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Daniel Dunaief

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From left, Deyu Lu (sitting), Anatoly Frenkel (standing), Yuwei Lin and Janis Timoshenko. Photo from BNL

By Daniel Dunaief

What changes and how it changes from moment to moment can be the focus of curiosity — or survival. A zebra in Africa needs to detect subtle shifts in the environment, forcing it to focus on the possibility of a nearby predator like a lion.

Similarly, scientists are eager to understand, on an incredibly small scale, the way important participants in chemical processes change as they create products, remove pollutants from the air or engines or participate in reactions that make electronic equipment better or more efficient.

Throughout a process, a catalyst can alter its shape, sometimes leading to a desired product and other times resulting in an unwanted dead end. Understanding the structural forks in the road during these interactions can enable researchers to create conditions that favor specific structural configurations that facilitate particular products.

First, however, scientists need to see how catalysts involved in these reactions change.

That’s where Anatoly Frenkel, a professor at Stony Brook University’s Department of Materials Science and Chemical Engineering with a joint appointment in Brookhaven National Laboratory’s Chemistry Division, and Janis Timosheko, a postdoctoral researcher in Frenkel’s lab, come in.

Working with Deyu Lu at the Center for Functional Nanomaterials and Yuwei Lin and Shinjae Yoo, both from BNL”s Computational Science Initiative, Timoshenko leads a novel effort to use machine learning to observe subtle structural clues about catalysts.

“It will be possible in the future to monitor in real time the evolution of the catalyst in reaction conditions,” Frenkel said. “We hope to implement this concept of reaction on demand.”

According to Frenkel, beamline scientist Klaus Attenkofer at BNL and Lu are planning a project to monitor the evolution of catalysts in reaction conditions using this method.

By recognizing the specific structural changes that favor desirable reactions, Frenkel said researchers could direct the evolution of a process on demand.

“I am particularly intrigued by a new opportunity to control the selectivity (or stability) of the existing catalyst by tuning its structure or shape up to enhance formation of a desired product,” he explained in an email.

The neural network the team has created links the structure and the spectrum that characterizes the structure. On their own, researchers couldn’t find a structure through the spectrum without the help of highly trained computers.

Through machine learning, X-rays with relatively lower energies can provide information about the structure of nanoparticles under greater heat and pressure, which would typically cause distortions for X-rays that use higher energy, Timoshenko said.

The contribution and experience of Lin, Yoo and Lu was “crucial” for the development of the overall idea of the method and fine tuning its details, Timoshenko said. The teaching part was a collective effort that involved Timoshenko and Frenkel.

Frenkel credits Timoshenko for uniting the diverse fields of machine learning and nanomaterials science to make this tool a reality. For several months, when the groups got together for bi-weekly meetings, they “couldn’t find common ground.” At some point, however, Frenkel said Timoshenko “got it, implemented it and it worked.”

The scientists used hundreds of structure models. For these, they calculated hundreds of thousands of X-ray absorption spectra, as each atom had its own spectrum, which could combine in different ways, Timoshenko suggested.

They back-checked this approach by testing nanoparticles where the structure was already known through conventional analysis of X-ray absorption spectra and from electron microscopy studies, Timoshenko said.

The ultimate goal, he said, is to understand the relationship between the structure of a material and its useful properties. The new method, combined with other approaches, can provide an understanding of the structure.

Timoshenko said additional data, including information about the catalytic activity of particles with different structures and the results of theoretical modeling of chemical processes, would be necessary to take the next steps. “It is quite possible that some other machine learning methods can help us to make sense of these new pieces of information as well,” he said.

According to Frenkel, Timoshenko, who transferred from Yeshiva University to Stony Brook University in 2016 with Frenkel, has had a remarkably productive three years as a postdoctoral researcher. His time at SBU will end by the summer, when he seeks another position.

A native of Latvia, Timoshenko is married to Edite Paule, who works in a child care center. The scientist is exploring various options after his time at Stony Brook concludes, which could include a move to Europe.

A resident of Rocky Point during his postdoctoral research, Timoshenko described Long Island as “extremely beautiful” with a green landscape and the nearby ocean. He also appreciated the opportunity to travel to New York City to see Broadway shows. His favorite, which he saw last year, is “Miss Saigon.”

Timoshenko has dedicated his career to using data analysis approaches to understanding real life problems. Machine learning is “yet another approach” and he would like to see if this work “will be useful” for someone conducting additional experiments, he said.

At some point, Timoshenko would also like to delve into developing novel materials that might have an application in industry. The paper he published with Frenkel and others focused only on the studies of relatively simple monometallic particles. He is working on the development of that method to analyze more complex systems.

This work, he suggested, is one of the first applications of machine learning methods for the interpretation of experimental data, not just in the field of X-ray absorption spectroscopy. “Machine learning, data science and artificial intelligence are very hot and rapidly developing fields, whose potential in experimental research we have just started to explore.”

 

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Cheese, milk, butter, ice cream, yogurt. You were all such good friends. I was lucky to have known you at all.

