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Authors Posts by Daniel Dunaief

Daniel Dunaief

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My brothers are getting ready to celebrate their birthdays, which are two days apart. OK, so, several years and two days apart, so, no, they aren’t twins who kept my mother in labor for more than 48 hours.

At times I thought perhaps I, the middle child, should have been born on the day in between them. That way, my parents would have gotten all the birthday parties for the year done in one week.

Then again, it would have been hard for any of us to own more than 24 hours if we were all making plans for something special in the same narrow window of time.

As a longtime baseball devotee and recreational player, I always imagined the best thing I could do on my birthday would be to attend a Yankees game.

Over time, the focus on my birthday has changed. Yes, I enjoy my wife’s chocolate chip cookies, which she bakes as often as I like and, yes, I enjoy the calls and the cards. However, I don’t anticipate the day the same way I did when I was my children’s age, as they count down the days, hours and minutes until their annual celebration.

My son, who also loves baseball — hmm, I wonder how that happened? — has often talked about going to a game on his birthday, which is, conveniently, during the summer. The biggest challenge to making that happen is that he plays baseball so often that his games often conflict with Yankee games. In fact, during some weeks in the summer, he plays more games than Alex Rodriguez. OK, well, maybe that’s a bad example because poor A-Rod, who is a shell of his former self, hasn’t gotten much playing time these days.

Back to birthdays, though, if I could choose between a summer and winter birthday, I’m not sure which way I’d go. Let’s lay out the advantages of a winter birthday: For starters, I might get one of those natural gifts, when a snow day would eliminate all the hustle and bustle as the world stops and is covered with a white blanket. Nice as that sounds, that never happened.

My school friends were around on my birthday. During the summer, some of my son’s friends go to camp, where they might send him a snapchat or a text message around his birthday, but they can’t hang out, eat cake and swim in a pool.

I could also go skiing on my birthday. I love racing fast enough down a mountain that my eyes water from speeding down a trail. And, after an incredible day at Killington or Mount Snow, both in Vermont, I could relax in a lodge, in front of a fireplace, with my tired feet and exhausted knees propped up on the hearth.

I also enjoyed going to the beaches during the winter, when the crowds were gone and I felt as if I owned the windswept landscape, from one end of West Meadow Beach to the other.

OK, how about the disadvantages? Tests were at the top of that list. When I was in school, a test on my birthday wasn’t as much of a wet blanket as a test the day after my birthday, when studying superseded any birthday celebration.

The movies around the middle of the winter never seemed as much fun to attend as the ones during the summer, perhaps because of the pressure to prepare for school.

Still, while the grass may be greener, literally, for summer birthdays and the baseball season may be in full swing, the winter birthdays give those of us looking for festivities during the colder, darker months something to celebrate.

Ideally, we can enjoy these festivities all-year round, as we celebrate with our friends and family, particularly during frenetic birthday weeks. 

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John Parise Photo courtesy of BNL

By Daniel Dunaief

Finding a proverbial needle in a haystack isn’t as hard as it once was. In fact, finding a needle with specific qualities has also become easier. Manufacturers and drug companies are constantly searching for a specific substance, whether it’s a drug that targets one part of an invading fungus or bacteria or a molecule that binds to a particularly harmful gas.

Indeed, it is in this latter category where John Parise, a distinguished research professor with joint appointments in geosciences and chemistry at Stony Brook University, and a team from Stony Brook, Brookhaven National Laboratory, the Lawrence Berkeley National Laboratory and Pacific Northwest National Laboratory recently shared their use of a metal organic framework, called SBMOF-1, that selectively binds to xenon, a gaseous by-product of nuclear reactions. Their findings, which were published recently in the journal Nature Communications, may point to a more effective and environmentally friendly way to manage nuclear waste.

“This [substance] is 70 times more effective than the current way scientists remove this dangerous gas,” said Parise, who has a joint appointment in photon sciences at BNL. “It allows krypton to pass through, but it retains xenon.” Parise said it acts like a sponge absorbing water until all the pores are filled, which can then be wrung out by passing a gas like nitrogen over it.

Researchers at Pacific Northwest National Laboratory, including Debasis Banerjee, who helped create this molecule when he was a graduate student at SBU, are continuing to work on this material.

The route SBMOF-1 took to becoming a potential xenon filter underscores the collaborative nature of a process that blends basic science with engineering, manufacturing, theory and potential commercial application.

