would provide adequate information for treatment.

Using genetic sequence data from patients who had at least two untreated metastases and a primary tumor, Reiter found that metastases and primary tumors overwhelmingly share a single driver gene. Reiter said this confirmed that a biopsy of the primary tumor should be sufficient to plan targeted therapies, because the risk of missing driver genes that are functional in the metastases proved to be negligible.

 In his next endeavors as a new member of the Canary Center for Cancer Early Detection, Reiter plans to use his knack for mathematical modeling to tackle problems of identifying cancer while still in its most treatable stage.  

Post by undergraduate blogger Sarah Haurin

Post by Sarah Haurin

First-Year Students Designing Real-World Solutions

In the first week of fall semester, four first-year engineering students, Sean Burrell, Teya Evans, Adam Kramer, and Eloise Sinwell, had a brainstorming session to determine how to create a set of physical therapy stairs designed for children with disabilities. Their goal was to construct something that provided motivation through reward, had variable step height, and could physically support the students. 

Evans explained, “The one they were using before did not have handrails and the kids were feeling really unstable.”

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Teya Evans is pictured stepping on the staircase her team designed and built. With each step, the lightbox displays different colors.

The team was extremely successful and the staircase they designed met all of the goals set out by their client, physical therapists. It provided motivation through the multi-colored lightbox, included an additional smaller step that could be pulled out to adjust step height, had a handrail to physically support the students and could even be taken apart for easy transportation.

This is a part of the Engineering 101 course all Pratt students are required to take. Teams are paired with a real client and work together throughout the semester to design and create a deliverable solution to the problem they are presented with. At the end of the semester, they present their products at a poster presentation that I attended. It was pretty incredible to see what first-year undergraduates were able to create in just a few months.

The next poster I visited focused on designing a device to stabilize hand tremors. The team’s client, Kate, has Ataxia, a neurological disorder that causes her to have uncontrollable tremors in her arms and hands. She wanted a device that would enable her to use her iPad independently, because she currently needs a caregiver to stabilize her arm to use it. This team, Mohanapriya Cumaran, Richard Sheng, Jolie Mason, and Tess Foote, needed to design something that would allow Kate to access the entire screen while stabilizing tremors, being comfortable, easy to set up and durable.

The team was able to accomplish its task by developing a device that allowed Kate to stabilize her tremors by gripping a 3D printed handlebar. The handlebar was then attached to two rods that rested on springs allowing for vertical motion and a drawer slide allowing for horizontal motion.

“We had her [Kate] touch apps in all areas of the iPad and she could do it.” Foote said. “Future plans are to make it comfier.”

The team plans to improve the product by adding a foam grip to the handlebar, attaching a ball and socket joint for index finger support, and adding a waterproof layer to the wooden pieces in their design. 

The last project I visited created a “Fly Flipping Device.” The team, C. Fischer, E. Song, L. Tarman, and S. Gorbaly, were paired with the Mohamed Noor Lab in the Duke Biology Department as their client. 

Tarman explained, “We were asked to design a device that would expedite the process of transferring fruit flies from one vial to another.”

The Noor lab frequently uses fruit flies to study genetics and currently fly flipping has to be done by hand, which can take a lot of time. The goal was to increase the efficiency of lab experiments by creating a device that would last for more than a year, avoid damaging the vials or flies, was portable and fit within a desk space. 

The team came up with over 50 ideas on how to accomplish this task that they narrowed down to one that they would build. The product they created comprised of two arms made of PVC pipe resting on a wooden base. Attached to the arms were “sleeves” 3D printed to hold the vials containing flies. In order to efficiently flip the flies, one of the arms moves about the axis allowing for multiple vials to be flipped that the time it would normally take to flip one vial. The team was very successful and their creation will contribute to important genetic research.

The Fly Flipping Device

It was mind-blowing to see what first-year students were able to create in their first few months at Duke and I think it is a great concept to begin student education in engineering through a hands-on design process that allows them to develop a solution to a problem and take it from idea to implementation. I am excited about what else other EGR 101 students will design in the future.

By Anna Gotskind


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