Long ago, I developed an intolerance for you. It’s not as if you’d kill me but, let’s just say, you’d incapacitate me for a prolonged and agonizing period of time if I ever decided to ignore all the earlier experiences and indulge again.

That doesn’t mean, however, that I can’t appreciate the quality time we shared together, the memories you forever embedded in my taste buds and in my satisfied stomach.

I’ll start with the unexpected. Yes, you, in the corner, looking all innocuous. Stand up custardy yogurt and let me recall the smooth, cool feel and consistent taste. My favorite was banana, even though I lost the second-grade spelling bee when I thought there had to be an extra “n” in there somewhere. Someone with as many vowels as there are in the name Dunaief should have recognized the superfluous nature of consonants, but alas I was too young.

Then there’s macaroni and cheese. The soft noodles and almost too-sweet cheese was like a warm, sweet bath for my mouth. After throwing snowballs at my brothers or coming in from the walk along Mud Road from Gelinas on a rainy day, the hot mac and cheese revived me enough to break out my homework and try to figure how to find a second derivative or identify feldspar (a rock-forming mineral).

Then there’s that tall carton of milk. How awesome were you with Oreos and chocolate chip cookies? I’d dip the cookies deep into the milk, hoping they’d break apart. At the end of that refreshing glass, I’d have a blend of cookie crumbs supersaturated in milk at the bottom. I tipped the cool glass toward my mouth and let those mushy morsels land gently on my unfolded tongue.

And then there’s ice cream. After a movie at Stony Brook Loews, I’d sit with my buddies at Friendly’s on Route 347 and wait as patiently as I could for everyone else to figure out what they wanted. I pretended to read the menu, particularly when I was on a date and was considering what to say next, but the choice was always the same: the mint chocolate chip sundae.

During cold winter days, particularly after a day of skiing with my family — who were patient enough for me to stop getting frustrated when I fell, learn from my mistakes and enjoy the ride — I looked forward to onion soup. Oh, the melted cheese on the top of that soup. As my wife would say, what’s better than that?

Busboys risked serious injuries to their fingers if they tried to take the Crock-Pot before I’d finished picking every piece of cheese off the sides. When I finally looked up from my cheese removal operation, I saw my mom flashing that same annoying grin I show our children when I see how satisfied they are in a moment.

Since we’re discussing cheese, how about a grilled cheese? Buttered bread with soft American cheese was an irresistible delight. I’d order several of these sandwiches at the old Jack in the Box at the corner of 25A and Main Street in Setauket.

When I was young, one of my late father’s favorite sandwiches was Swiss cheese on rye with lettuce, tomato and mustard. The first time I tried it, I smiled politely and gave it back to him. Before the end of the dairy road for me, I ordered it again and thoroughly enjoyed it. Maybe it was an acquired taste or maybe it brought me closer to my father, who I could imagine enjoying the life and the food as much as I did. Oh, those dairy delights.

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John Daly racing down the slope. Photo from Jonn Daly

Four years ago, Smithtown resident James Daly took his son John aside. The younger Daly had been in position to realize a long-held dream, only to see that dream slip away, as if it, and his sled, had slipped into a nightmare on Russian ice.

Competing in his second Olympics in the fast-paced sport of skeleton racing, John Daly was in fourth place in the Sochi Winter Olympics going into the final run of a four-heat race when his sled popped out of the grooves at the top of the mountain. That slip cost him time he could not afford to lose, sending him down to 15th place, and after the race, into retirement.

John Daly is a professional skeleton racer. Photo from Jonn Daly

Daly’s father grabbed him and said, “What happens to you today will make you the man that you’ll be tomorrow,” the son recalled.

At the moment, Daly barely registered the words, as the agony of defeat was so keen that he walked away from a sport that had helped define his life over the last 13 years.

His retirement, however, only lasted two. Daly wanted to rewrite his Olympic script.

The Smithtown native recently learned that he would represent the United States for a third time at the Winter Olympics, completing a comeback that required him to make marathon nine-hour drives from Virginia, where he’d gotten a job as a sales representative at medical technology company Smith & Nephew, to Lake Placid, where he returned to familiar stomping grounds.

A race official for bobsled and skeleton, the elder Daly continued to trek to the top of snowy and wind-whipped mountains, recognizing in the back of his mind that the middle of his three children might one day return to a sport where competitors sprint with a hand on their sled for five seconds and then dive headfirst onto a brakeless vehicle that can reach speeds in excess of 80 miles per hour.

When he learned his son made the Olympic team that will compete in Pyeongchang, South Korea next month, Daly couldn’t contain his enthusiasm.

“I’ve been telling everybody,” the retired EMS worker for the FDNY said with a laugh, even including random people he meets at the gym.

“When people watch the Olympic games on TV, they see a person from a town they never heard of,” James Daly said. “Now, all of a sudden, they see Smithtown. It’s great.”

The racing Daly, who is now 32, had a long road back to reclaim a spot on the American team. For starters, he had to go back to North America Cup races, the junior circuit of racing.

“Daly never really lost it. It was quite amazing to see.”