Banerjee won the President’s Award as a distinguished doctoral student at Stony Brook for his research, which involved creating this framework in 2012. When Banerjee designed this material, he didn’t have xenon or nuclear energy on his mind — he was focused on trying to extract carbon dioxide at room temperatures in a humid environment during industrial processes. “We tested this material on numerous gases except xenon,” Parise said.

What they did that led to the next step, however, was critical to the search scientists at Berkeley were conducting to find their proverbial needle. The Berkeley researchers were looking for a better way to remove xenon from nuclear waste. The Stony Brook scientists put their compound in a searchable database online, which met the criteria the Berkeley scientists had established in their search.

Instead of trying to create something new, however, the Berkeley scientists did the equivalent of digging through massive piles of haystacks to search for something that already existed, perhaps for a different purpose, that might be a candidate for the job. Sure enough, they found SBMOF-1.

“While experimentally we need to sift through a fair amount of ‘hay’ — the computer, once programmed correctly (and this is nontrivial) works rapidly to locate the needle,” Parise said.

Indeed, when the theory met the reality, krypton passed through in 10 to 15 minutes, while xenon remained trapped for close to an hour. A nuclear facility can blow air back through the material and recover most of the xenon, Parise explained.

“It’s a beautiful compound and is so much better than anything else,” Parise said, although he cautioned that “it’s not to say something else can’t do better.”

In making the material, Bernjee started looking at sodium and calcium and phenyl ring compounds. He set out to create something that was environmentally friendly.

Banerjee is continuing to work on nuclear energy at PNNL. He reflected positively on his experiences at Stony Brook University, where he conducted research from 2007 to 2012. “Stony Brook is a great place to work, particularly for research,” he explained in an email. “I still actively collaborate with [Parise’s] group.”

He described Parise as a “great mentor” and said many of his current collaborators share a similar background of working in Parise’s lab. Banerjee’s scientific teammates are either in different national laboratories or are at other universities.

Parise is a strong advocate of the process that led to this uniting of theory and practice. This procedure will give the United States a research and development edge, because the theory makes the experiments more effective and the more effective experimental results reinforce the theory.

Parise works together with people like Artem Oganov, a professor in the Department of Geosciences at Stony Brook. They are exploring new compounds to split water from sunlight. “Computational materials discovery is an ongoing scientific revolution,” explained Oganov in an email. “Calculations are playing an increasingly critical role in materials science.”

Oganov said Parise is “known as a very creative and most versatile synthetic chemist.” Banerjee added that Parise “has major contributions in the field of materials characterization using X-ray and neutron diffraction.”

A native of North Queensland, Australia, Parise started working at SBU in 1989. He is married to Alyse Parise, who is a business coach and psychotherapist, who has a private practice in Setauket. Residents of Poquott, the Parises enjoy the beaches and kayaking on Long Island. At the end of July, they will join friends to raft down the Salmon River in Idaho.

As for his work, Parise said he is dedicated to determining how the structure of compounds are arranged. “We’re interested in where the atoms are” in a wide range of materials, he said.

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Chances are the day of this publication, July 7, i.e., 7/7, is your lucky day. Why? Many people believe seven brings them luck, whether it’s because of the seven days of the week, seven colors in the rainbow, seven continents or even the “7” Mickey Mantle wore on his back.

If you believe in lucky numbers, seven might give you the kind of confidence you need to say exactly the right thing in a job interview, to seek a date with a long-term love interest, or to swing at a fastball at just the right moment, sending the ball deep into the night.

Practically speaking, all those people who share that lucky No. 7 can’t be winners at the same time. What if a pitcher in a tight game, who is the seventh child in a family of seven and might have been born at 7:07, is pitching to a hitter, who grew up on 77 Main Street and who always bats seventh? Who would win?

Taking a step back from the “7” sports quagmire, what is it about numbers that can make or break our confidence, that can inspire or deflate us? Even for those indifferent to theorems and patterns, numbers can be beautiful and comforting. They can create order in a chaotic world, offering support and structure in their patterns and predictability.

There’s the alternating odds and evens. That’s a pattern that’s like looking at a checkerboard, with its alternating tiles. According to some news reports, zero presents a problem for some people because they are not sure whether it is odd or even and most odd/even discussions begin with “1” while evens begin with “2.” (Zero is an even number under the standard mathematical definition.)

Then there are those rules of numbers that can help in the prime versus non-prime consideration. If you’re looking at an odd number, how do you know whether it’s divisible by three? You add up the digits in the number and see if the sum is divisible by three. Take, for example, 4,197. The sum of four, one, nine and seven is 21, which means it’s divisible by three.

