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Anne Churchland. Photo from CSHL

By Daniel Dunaief

Someone is hungry and is walking through a familiar town. She smells pizza coming from the hot brick oven on her left, she watches someone leaving her favorite Chinese restaurant with the familiar takeout boxes, and she thinks about the fish restaurant with special catches of the day that she usually enjoys around this time of year. How does she make her decision?

While this scenario is a simplified one, it’s a window into the decision-making process people go through when their neurons work together. A team of 21 neuroscientists in Europe and the United States recently created a new collaboration called the International Brain Laboratory to explore how networks of brain cells support learning and decision-making.

“We understand the simple motor reflex,” such as when a doctor taps a knee and a foot kicks out, said Anne Churchland, an associate professor at Cold Spring Harbor Laboratory and the American spokesperson for this new effort. Scientists, however, have only a limited understanding of the cognitive processes that weigh sensory details and a recollection of the outcomes from various courses of action that lead to decision-making, Churchland said.

Scientists likened the structure of the new multilaboratory effort to the circuitry involved in the brain itself. The brain is “massively parallel,” said Alexandre Pouget, a professor at the University of Geneva and the spokesperson for the IBL. “We know it’s working on consensus building across areas so, in that respect, the IBL is similar.”

A greater awareness of the decision-making process could provide a step into understanding the brain network problems involved in mental health disorders.

Churchland’s lab is one of three facilities that will house a new behavioral apparatus to study decision-making in mice. The other sites will be in the United Kingdom and in Portugal. Eventually, other labs will use this same technique and house the same apparatus.

An ongoing challenge in this field of research, Churchland said, is that scientists sometimes create their own models to test the neurological basis of behavior. While these approaches may work in their own labs, they have created a reproducibility problem, making it difficult for others who don’t have expertise in their methods to duplicate the results.

Creating this behavioral apparatus will help ensure that the collaborators are approaching the research with a reliable model that they can repeat, with similar results, in other facilities.

While the scientists will all be exploring the brain, they will each be responsible for studying the activity of circuits in different parts. The researchers will collect a wealth of information and will share it through a developing computer system that allows them to maneuver through the mountains of data.

To address this challenge, the IBL is creating a data architecture working group. Kenneth Harris, a professor of quantitative neuroscience at the University College London, is the chair of the effort. He is currently looking to hire additional outside staff to help develop this process.

Harris suggested that the process of sharing data in neurophysiology has been challenging because of the complex and diverse data these scientists share. “In neuroscience, we have lots of different types of measurements, made simultaneously with lots of different experimental methods, that all have to be integrated together,” he explained in an email.

The IBL collaboration will make his job slightly easier than the generic problem of neurophysiology data sharing because “all the labs will be studying how the brain solves the same decision-making task,” he continued.

Harris is looking to hire a data coordinator, a senior scientific programmer and a scientific MATLAB programmer. He has a data management system already running with his lab that he plans to extend to the IBL.

Pouget said there are two milestones built into the funding from the Wellcome Trust and the Simons Foundation for this new collaboration. After two years, the researchers have to have a data sharing platform in place, which will allow them to share data live as they collect it.

Second, they plan to develop standardized behaviors in all 11 of the experimental labs, where the behavior has to be as indistinguishable from one lab to another as possible.

In addition to the experimentalists involved in this initiative, several theoretical neurobiologists will also contribute and will be critical to unraveling the enormous amounts of data, Pouget suggested. “If you’re going to tackle really hard computational problems, you better have people trained in that area,” he said, adding that he estimates that only about 5 percent of neuroscientists are involved in the theoretical side, which is considerably lower than the percent in an area like physics.

Researchers involved in this project will have the opportunity to move from one lab to another, conducting experiments and gaining expertise and insights. The principal investigators are also in the process of hiring 21 postdoctoral students.

Churchland said each scientist will continue to conduct his or her own research while also contributing to this effort. The IBL is consuming between a quarter and a third of her time.

Pouget suggested that Churchland was “instrumental in representing the International Brain Laboratory to the Simons Foundation,” where she is the principal investigator on that grant. “Her role has been critical to the organization,” he said.

Churchland said the effort is progressing rapidly. “It’s moving way faster” than expected. “This is the right moment, with an incredible team of people, to be working together. Everyone is dedicated to the science.”

Harris indicated that he believes this effort could be transformative for the field. “Neuroscience has lagged behind many other scientific domains” in creating large-scale collaborations, he explained. “If we can show it works, we will change the entire field for good.”