— Tuffy Latour

Daly “never really lost it,” said Tuffy Latour, the head coach of the USA skeleton team. “It was quite amazing to see. We were quite pleased.”

In January of last year, Daly earned a gold medal at Salt Lake City and followed that up with a gold and silver at Lake Placid.

Not only was his proud father there to celebrate John’s return, James also put the hardware around his neck.

“He’s been there from the time I went down the mountain the first time,” John said. “He’s always been there and for him to be there again, to put the medal on me for my first race back, it felt right.”

The pair joked while celebrating the first of several America’s Cup medals that the success felt familiar, like Daly was never gone.

At this point, Daly said he feels that the track in South Korea where he will square off against veteran sliders, including his longtime friend and teammate Matt Antoine, plays to his strengths. Latour said the American team is in a similar position preparing for South Korea as it was going into Sochi.

“We had a test of it last year in the World Cup,” the coach said. “The results were similar to what we had [in 2014].”

Latour said it sometimes helps to walk away for a few years and come back refreshed. He highlighted Daly’s experience as an asset in preparation for the 2018 games.

“He has nothing to lose,” said Latour, who appreciates how Daly’s comedic side helps steady his teammates during competition. He said Daly has the same energy he had before he left the race. “It’s great to have him around.”

John Daly, with father James, has had a successful season leading up to the Olympics in North Korea, grabbing gold in Lake Placid last year. Photo from John Daly

Daly said he’s proud to represent the United States. After he retired, he went to the gym, where he’d see people wearing sweatshirts emblazoned with the names of the colleges they’d attended. His sweatshirts read “USA.”

“That USA represents every college,” said Daly. “It’s a good feeling to wear it.”

At the South Korea games, Daly will be without teammate and friend Steve Holcomb, who died last year at 37. Holcomb’s story, including a recovery from an eye disease that made him nearly blind to a gold medal-winning driver of the celebrated Night Train sled, inspired people around the world, as well as his teammates.

As with his fellow bobsled and skeleton racers, Daly will be flying down the mountain in a suit that has Holcomb’s initials on it.

Daly will spend a next few weeks preparing for one more chance in the Olympics.

During the training to get back, Daly said his body and his mind demanded to know why he’s going through this work again.

He told himself: “I’m here to finish my career off the way I’d like.”

Bennarda Daly, who will attend the Olympics with her husband, said the South Korea Olympics will give her son something he didn’t get from the games in Russia.

“In South Korea,” she said, “he will finally get closure.”

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From left, Brenna Henn and Meng Lin at a conference last year in New Orleans. Photo from Meng Lin

By Daniel Dunaief

The story of the genetics of skin pigmentation in humans may have even more layers than the skin itself, depending on how close people live to the equator. The conventional wisdom for skin pigmentation is that it is a relatively simple trait, with a small number of genes accounting for almost half of the variety of skin tones.

That, however, isn’t always the case. Pigmentation genetics likely becomes more complex in populations near the equator or with greater variation in pigmentation, like with the Khoisan living in southern Africa.

Above, Brenna Henn, right, with an elder in the Khomani San community who gave her a book on the language formerly spoken in the southern Kalahari Desert. Photo from Brenna Henn

“As you move further toward the equator, the distributions are wide,” Brenna Henn, an assistant professor in the Department of Ecology and Evolution at Stony Brook University, said about the results she, along with collaborators from her lab and from Stanford University, recently published in the journal Cell.

Exploring the genetic determination of skin can serve as a model to understand the broad implications for various genetic variations for different populations as they confront a range of health challenges.

Henn has also worked with tuberculosis studies in South Africa. About one in three people in the world has a latent tuberculosis infection. Researchers have conducted studies to see which genes might be responsible for the different reactions to this disease. Tuberculosis susceptibility studies indicate that different genes may be responsible for infection in different populations, in areas including Russia, West Africa and South Africa.

According to Henn, scientists need to study and understand the disease in different populations to identify, through gene interactions, who will benefit from specific treatments in a vaccination campaign.

When Henn, who is a native of California, started the pigmentation study seven years ago when she was a graduate student at Stanford University, she had considerably different expectations. “When I was a post doc at Stanford, I expected the project to be quick because the genetics of pigmentation in Europeans was relatively well understood,” she explained in an email. When she started analyzing the results, she found that her hypothesis “was not true at all. There are so many different things involved.”

Calling this analysis the “tip of the iceberg,” Henn said she discovered many new genes beyond the ones scientists already knew contributed to skin pigmentation. She estimates that there are 50 if not more genetic sequences involved in skin pigmentation near the equator.

The range of skin pigmentation in South African populations reflected this increased genetic blueprint, with people in these areas demonstrating about twice the variation as people might encounter in a western European population.

These studies require the analysis of considerable data, through a field called bioinformatics, in which researchers analyze and process information through programs that search for patterns. “There’s a huge computational component” to this work, Henn said. “We don’t know where the genes are. We have to sample the entire genome” for as many as 500 people. “This blows up into a computational problem.”