But then there are those well-known irrational numbers that provide memory challenges for schools. Some schools, on March 14 each year, hold a contest about the famous constant, pi, which is the ratio of a circle’s circumference to its diameter. Students commit as many digits of pi as they can to memory. Most people recall the 3.14 part of pi, which is why those competitions are held on March 14, but some push themselves to memorize more than a hundred digits.

Then there are those numbers that signal the beginning or the end of something. The famous countdown to a rocket launch that carries with it the hope of finding something new, of taking humans somewhere we’ve never gone, or of exploring or seeing the Earth from a different perspective. Parents know the famous mantra, “I’m going to count to three,” before a potential liftoff of another kind.

For the sports fanatics out there, numbers are the game within a game. For example:

• How fast did he throw that pitch?

• How many goals did he score in the World Cup?

• How great was this player compared with another player?

Numbers are sliced and diced to make predictions, reconsider greatness or understand a player’s potential.

Perhaps the corollary to the question, “Would a rose by any other name smell as sweet?” should be, “Would a superstar with a different uniform number play as well?” The answer might depend on the date of the game.

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Ute Moll in her lab at Stony Brook University. Photo by John Griffin

Some day, people may be able to breathe easier because of a cancer researcher.

No, Ute Moll doesn’t work on respiration; and, no, she doesn’t study the lungs. What Moll, research scientist Alice Nemajerova and several other collaborators did recently, however, was explain the role of an important gene, called p73, in the formation of multiciliated cells that remove pollutants like dust from the lungs.

Initially, scientists had studied a knockout mouse, which lacked the p73 gene, to see if the loss of this gene would cause mice to develop cancers, the way they did for p73’s well-studied cousin p53. Researchers were surprised that those mice without p73 didn’t get cancer, but found other problems in the development of their brains, which included abnormalities in the hippocampus.

While each of these mice had a respiratory problem, researchers originally suspected the breathing difficulties came from an immune response, said Moll, the vice chair for experimental pathology and professor of pathology at Stony Brook University.

A board-certified anatomical and clinical pathologist who does autopsies and trains residents at Stony Brook, Moll took a closer look and saw an important difference between these mice and the so-called wild type, which has an intact p73 gene.

Moll on a recent trip to Africa says hello to Sylvester the cheetah who is the animal ambassador in Zimbabwe. Photo from Moll
Moll on a recent trip to Africa says hello to Sylvester the cheetah who is the animal ambassador in Zimbabwe. Photo from Moll

“Microscopic examinations of many types clearly showed that the multiciliated cells in the airways were severely defective,” she explained. “Instead of a lawn of dense long broom-like motile cilia on their cell surface which created a strong directional fluid flow across the windpipe surface, the [knockout] cells had far fewer cilia, and the few cilia present were mostly short stumps that lost 100 percent of their clearance function.”

This finding, which was published in the journal Genes & Development, could have implications for lung diseases such as chronic obstructive pulmonary disease, or COPD, which affects more than 330 million people around the world and is the third leading cause of death.

The discovery provides “the long-awaited explanation for the diverse phenotypes of the p73 knockout mice,” wrote Elsa Flores, a professor of molecular oncology at the UT MD Anderson Cancer Center, in a commentary of the work.

In an email, Flores said Moll is a “wonderful collaborator and colleague” whose “meticulous” work is “held in high regard.”

Carol Prives, Da Costa professor in biological sciences at Columbia University, suggested this was a “very significant finding.”

Moll and her scientific team went beyond showing that the loss of the p73 gene caused the defective or missing cilia. They took stem cells from the trachea, which can grow on a culture dish into a range of other cells. With the proper nutrients and signals, these stem cells can grow back into a fully differentiated respiratory epithelium.

The organotypic culture had the same defects as the knockout mice. The scientists then used a lentivirus to insert a copy of the functioning p73 gene. The cells in the culture developed a complete set of long, motile cilia.

“It’s a complete rescue experiment,” Moll said. “This closes the circle of proof that” p73 is responsible for the development of these structures that clean the lungs.

In addition to the lungs, mammals also develop these cilia in two other areas, in the brain and in the fallopian tubes.

There could be a range of p73 deficiencies and some of these could be indicative of vulnerability or susceptibility to lung-related problems that are connected to incomplete cilia. This could be particularly valuable to know in more polluted environments, where the concentration of dust or pollutants is high.

Moll plans to “find tissue banks from COPD patients” in which she might identify candidate alleles, or genes, that have a partial loss of function that would contribute to the reduction in the cilia cells.