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Baba Ghanoush

By Barbara Beltrami

Actually, eggplant comes in many more shapes and sizes than the large purple global variety with which we are all familiar. A member of the nightshade family, its flowers, not the eggplant itself, can be female or male. So the preference for one or the other is based on myth. What you should concentrate on when choosing an eggplant is the skin, the weight and the hardness or softness of it. A fresh, ripe eggplant has glossy, taut skin, feels somewhat heavy and can be depressed with the thumb with just a little resistance and then return to its form.

While most people think of eggplant as one of the basic ingredients in the popular Italian American dish, eggplant parmigiana, it is, in fact, a staple of many diets, particularly in the Near and Far East. From the Syrian baba ghanoush to the Indian bhurtha to the Thai pud makua yow, eggplant crosses most ethnic boundaries to remind us that we’re not very much different from one another. I don’t often feature Asian recipes in this column simply because I have little experience with them. However, research among some acquaintances for whom the following recipes are traditional has expanded my repertoire.

Bhurtha

Bhurtha

YIELD: Makes 4 servings

INGREDIENTS:

1 medium eggplant

3 tablespoons vegetable oil

1 medium onion, chopped

1 teaspoon grated fresh ginger

1 large tomato, diced

1 clove garlic, minced

1 teaspoon ground cumin

½ teaspoon turmeric

½ teaspoon ground coriander

¼ teaspoon cayenne pepper

Salt and freshly ground black pepper

1 handful fresh cilantro, chopped

DIRECTIONS: Preheat broiler. Rub eggplant skin with oil. Place under broiler and turn frequently until skin is charred and inside pulp is soft and mushy. Cut eggplant in half, scoop out flesh, cut into cubes and set aside. In a medium-large skillet, heat the oil, then add the onion, ginger, tomato, garlic, cumin, turmeric, coriander, cayenne, salt and pepper. Cook over medium heat, stirring frequently, just until onion turns opaque. Add eggplant and cook another 10 to 15 minutes, stirring frequently, until most of the moisture is evaporated. Transfer to serving dish and sprinkle with cilantro. Serve with naan (oven-baked flatbread), jasmine rice and peas.

Baba Ghanoush

Baba Ghanoush

YIELD: Makes 6 to 8 servings

INGREDIENTS:

2 large eggplants

Juice of 2 lemons

2 tablespoons tahini

One large clove garlic, finely minced

Coarse salt, to taste

¹/3 cup chopped flat-leaf parsley

3 tablespoons extra virgin olive oil

DIRECTIONS: Wash eggplants and grill whole on gas grill over medium-low heat. Turn frequently until eggplant is cooked on all sides, skin is charred and pulp is soft. Remove from heat, place on a platter and let cool for one hour. Do not be alarmed if it collapses. Peel the eggplant, scrape any flesh that adheres to the skin and put that plus the remaining flesh into a bowl; immediately add lemon juice and mash it in with the eggplant. Add tahini, garlic and salt and mix well. Cover tightly with plastic wrap and chill. Transfer mixture to a shallow bowl, sprinkle with parsley, and drizzle with olive oil. Serve with pita bread and black olives.

Pud Makua Yow

Pud Makua Yow

YIELD: Makes 4 servings

INGREDIENTS:

2 tablespoons vegetable oil

2 garlic cloves, minced

2 serrano chiles, stemmed and minced

2 to 3 medium eggplants (preferably the long Japanese ones), cut into one-inch cubes

1 cup water

2 to 3 tablespoons soy sauce

1 tablespoon fish sauce

1½ cups Thai sweet basil leaves, packed

DIRECTIONS: Pour oil into a wok or large skillet; add garlic and chiles. Over medium heat, cook, stirring constantly, until garlic releases its aroma. Add eggplant and one cup water; stir, cover and cook, stirring occasionally and adding more water if necessary, until eggplant is tender, about 5 to 10 minutes. If too much liquid remains, uncover and continue cooking until it is evaporated. Add soy and fish sauces and stir; then add basil and stir again. Serve immediately with rice, tofu or chicken.

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Rheumatoid arthritis typically begins with stiffness in the joints of the hands.
RA medications may increase other risks

By David Dunaief, M.D.

Dr. David Dunaief

We know that inflammation is a critical part of many chronic diseases. Rheumatoid arthritis (RA) is no exception. With RA, inflammation is rampant throughout the body and contributes to painful joints, most commonly concentrating bilaterally in the smaller joints of the body, including the metacarpals and proximal interphalangeal joints of the hand, as well as the wrists and elbows. With time, this disease can greatly diminish our ability to function, interfering with our activities of daily living. The most basic of chores, such as opening a jar, can become a major hindrance.