Above, from left, Meng Lin and Brenna Henn at Lin’s graduation ceremony where she earned her PhD. Photo from Brenna Henn

Meng Lin, who worked in Henn’s lab for four and a half years and recently earned her doctorate, performs just such analyses. “We were hoping we’d be able to find some signals that had never been found before, to demonstrate the difference” in the genetic architecture, said Lin, who is now applying for postdoctoral research positions. “Given the prior studies on skin pigmentation traits, the complexity of the genetic architecture we found out was unexpected.”

People near the equator would likely need to have pigmentation that balanced between producing vitamin D from sunlight with protecting their skin from too much exposure to ultraviolet light. In areas such as in Africa, the ultraviolet light can be so strong that “the primary selection factor would be to avoid the photo damage from the strong UV, which favors melanin enriched dark skin pigmentation for photo protection,” Lin explained in an email.

Generally, people further from the equator, such as Scandinavian populations, have lighter skin because they need to process the limited vitamin D they can get, particularly during the darker months. That, however, isn’t the case for the Inuit people, who have darker skin in an area that gets limited sunlight. “Anyone who lives there should be under pressure for light skin,” Lin said. The Inuit, however, are darker skinned, which might be because their diet includes fish and fish oil, which is a rich source of vitamin D. “That would relax the selection force on lighter skin color,” she said.

With people able to travel and live in a wide range of regions across the Earth, selection pressures might be harder to decipher in the modern world. “Travel across continents is a recent” phenomenon, Lin said. The history of such travel freedom is “way too short for changing the genetic components.” Selection pressure occurs over tens of thousands of years, she added.

Diversity and the intake of vitamin D interact closely with each other. They can have impacts on the balance point. Using vitamin supplements could relax the selection on lighter skin, so the balance might shift to a darker population, Lin explained. Other modern lifestyles, such as wearing clothes, staying indoors and consuming vitamin D could complicate this and relax the strength of selection in the future, she added.

A native of China, Lin lives in Port Jefferson Station and enjoys applying math and computer skills to biology. “It’s great fun to solve the questions we have by developing and applying computational methods to existing data,” she said.

After five years at Stony Brook, Henn is transitioning to a position at the University of California at Davis, where she hopes to continue this ongoing work. “We want to follow up on how quickly these selective events occur,” Henn said. She’d like to discover how long it takes for the genetic average of the population to shift.

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He was so close and then, poof, everything he’d worked for and imagined for 13 years disappeared in an instant.

John Daly, a Smithtown native who hates the cold, was competing in his second winter Olympics in Sochi, Russia, and was in fourth place, in the hunt for a medal after three of the four legs of his skeleton race.

In skeleton, athletes sprint at top speed hunched over with their hands on the sleds for five seconds, then dive headfirst on the sleds, navigating around the curved icy track by shifting their weight while traveling at speeds of more than 80 miles per hour.

And then, in the fourth race, at the top, where he needed to generate the kind of speed that would allow him to race against his rivals and the clock, Daly’s sled popped out of the grooves in the ice, slowing him down and sending him back to 15th place.

After such a crushing defeat, Daly decided to move on with his life, retiring from a sport where he’d won numerous other medals and where he was one of the country’s best sliders.

For two years, he stayed retired, taking a job in Virginia at medical technology company Smith & Nephew.

Then, a funny thing happened in retirement. Daly missed the sport. He didn’t have the same passion for other parts of his life, the bitter cold from mountains around the world notwithstanding, that he felt when he was racing.

He spoke to numerous people about what he might do.

People his age, he’s 32, could understand the hesitation about throwing himself back into a sport that required physical and mental commitment. To get back into prime condition, Daly would need to make nine hour drives from Virginia, where he was living, up to Lake Placid, a familiar training ground and site of the 1980 Miracle on Ice.

People older than he is, however, couldn’t understand the agony of the decision.

“Why wouldn’t you go back?” they asked. When you’re older, they argued, “Do you want to look back and say, ‘I might have gotten a little further ahead at work,’ or do you want to go back for one more Olympic games?”

Unlike other competitions, the Winter Olympics only occur once every four years. And, unlike the World Cup competitions, a global TV audience seems to pause to watch the games.

The Olympics can make the improbable possible, including the unexpected warming of tensions between North and South Korea, who are marching together in the opening ceremony and sending a combined women’s ice hockey team to the games.

As we age, we don’t always spring out of bed the same way and we may lose a step or two in our reaction time. We gain, however, the benefit of each year of life experiences, observing how we, and the world around us, change.

Daly decided to return to the sport, where he has made his third Olympic team. The poet Horace, who published the immortal Latin phrase “carpe diem,” meaning “seize the day,” would be proud.

No one knows how Daly will do in a few weeks. Could he medal? His coach Tuffy Latour thinks so.

Latour said that Daly “never really lost it.”

Sometimes, Latour said, the time away helps athletes better prepare for the next Olympics, allowing them to gain a fresh perspective.

Coming back, however, may prove equally important for Daly, who is hoping to rewrite the final chapter of a sliding odyssey. Many years from now, he hopes he may one day offer the same kind of support to his kids that he received from his parents James and Bennarda, whom he jokingly called “sliding enablers.”