While Moll will continue to work on respiration and p73 in mice, she described her broader research goals as “gene-centric,” in which she studies the entire p53 family, which includes p53, p63 and p73.

Colleagues suggested that she has made important and unexpected discoveries with p53.

“She was among the first to show that in some pathological states, p53 is sequestered in the cytoplasm rather than in the nucleus,” Prives, who has known Moll for 25 years, explained in an email. “This led to her original and very unexpected discovery that p53 associates with mitochondria and plays a direct role in mitochondrial cell death. She was very courageous in that regard since the common view was that p53 works only in the nucleus.”

Moll was raised in Germany and earned her undergraduate and medical degrees in Ulm, the same town where Albert Einstein grew up. She lives in Setauket with her husband, Martin Rocek, a professor of theoretical physics at SBU. The couple has two sons, 26-year-old Thomas, who is involved in reforestation in Peru, and 29-year-old Julian, a documentary filmmaker focusing on environmental themes.

Moll is also focused on the environment.“If humankind doesn’t wake up soon, we are going to saw off the branch we’re sitting on,” she warns. One of Moll’s pet peeves is car idling. She walks up to the windows of people sitting in idling cars and asks if they could turn off the engine.

As for her work with p73, she feels as if she is “just at the beginning. This is a rich field.”

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We all have them and we can laugh about them — later. In the moment, they are the shortening fuse that converts us from rational people capable of responding to any challenges into people who can’t control the frustration boiling inside us.

Recently, I visited with a friend who couldn’t get through a security gate on the way to a party. She had to wait as several people working at a gated community discussed whether to admit the car in front of her.

My friend is a brilliant person who is capable of erudite speeches, has keen insights and is informed about a wide range of subjects. She is among the most charming people in a room — most of the time.

Sitting in a line that came to a complete standstill, however, she “lost it.” She walked up to the glass partition, shouted at the security guards and demanded that they let her enter a party that would last for hours.

Even in the moment, she says, she could see herself saying things out of intense frustration, but she couldn’t regain control.

Those raw and exposed moments can be — and often are — the subjects of YouTube videos, as people around the action whip out their phones to chronicle someone who reached the point of no return in his or her actions.

From what I understand, our fuses get shorter during the summer months. It’s an ironic time for us to become so irate, when we dial back the pressure and take trips to our national parks, to Niagara Falls, or to a college or high school reunion. Maybe the heat shortens the fuse or speeds up the travel from when the fuse is lit to when it triggers us to react in a way we would just as soon avoid?

To some degree we need moments to blow off steam, to let it go and to release the toxins that have built up in us over the preceding days, weeks, months or, in some cases, years. Letting go of the control we maintain over ourselves through all the hundreds or thousands of nuisances and annoyances can cleanse us and restore our equanimity in a way that yoga classes, deep-breathing exercises or a repetition of a mantra like “serenity now” doesn’t quite cover.

To be clear, I’m not talking about those moments when someone commits some grievous act but, rather, the times when those of us with considerable calm suddenly throw spirited temper tantrums that are visual or verbal displays, without injuries to anyone other than our pride.

In those contained but still surprising displays, is it possible to stop the reaction before we start flapping our arms, jumping up and down, banging on glass doors, or unintentionally releasing saliva when we make our anger-laden point about the inconvenience someone is causing?

Generally, I’ve found that a lit fuse finds its mark, no matter how many James Bond movies I’ve seen where he stops a detonation with 007 seconds left.

So, who lights our fuses? I think it’s people on either extreme: those we know incredibly well, who have a talent for throwing darts at our anger bull’s-eye; and those people we may interact with only once, whose commitment to a process keeps us from accomplishing some task.

Then again, no one can light our fuse if we didn’t let them. We bear responsibility for a lit fuse because we ultimately sit in the control rooms of our brains, like those characters in the animated movie “Inside Out.” So, when the red guy in our brains takes over and he starts stomping our feet and demands that the car in front of us should “go, go, go,” what’s the solution?

Maybe if we anticipate laughing afterward, we can short-circuit that red guy and neither laugh at him nor with him, but laugh about what he might have done.

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We’ve got hot summer nights on the horizon. Come on, it’s an election year. In thinking about the days ahead of heated debates, accusations and counter accusations, I made some resolutions I’d like to share:

• I resolve not to get too caught up in politics. No, seriously. I’m not going to count the days — 138, but who’s counting? — before the election.

• I resolve not to study a single political poll between now and Nov. 8, which is, as I mentioned but we’re not going to talk about, 138 days away.