Regardless of the outcome, that older version of himself may thank him for giving it one more try.

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How old were you when you kissed your first partner, had your first alcoholic drink, met the person of your dreams, had your first child, dealt with your first serious loss, got your first big job or made your first million?

We can use age to motivate us, give us a sense of time and place, and allow us to hear the alarm bells, or to hit the snooze button for the next phase of our lives.

We compare ourselves to those around us to see if we’re approaching the landmarks at the right pace. We take pride in our accomplishments, or in the accomplishments of our children, as in, “My son started walking when he was 7 months old.”

The comparisons often start with our parents, even though we come from a different generation. I wasn’t anywhere close to getting married at the same age as my parents were when they wed. I thought about that when I passed that landmark age. Was I moving too slowly? Was I missing something or someone? Was I falling behind?

I took comfort in knowing that I lived at a different time. Then again, I also passed the age at which my brother got married. Did I need to do a hard target search of every outhouse, henhouse and farmhouse to find my fugitive wife?

Fortunately, the answer had nothing to do with age. I could have married other women, but I hadn’t met the right person.

Before my wife and I got married, we were in sync about when we wanted to try to make that wonderfully challenging transition toward parenthood.

Now, as the years have passed and our children have learned to drive the car — and us crazy — we have reached other milestone ages.

They have celebrated academic landmarks, graduating from elementary and middle schools while working their way through high school.

Our milestone birthday numbers don’t come as frequently as 16, 18, 21, and 25 do for our kids.

But, every so often, we hit a number that has significance either on its own, ending in a zero or a five, or because of some family connection.

I am approaching just such a challenging milestone. My father was this old when he died. I know there are people like Mickey Mantle, who expected to live a relatively short life. Mantle’s grandfather died at 60 and his father passed away at 40, both from Hodgkin disease. In the event, the baseball legend lived until he was nearly 64.

At every annual physical, my doctor and I review my family history. We are aware of the diseases that may be lurking somewhere in my genes. It makes sense to monitor my health and to catch anything early, particularly something that may run in the family.

Still, I don’t share Mantle’s sense of predestination, just as I didn’t feel an overwhelming urge to grab the nearest woman I found relatively unobjectionable because I had to get married at the same age as my parents or my brother.

My life doesn’t come with a playbook or a chapter outline. Maybe I would have made more money by now, reached more personal milestones, or run a few more marathons — OK, one — if I’d recognized all the age-related alarm bells.

Then again, if I had, I would have missed out on knowing my wife and our children, three people whose lives enrich and define my own.

So, yes, while I keep an eye on the genetic footprints in the sand ahead of me, I also hope to follow my own compass as I imagine the days ahead when I become older than my father.

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Yali Xu and Christopher Vakoc at the 2013 Don Monti Memorial Research Foundation’s Anniversary Ball. Photo from Yali Xu

By Daniel Dunaief

It’s like a top scorer for another team that the greatest minds can’t seem to stop. Whatever they throw at it, it seems to slip by, collecting the kinds of points that can eventually lead to a life-threatening loss. The scorer is a transcription factor called MYB, and the points it collects can, and often do, lead to breast and colon cancer and leukemia.

Researchers have known for over 30 years that stopping MYB could help with cancer treatment. Unlike other possible targets, however, MYB didn’t seem to have the kind of structural weakness that pharmaceutical companies seek, where developing a small molecule could prevent the cancer signals MYB delivered. Some researchers have decided that drugs won’t stop this high-profile cancer target.

Cold Spring Harbor Laboratory Associate Professor Christopher Vakoc and his graduate research assistant Yali Xu, however, have figured out a way around this seemingly intractable problem. The CSHL scientists recently published their results in the journal Cancer Cell.

MYB binds at a small nub to a large and important coactivation protein called TFIID (which is pronounced TF-two-D). This protein is involved in numerous life functions and, without it, organisms couldn’t survive. Vakoc and Xu found that they could use a small peptide decoy to trick MYB into believing it had attached to this protein when, it reality, it hit the equivalent of a molecular dead end.

In a mouse model of acute myeloid leukemia, this peptide caused leukemias to shrink in size by about 80 percent. “What we’ve discovered is head and shoulders above anything we’ve come across before,” Vakoc said.

As with many scientific discoveries, researchers have to clear numerous hurdles between this conceptual discovery and any potential new cancer therapy. “This is not a medicine a person can take,” Vakoc said.

Indeed, scientists and pharmaceutical companies would need to study what leukemia cells escaped this type of treatment to understand how a cancer might rebound or become resistant after an initial treatment. “Our goal is to develop something with longer lasting effects” that doesn’t become ineffective after three to six months, Vakov said. He described understanding the way a disease reacts to a treatment as an “arms race.” Nature inevitably “finds a way to outsmart our decoy. We’d like to know how [it] does it. We’re always trying to study both sides and trying to anticipate” the next steps.

Down the road, Vakoc could foresee researchers and, ultimately, physicians using this kind of approach in combination with other drugs or therapies, the way doctors now provide patients who have the HIV infection with a cocktail of drugs. Conceptually, however, Vakoc is thrilled that this work “highlights what’s possible.”