• I resolve I will not watch too many debates when I have better things to do. I might need to clip my toenails. Or, maybe, a movie I’ve seen 20 times, like “Bull Durham” will be on TV and I’ll just have to watch that scene one more time when the players come to the mound to discuss wedding gifts and cursed gloves.

• I resolve not to focus on the number of times either candidate calls the other one a liar. If they do, however, I resolve to imagine that candidate adding, “liar, liar, pants on fire,” to add some levity to the accusation.

• I resolve not to worry too much that one of these two people whom I don’t particularly like will be president. Seriously, we’ve got all these people eager for power and these two are the best we can find? Not everyone wants to be president, but doesn’t this seem like the perfect time for a dark horse to throw his or her hat in the ring?

• I resolve to avoid listening to pundits. I don’t want to hear how you absolutely think your candidate won the debate and the other candidate completely lost the debate, the election and his or her mind the other night. Can you imagine two pundits watching everything you did in a day?

Pundit 1: “Oh, he totally nailed that plaque on his teeth. He won’t need to brush his teeth for a week after a performance like that.”

Pundit 2: “Are you kidding? Do you think he gave the molars any attention? I’ve spoken to the molars and they are feeling neglected. I have a way to brush that would fight for every tooth and not just the ones on top.”

My only pundit exception is David Gergen: He’s smart and funny, has a deep authoritative voice and he’s really tall, so it looks like he’s observing everything from on high. Besides, in the early 1990s I met him, not to name drop or anything, and he actually listened carefully to a question I asked.

• I resolve to do 10 push-ups every time I hear one of the candidates, in an advertisement or during a TV or radio news program, use the word “fight.” I figure if they argue that they’ll fight for me, I might as well fight for my own fitness. Maybe I’ll do 20 sit-ups every time I watch them shake their heads in frustration when describing the ridiculous and calamitous choice on the other side of the aisle.

• I resolve to think of the two candidates as the leaders of their packs on a middle school playground. Each time one of them is emotionally wounded and levels accusations against the other, I will imagine that they are just going through a difficult phase in their political career and that they’ll be OK once they get to high school.

• Finally, no matter what, I resolve to remind myself that the Constitution guarantees us checks and balances. That means, regardless of the final “winner,” other leaders can protect all our interests.

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Christopher Vakoc in his lab at Cold Spring Harbor Laboratory. Photo courtesy of CSHL

We create buildings that climb into a sky crowded with airplanes and supersonic jets. We harness the energy of the atom, design intricate artwork, compose and perform inspirational music, travel miles below the surface of the ocean and send satellites deep into space. Sometimes, we tap into unlikely sources to learn new ways to improve our lives, even in the fight to understand and attack cancer.

Bacteria have been battling against viruses for so long that they have evolved to disarm these intruders. The bacterial immune system uses a gene-editing system called CRISPR. Researchers have taken some of the CRISPR machinery from bacteria and are using it in human cells. CRISPR was named the American Association for the Advancement of Science’s Breakthrough of the Year for 2015.

Using a bacterial enzyme called Cas9, which isn’t found naturally in humans but can be used in our genetic code, scientists can edit out DNA that contributes to the proliferation of cancer.

Christopher Vakoc, an associate professor at Cold Spring Harbor Laboratory, has used his expertise with CRISPR to study cancer.

Starting in the fall of 2014, he and Charles Keller, the scientific director at Children’s Cancer Therapy Development Institute in Oregon, collaborated to study the disease rhabdomyosarcoma, a rare form of deadly pediatric cancer of the connective tissue that typically involves muscle cells attached to bones. Vakoc’s lab is using CRISPR to discover new vulnerabilities in RMS.

At this point, Keller has found a potential treatment in animal models that shows positive results, while Vakoc has determined how that specific drug is working. They have submitted their work for publication in a scientific journal and are awaiting word back from reviewers.

Starting this fall, Vakoc will add Ph.D. scientist Bryan Lanning, who will try and identify new targets in RMS using CRISPR.

“It’s great to contribute more resources to this effort,” Vakoc said.

In an email, Keller detailed how “we have more insight into how the drug for rhabdomyosarcoma works.” He credits Eric Wang from Vakoc’s lab for contributing “instrumental” results to the early findings. Keller is “grateful for the support of [Vakoc’s] lab and the collaboration it empowers.”

At the same time, Vakoc’s lab continues to work in an area where they have made some breakthroughs with CRISPR, on a site called BRD4. Collaborating with several other labs, Vakoc showed that chemical inhibition of BRD4 provides a therapeutic benefit in mouse models of leukemia, which has led to clinical trials in humans. Using a drug called JQ1, scientists have generated positive results with humans in Phase I of the Food and Drug Administration’s process for therapeutic approval.

Christopher Vakoc/photo courtesy of CSHL
Christopher Vakoc/photo courtesy of CSHL

“Some of the patients at tolerated doses have had complete remission,” he said. He called those early findings “encouraging.”

A major area of focus, Vakoc explained, involves continuing to try to understand on a molecular level how these drugs are working and why BRD4 is a drug target. “It was not clear in the beginning, but we are slowly revealing the special properties of BRD4,” he said.

As the tests move into the next stage, called Phase 2, an important question in order for this therapy to work, Vakoc said, is to anticipate “how we are going to overcome these resistant states.”

While he doesn’t have an answer yet, he said, he hopes a combination of agents can be more active than any one treatment individually. “A lot of what we’ve been doing, while we are waiting for clinical trials to get under way, is to study resistance and therapies in animal and culture models,” Vakoc said.

Vakoc and Johannes Zuber, a group leader at the Research Institute of Molecular Pathology in Vienna, Austria, recently published a paper in which they outlined how some cells become resistant through nongenetic changes. As they described, the cells are rewiring gene expression without introducing new DNA. A cell can evolve to this new state, Vakoc said. In the battle to defeat the disease, this requires a readiness to defeat what he expects will be some level of resistance to this new treatment.

The inhibitors Vakoc and Zuber have worked on have “very broad and desired activity,” but to find a cure “we have to find effective combination therapies,” explained Zuber, who collaborated on BRD4 projects at Cold Spring Harbor when he was a postdoctoral researcher in Scott Lowe’s lab as early as 2008.

“Assuming that cancer drugs can be well-tolerated enough to be combined and administered as chronic therapy, I hold out hope that we can combine numerous agents and apply them upfront, based on information in the lab and real-life information from patients,” Vakoc said. This could mean a cocktail of three, four or five well-tolerated drugs that he hopes won’t increase chemotherapy toxicity.

In an email, Zuber wrote that Vakoc’s CRISPR system will allow systematic CRISPR screens that point toward domains and identify structures for drug development.

Vakoc lives on campus at CSHL with his wife Camila Dos Santos, who studies epigenetic changes that occur after pregnancy. The couple is collaborating in their research. “CRISPR technology is useful for all biologists and my wife is no exception,” he said.

As for his own work, Vakoc expressed an appreciation for the scientific tools bacteria are providing.“Biologists have always been learning from naturally occurring mechanisms used by various organisms” and using them to approach a range of challenges, Vakoc explained.

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I am you and you are me. We, the people of this country and this planet, share something people hundreds of years before and hundreds of years hence can’t possibly have in common with us: now.

What defines “now”? Labels. We are tremendously caught up in them. Who are the good guys and who are the bad guys? And then, something happens, something unimaginable in Florida, and it’s clear at least one person directed his hatred toward one particular group.

This was an attack on the gay community. Other labels will undoubtedly stick and motives will undoubtedly be uncovered, but it was an attack on gay America. Sure, it was terrorism, because it was terrible and it was shockingly violent, but it was, first and foremost, an attack on a community.

There’s a moving scene at the end of the Kevin Kline film, “In & Out,” at a high school graduation in which everyone stands up and says they are gay in support of Kline, who is on the verge of losing his job because of his sexual orientation.

As we watched a moving Tony Awards ceremony, I hoped someone would step to the microphone and say, “I’m gay and anyone else who is gay today, please stand with me.” I’m sure the entire audience would have stood up.

For today, tomorrow and for the foreseeable future, we are all gay. We are all lesbian, bisexuals and transgender. We are like the Danish people who, legend has it, put yellow stars on their clothing to make it impossible to distinguish Jewish Danes from fellow Danes during World War II. There is some debate about whether Christian X, the king of Denmark, put the Jewish star on his clothing. What is clear, however, is that the Danes did what they could in a horrible time to save their citizens from discrimination and death by helping them escape to Sweden.

In the here and now, with so much blood, so many tears and such incomprehensible loss, there is something we can do for our fellow Americans: We can be gay. I’m not suggesting we all need same-sex partners, merely, that the label that seems so toxic to some applies to all of us.

We live with such random acts of terror and violence. Far too often, the president of the United States has become the Mourner in Chief. Maybe, instead, he should be gay, too.

Let’s not wait for a reluctant and divided Congress to act and to take action on guns, or on hate, or on love. Let’s embrace and understand each other.