One of the most encouraging elements of this approach, Vakoc said, is that it combats MYB without harming organ systems. When the researchers gave the treatment to rodents, the mice were “running around, eating and gaining weight.” Their body tissues appeared normal, and they didn’t demonstrate the same sensitivity that is a common byproduct of chemotherapy treatment, such as losing any hair or having problems in their gut.

An important step in this study, Vakoc said, was to understand the basics of how MYB and TFIID found each other. That, Xu said, was one of the first steps in her graduate work, which took about five years to complete.

In Vakoc’s lab, which includes 13 other researchers, he described how scientists make thousands of perturbations to cancer and normal cells, while they are hunting for cancer-specific targets. By using this screening technique, Vakoc and his team can stress test how cancer cells and normal cells react when they are deprived of certain proteins or genes.

“This began as a screen,” he said. “We took leukemia and normal blood cells and did a precise comparison of the perturbation.” They searched for what had the most specific toxicity and, to their surprise, found that interfering with the binding between MYB and TFIID had the strongest effect. “Once we understood what this nub was doing, we applied all kinds of biochemical assay experiments,” Vakov added.

Ultimately, the peptide they found was a fragment of a larger protein that’s active in the cell. Vakoc credits Xu for her consistent and hard work. “When we started on this hunt, we had no idea where this was headed,” he said. Xu was “relentless” in trying to find the answers. “She pieced it all together. It took a great amount of imagination and intellect to solve this puzzle.”

Vakoc suggested that Xu, who plans to defend her thesis this spring and graduate this summer, has set a great example for the other members of his lab. “I now have 13 other people inspired to outdo her work,” he said. “We know we have a new standard.”

Xu is grateful for the support she has received from Vakoc and appreciates the journey from her arrival as a graduate student from China to the verge of her graduation. “It’s very satisfying when you look back and think how things evolved from the beginning to the end” of her graduate work, said Xu, who lives near Huntington Village and enjoys the chance to visit local restaurants and sample coffee and ice cream when she isn’t conducting research toward her doctorate.

The scientific effort, which was published recently, has attracted the attention of others, particularly those who are studying MYB. Vakoc recently received an email from members of a foundation that is funding research on a solid tumor in which scientists believe MYB plays a role. He is writing grants to get more financial support to pursue this concept. Vakoc is encouraged by the opportunity to make progress with a protein that has been “staring [scientists] in the face for three decades.”

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Furie, above sailing on her 26-foot boat that is moored at Manhasset Bay, is navigating the American Journal of Pathology toward new waters. Photo by Richard Furie

By Daniel Dunaief

Martha Furie has a job no other woman has held in the 122-year history of a highly regarded scientific periodical. A professor of pathology and molecular genetics and microbiology at Stony Brook University, Furie is the new editor-in-chief of the American Journal of Pathology, taking over the top editorial job at a journal where she has been a contributor since 1993.

Martha Furie. Photo by SBU

“As a woman, it is certainly gratifying to see an accomplished and capable woman such as Martha being chosen to lead the way,” said Kari Nejak-Bowen, an assistant professor in the Department of Pathology at the University of Pittsburgh, School of Medicine, in an email. “Seeing women such as [Furie] in positions of power and visibility will empower other female scientists to dream that they can accomplish similar goals.”

Richard Mitchell, a senior associate editor at the journal and a professor of pathology and health sciences and technology and vice chair for education at Brigham and Women’s Hospital also applauded the choice. Furie “was probably the very best person we could recruit for the job and is someone who has the energy and vision for leading us into the challenging future,” Mitchell said.

From 1986 through 2014 Furie ran a lab that focused on the study of the body’s immune response to infections from Lyme disease and tularemia, which is cause by a bacterium that is classified as a potential agent of bioterrorism. In 2014, she became the director of the Graduate Program in Genetics at Stony Brook.

Kenneth Shroyer, the chair of the Department of Pathology at SBU, described the periodical Furie starts leading in 2018 as the “top pathology journal.”

As she takes the helm of the journal, Furie plans to navigate the periodical toward more translational research. “The Journal has been very focused on understanding the basic mechanisms of disease,” she said. “Research in all areas is getting much more translational: The bench-to-bedside thinking is where funding agencies are focusing their efforts,” and it’s also where the periodical she now leads is heading.

The tagline for the journal, which Nejak-Bowen said helped pioneer the current understanding of cell death, used to be Cellular and Molecular Biology of Disease. Furie changed that to Discoveries in Basic and Translational Pathobiology.

Shroyer believes the new direction should help the journal compete and redefine its niche for a wider range of readers. While Furie is excited about the opportunity, she acknowledges the increasingly challenging nature of the business. “Scientific publishing is a tough area right now,” she said. “There are fewer people in research because funding has diminished,” while, at the same time, more journals are competing to highlight research discoveries.