There will be plenty of people pointing fingers. The FBI was watching this killer through different points in his life. Did they miss anything? I’m sure there’ll be plenty of people who will suggest that if the clubgoers had had guns, this killer wouldn’t have been as effective because someone would have been able to take him out before he did all that damage. Is that really what we want, a bunch of people in a club with guns? Would that really make us safer? It’s a bit like the mutually assured destruction argument during the Cold War. Maybe it was so irrational to consider destroying the world that no one pushed the button, but we still have all those weapons and there is still plenty of hate and fear. We and the former Soviet Union spent billions on weapons when those resources might have cured cancer, improved food crops or developed cheaper, cleaner energy.

So, how do we stop the hate? We stand up, we unite, we share — and we recognize that I am you and you are me.

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Maurizio Del Poeta in his laboratory at Stony Brook University. Photo by Antonella Rella

Like the fictional Steve Austin, Stony Brook University’s Maurizio Del Poeta has become the ““Six Million Dollar Man.”

No, Del Poeta didn’t crash in an experimental spacecraft; and no, he doesn’t have bionic limbs. Instead, work with a potentially deadly fungus in his laboratory helped Del Poeta, a professor in the Department of Molecular Genetics & Microbiology at Stony Brook University, earn two, multiyear $3 million grants from the National Institutes of Health.

Del Poeta is attacking a fungus that can be deadly, particularly for people with weakened immune systems. Recently, his approach yielded an unexpected result that may lead to a vaccine. “We were looking for a gene that would metabolize a fungal sphingolipid on the surface of the fungus,” he said.

The gene he mutated caused a different function than expected, leading mice with exposure to this strain to become resistant to fungal infection, Del Poeta said.

This change may be the key to providing a vaccination against Cryptococcus neoformans, a fungus present in numerous places, including in bird droppings.

Postdoctoroal student Antonella Rella who is working on an antiviral vaccine in Del Poeta’s laboratory at SBU. Photo by Maurizio Del Poeta
Postdoctoroal student Antonella Rella who is working on an antiviral vaccine in Del Poeta’s laboratory at SBU. Photo by Maurizio Del Poeta

“We think that this discovery will open the road to a new vaccination strategy against fungi” including candidiasis caused by Candida albicans or aspergillosis, caused by Aspergillus funigatus, Del Poeta said.

The same gene for sterol glucosidase that Del Poeta and the researchers in his lab mutated is also found in the genome of these other fungal species. “One could potentially make a vaccine containing the three fungal mutants combined and inject them together to protect simultaneously” against all three species, he said. These three infections account for over 1.3 million deaths per year, according to the Centers for Disease Control and Prevention.

This vaccine could prove effective for immunocompetent and immunocompromised individuals. A potential vaccine is particularly important for the latter group.

Del Poeta and his colleagues injected the mutated version of the fungus into an animal model that mirrored the conditions of a patient with the human immunodeficiency virus. The vaccine “protected 100 percent” against an infection, Del Poeta said. “Whatever this mutant is doing, the protection is not determined by the presence of CD4 cells.”

CD4 cells are a type of white blood cell that fights infection. They are at the center of vaccines that train the immune system to recognize and destroy live versions of infections. Without those cells, vaccination becomes more difficult, but, clearly, not impossible.

His results earned him a 1 score, the top mark from reviewers, from the National Institutes of Health, which recently awarded him a $3 million grant to study this mutated fungus. The grant should become active on July 1.

John Perfect, the James B. Duke Professor of Medicine and chief of the Division of Infections Disease at Duke University, brought Del Poeta into his laboratory from Italy. He is proud of his protege, describing Del Poeta in an email as a “major investigator in fungal pathogenesis.”

An important question Del Poeta can’t answer is how this attenuated strain conveys resistance.

Before this promising early work can become a part of preventive treatment, Del Poeta said he and his team will look for a different formulation of this potential vaccine.

“It will be difficult to convince the FDA to administer a live fungus to an immunocompromised patient, even if the fungus will be attenuated,” he explained. “So, we need to make a better vaccine.”

His postdoctoral researcher, Antonella Rella, who is the first author on a paper published in Frontiers in Microbiology describing their results, is making and testing new formulations. She has already found promising results using only certain portions of the cell, Del Poeta said.

Maurizio Del Poeta in front of the brick oven he built in the backyard of his Mount Sinai home. Photo by Chiara Luberto
Maurizio Del Poeta in front of the brick oven he built in the backyard of his Mount Sinai home. Photo by Chiara Luberto

Del Poeta is also working in drug development. He received a $3 million grant this past December from the NIH for his continued work on drugs to treat fungal infections.