She will try to raise the journal’s profile for research scientists. Furie plans on expanding the journal’s social media presence and will do more marketing, while working with expert associate editors and getting them more involved in soliciting submissions. She also plans to make collections of highly cited papers in targeted areas and intends to use these to market the journal to attendees at specialized conferences.

Furie will spend this month contacting each of the associate editors and will solicit suggestions for people who might like to join the publication. She will also seek ideas for the journal. Mitchell suggested that Furie would likely benefit from these interactions. She is a “very good listener and is thoughtful in the questions she asks,” he said. “She is very discerning in assimilating the answers she gets back.” Shroyer expressed confidence in Furie’s leadership, citing a string of accolades and accomplishments in an SBU career that began in 1986.

Above, Furie welcomes students and faculty to the graduate program’s retreat in 2016. Photo by Constance Brukin

Furie was the president of the American Society for Investigative Pathology from the middle of 2011 through the middle of 2012. She was also the recipient of the Robbins Distinguished Educator Award in 2017, which recognizes people whose contributions to education in pathology had an important impact at a regional, national or international level.

Furie and Nejak-Bowen co-organized and co-chaired the ASIP Scientific Sleuthing of Human Disease for High School Teachers and Students in April 2017. With this effort, Furie has already had some success in changing the direction and target audience of an ongoing program. The session, which provides high school teachers with concepts of human disease that they can incorporate into their classroom, now includes high school students.

“This has really revitalized the program, as the students are inquisitive and very engaged with the material,” Nejak-Bowen explained. Furie was “instrumental in encouraging this change in focus, and is passionate about building an improving this session every year.”

The opportunity Furie has as editor-in-chief of the Journal of Pathology “continues her role as a national leader that she’s established,” Shroyer said.

Furie said she benefited from a diverse staff at Stony Brook, that included women like current Professor Emeritus Gail Habicht, when she first arrived. One of the best pieces of advice she received from Habicht was to understand that you can have a family and a successful career.

“You might not be able to do it to the same standard of perfection you did before you had children, but you can have a meaningful career and raise successful children and be happy doing both,” recalled Furie, who has two sons, Jon and Dan, and a 10-month-old grandson Tyler, who lives in Bedford, New York. She is married to Richard Furie, the chief of the Division of Rheumatology at Northwell Health, whom she met in a physics class at Cornell over 45 years ago.

Nejak-Bowen said Furie “leads by example when it comes to work/life balance.” Nejak-Bowen urges women scientists to find a mentor who can offer advice through all stages of a career. She has long considered Furie “a friend, mentor and inspiration.”

Based on Furie’s track record, Shroyer is confident in her continued success and anticipates that the journal will “thrive under her direction.”

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In the dark of night, it silently slithered toward the back of the car, spray painting the windows with a sheen of opaque white.

It made its way around the car, finding the seam in the doors and filling it with surprisingly strong epoxy. It glided down to the ground and sucked some of the warm air out of the tires. The car was trapped on the driveway with no way to fight off this unwelcome intruder. If its alarm could have gone off, it would have warned us. But, no, that alarm only goes off early in the morning on the weekends, when someone opens the door with the key instead of deactivating the alarm system with a button, annoying the neighbors and embarrassing our kids and us in equal measure.

It slid under the hood. It paused over the heart of the machine, looking for places to extend its icy fingers into the exposed engine, snickering with delight at the opportunity to turn 3,000 pounds of metal into a frozen couch.

It reached into the battery and deactivated the power.

On my way to the car, it issued a warning, or was it a challenge, when it wrapped its icy fingers around my neck. I tried to ignore it and stick with my routine. When I turned the key, however, the car coughed weakly.

“Come on,” I pleaded, as the cold scraped its icicle hands against my exposed calf. I tried again. The third time was not the charm, either.

After getting a jump start, I decided to outsmart the wretched cold. I cleared space in the garage, hauling all the heavy items parked there into the basement. The garage door and the walls of the house would offer greater protection. No, I wasn’t giving the car a blanket and pillow and setting it up with reruns of “Knight Rider,” but I was protecting the family car.

The next day, I went through the basement into the garage, put the key in the ignition and beamed broadly as the internal combustion engine roared to life. Ha! I foiled the frigid air. I told the kids to climb in the car, which warmed up rapidly as a reward for keeping it in the garage, and drove triumphantly to school. The cold wouldn’t undermine my day, I thought, as I maneuvered through the responsibilities of the day.

When I returned home, I found that the cold had recruited my garage door to its unworthy cause. I didn’t look carefully enough when I had pulled away from the house. The garage door, fooled by a small piece of snow in the corner of the floor, thought it had hit something and reopened, where it stayed all day.

I pulled the car in, closed the garage and waited for the door to close. When the metal door reached the ground, it reopened. I played a short game with the door, pushing the button just after it started to open again so that the cold air had only a small opening.

“I win,” I announced as I entered the warm house.

When I turned on the water in my bathroom the next morning, I realized I had lost. The combination of the cold from the open garage from the day before and the small crack at the bottom of the door was enough to enable the cold to lay its frozen hands on my pipes.

Several hours later, the plumber, who was busier than a foraging ant during a Fourth of July picnic, shivered in the garage and proclaimed the small opening under the door as the culprit.

This cold snap, which finally left the area earlier this week, won this battle.

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Alexander Krasnitz. Photo by Gina Motis?CSHL

By Daniel Dunaief

Seeing into the future is one of the most challenging, and potentially rewarding, elements of studying cancer. How, scientists and doctors want to know, can they take what evidence they have —through a collection of physical signs and molecular signatures — and determine what will be?

Researchers working on a range of cancers have come up with markers to divide specific types of cancers to suggest the likely course of a disease.

With prostate cancer, the medical community uses a combination of the prostate-specific antigen (PSA), magnetic resonance imagining (MRI) and biopsy results, which are summarized as the Gleason score, to diagnose the likely outcome of the disease. This analysis offers probable courses for developing symptoms.

Cold Spring Harbor Laboratory Professor Michael Wigler and Associate Professor Alexander Krasnitz recently published an article in the journal Cancer Research of a promising study of eight patients that suggests a way of using molecular signatures to determine whether a prostate is likely to contain cells that will threaten a patient’s health or whether the cells are in a quieter phase.

The third most common cancer among Americans, prostate cancer kills an average of 21,000 men each year. Doctors and their patients face difficult decisions after a prostate cancer diagnosis.

“A major challenge is to determine which prostate cancers have aggressive potential and therefore merit treatment,” Herbert Lepor, a professor and Maritin Spatz Chair of Urology at the NYU Langone Medical Center School of Medicine, explained in an email. A collaborator on the study, Lepor provided a clinical perspective and shared patient samples.

A conversation with a doctor after such a diagnosis may include a discussion about how the cancer is not likely to pose an immediate risk to a patient’s life, Krasnitz explained. In that case, doctors do not recommend surgery, which might cause other problems, such as incontinence.

Doctors typically recommend active surveillance to monitor the disease for signs of progression. Some patients, however, make their own decisions, electing to have surgery. The Gleason score, which is typically 3, 4 or 5, can’t provide “meaningful information regarding aggressiveness of the disease,” Lepor explained. “The unique genetic profile of a cancer cell should have infinite more prognostic capability.”

Wigler and Krasnitz, who have been collaborating since Krasnitz arrived at CSHL in 2005, use several hundred single cells from biopsy cores. The research group, which Krasnitz described as a large team including research investigator Joan Alexander and computational science manager Jude Kendall, look for cells with a profile that contains the same irregularities.

“If you take two cells and their irregularities are highly coincident, then perhaps these two cells are sisters or cousins,” Krasnitz explained in an email. “If they are less coincident, then the two cells are more like very distant relatives. We looked for, and sometimes found, multiple cells with many coincident irregularities. This was our evidence for a clonal population.”

By looking at how many biopsy cores contain clonal cells, and then determining how far these clonal cells have spread out through the prostate, the researchers gave these patient samples a score. In this group, these scores, determined before any intervention, closely tracked a detailed analysis after surgery.

“We get a high correlation” between their new score and a more definitive diagnosis that comes after surgery, Krasnitz said. “Our molecular score follows the final verdict from the pathology more closely than the pathological score at diagnosis from the biopsy.”

Wigler, Krasnitz, Lepor and other researchers plan to continue to expand their work at Langone to explore the connection between their score and the course of the disease. Lepor explained that he has been collaborating with Wigler and Krasnitz for five years and suggested this is “an exceptional opportunity since it bridges one of the strongest clinical programs with a strong interest in science (NYU Urology) and a world-class research program interested in clinical care (CSHL).

The research team has submitted a grant to the National Institutes of Health and hopes to expand their studies and provide “compelling evidence” that single-cell genomic mapping “will provide an unmet need defining aggressiveness of prostate cancers,” Lepor said.

While Krasnitz is encouraged by the results so far, he said the team has work ahead of them to turn this kind of analysis into a diagnostic tool physicians can use with their patients.

Realistically, it could take another five years before this score contributes to clinical decision-making, Krasnitz predicted. “You can’t do it overnight,” he cautioned. When this test offers specific signals about the likely outcome for a patient, a researcher would likely need to wait several years as the patient goes on active surveillance to see whether the score has predictive value for the disease in a larger population.

Krasnitz has a sense of urgency to produce such a test because there is “no point in delaying something that potentially looks promising and that one day might well be a part of a clinical practice.”

The work that led to their article took three or four years to complete. The study required technical improvements in the way the researchers processed DNA from single cells. They also had to develop algorithmic improvements that allowed them to use copy number variation to determine clonal structure. The scientists tapped into a wealth of information they gained by taking cells from several locations within the prostate.

Krasnitz was born in Kiev, now part of the Ukraine, and grew up in the former Soviet Union. A resident of Huntington, he lives with his wife Lea, who produces documentaries, including “Maria — The Russian Empress” on Dagmar of Denmark, who was also known as Maria, mother of Nicholas II, the last Romanov czar who was overthrown in 1917. As for his work with Wigler, Krasnitz is excited about the possibilities. “It’s very encouraging,” he said. “We look forward to a continuation of this.”

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