Last June, Del Poeta published a study in mBio, the online journal of the American Society for Microbiology, in which he found two compounds, BHBM and its derivative DO, that decreased the level of a lipid fungal cells need to reproduce.

Since then, he has found that some derivatives are more potent and less toxic.

He has teamed up with Iwao Ojima, the director of the Institute of Chemical Biology and Drug Discovery at Stony Brook University, and John Mallamo, who was a director in drug discovery at Cephalon. The scientific team is working with Brian McCarthy, an entrepreneur-in-residence, as a part of a new company called MicroRid Technologies.

The first milestone in the next three to four years is to raise additional funds for FDA filing and to perform a Phase 1 clinical trial some time between 2018 and 2020.

Del Poeta “exudes optimism” and his “scientific rigor and thoughts are simply first rate,” said Perfect.

When he’s not working to stop potentially deadly fungal infections, Del Poeta lives in Mount Sinai with his wife Chiara Luberto, who is studying leukemia at the Cancer Center at Stony Brook, and his sons Matteo, who is 9, and Francesco, who is 6.

Originally from Treia, Italy, which is near Florence on the Adriatic coast, Del Poeta worked in a pizzeria when he was younger. He built a brick oven in his backyard, where he hosts neighbors and the families of his sons’ classmates. His favorite pizza, called Amir Pizza after a former talented postdoctoral student in his lab, is a white pizza with extra-thin-sliced white onions, one thin-sliced hard avocado, a generous portion of pistachios and mozzarella.

While the work Del Poeta does has clinical implications, he has no expectations to move to a biotechnology company. “I love what I do,” he said. “If I can make the life of a patient a little better, if I can bring a new drug to the clinic or even contribute a little bit to improve the survival of a patient, I would be so grateful.”

Readers who would like to know more about the battle against fungal infections can gather information at the Global Action Fund for Fungal Infections web site, www.gaffi.org.

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We all have addictions. I don’t mean we’re all addicted to a narcotic, to alcohol or to something that can cause harm to us, to our families or to our communities.

We think of addictions as negatives, because they suggest a dependency or a need for something without which we find ourselves unbalanced, uncomfortable or unhinged.

There are plenty of positive addictions. Many of us are, for better or worse, addicted to our children. We want them to succeed, to be happy, to live better lives than we’ve had and to have every opportunity to find their niche.

When they’re born, we become addicted to the sound of their giggling and laughter, which helps us get through those sleepless nights just as effectively as a caffeinated beverage. That sound is more pleasant than the most magnificent music we’ve ever heard, than the calls of birds outside our windows in the morning, or than the school bell that signaled the end of another week and the start of a much-anticipated weekend.

Outside of the home, we can become addicted to victory, whether it’s at work, on a softball field where we are competing against a group of people from another company, or at a traffic light where we want to beat the car next to us to the on-ramp for the Long Island Expressway.

Our bodies become accustomed to these addictions. Runners receive chemical endorphins in the brain that give them a high, allowing them to run much longer than someone whose would-be endorphins are knocked unconscious by alcohol or are far too overwhelmed from sugar overload to become active. When you’re driving in extreme heat or cold and you see runners pushing themselves up a steep hill, they are feeding that addiction.

Speaking of feeding, we are addicted to particular foods, or food groups. If we eat cookies every night, our bodies send signals to our brains to find those chocolate chip cookies. We can also become addicted to foods that are healthy for us, like broccoli, blueberries or gluten-free kale pizza.

We can also become addicted to long days of summer sun. When the fall and winter come, we might miss the light, craving it the way we would another cup of mid-afternoon coffee when we’re feeling run down through the day.

But is addiction really the right word? Aren’t these habits and not addictions? I see addictions and habits as a spectrum, somewhat akin to the discussion about what is normal. We all tend to believe we’re normal, but as we know from our own families and from the families we marry into, the range of normal is broad. Every family has its crazy uncles, its eccentric aunts and its oddball distant cousins. Much as we might like to believe the grass is greener with other families, we know that the more we interact with extended family groups, the more likely we are to observe behaviors that fall outside the range of what we consider normal.

So, if we recognize our addictions, can we change them?

Like any addiction, change is challenging. Plenty of support groups offer help, especially with addictions to alcohol, drugs or other substances. There are also groups like Jenny Craig, which offer to provide balanced meals that help people transition to a different diet.

Even without support groups, though, people can fundamentally change some of their addictions, often when they are so concerned with the happiness of someone else — a spouse, a child, a niece or a parent — that their own needs no longer come first.

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