In addition, RA can cause extra-articular, a fancy way of saying outside the joints, manifestations and complications. These can involve the skin, eyes, lungs, heart, kidneys, nervous system and blood vessels. This is where it gets a bit dicier. With increased complications comes an increased risk of premature mortality (1).

Four out of 10 RA patients will experience complications in at least one organ. Those who have more severe disease in their joints are also at greater risk for these extra-articular manifestations. Thus, those who are markedly seropositive for the disease, showing elevated biomarkers like rheumatoid factor (RF), are at greatest risk (2). They have an increased risk of cardiovascular disease events, such as heart attacks and pulmonary disease. Fatigue is also increased, but the cause is not well understood. We will look more closely at these complications.

Are there treatments that may increase or decrease these complications? It is a very good question because some of the very medications used to treat RA also may increase risk for extra-articular complications, while other drugs may reduce the risks of complications. We will try to sort this out, as well. The drugs used to treat RA are disease-modifying anti-rheumatic drugs (DMARDs), including methotrexate; TNF (tumor necrosis factor) inhibitors, such as Enbrel (etanercept); oral corticosteroids; and NSAIDs (nonsteroidal anti-inflammatory drugs).

It is also important to note that there are modifiable risk factors. We will focus on two of these, weight and sugar. Let’s look at the evidence.

Cardiovascular disease burden

We know that cardiovascular disease is very common in this country for the population at large. However, the risk is even higher for RA patients; these patients are at a 50 percent higher risk of cardiovascular mortality than those without RA (3). The hypothesis is that the inflammation is responsible for the RA-cardiovascular disease connection (4). Thus, oxidative stress, cholesterol levels, endothelial dysfunction and high biomarkers for inflammation, such as ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein), play roles in fostering cardiovascular disease in RA patients (5).

The yin and yang of medications

Although drugs such as DMARDs (including methotrexate and TNF inhibitors, Enbrel, Remicade and Humira), NSAIDs (such as celecoxib) and corticosteroids are all used in the treatment of RA, some of these drugs increase cardiovascular events and others decrease them. In meta-analysis (a group of 28 studies), results showed that DMARDs reduced the risk of cardiovascular events by up to 30 percent, while NSAIDs and corticosteroids increased the risk (6).

The oral steroids had the highest risk of heart complications, approximately a 50 percent rise in risk. This may be one reason rheumatologists encourage their RA patients to discontinue oral steroid treatments as quickly as possible.

In an observational study, the results reaffirm that corticosteroids increased the risk of a heart attack in RA patients, this time by 68 percent (7). The study involved over 8,000 patients with a follow-up of nine years. Interestingly, there was a dose-response curve. In other words, the results also showed that for every 5 mg increase in dosage, there was a corresponding 14 percent increase in heart attack risk.

Baffling disease complication

Most complications seem to have a logical connection to the original disease. Well, it was a surprise to researchers when the results of the Nurses’ Health Study showed that those with RA were at increased risk of cardiovascular disease and of respiratory disease (8). In fact, the risk of dying from respiratory disease was 106 percent higher in the women with RA, compared to those without, and the risk was even higher in women who were seropositive (had elevated levels of rheumatoid factor). The authors surmise that seropositive patients have greater risk of death from respiratory disease because they have increased RA severity compared to seronegative patients. The study followed approximately 120,000 women for a 34-year duration.

Why am I so tired?

While we have tactics for treating joint inflammation, we have yet to figure out how to treat the fatigue associated with RA. In a Dutch study, results showed that while the inflammation improved significantly, fatigue only changed minimally (9). The consequences of fatigue can have a negative impact on both the mental and physical qualities of life. There were 626 patients involved in this study for eight years of follow-up data. This study involved two-thirds women, which is significant; women in this and in previous studies tended to score fatigue as more of a problem.

Lifestyles of the painful and more debilitating

We all want a piece of the American dream. To some that means eating like kings of past times. Well, it turns out that body mass index plays a role in the likelihood of developing RA. According to the Nurses’ Health Study, those who are overweight or obese and are ages 55 and younger have an increased risk of RA, 45 percent and 65 percent, respectively (10). There is higher risk with increased weight, because fat has pro-inflammatory factors, such as adipokines, that may contribute to the increased risk. Weight did not influence whether they became seropositive or seronegative RA patients.

With a vegetable-rich, plant-based diet you can reduce inflammation and thus reduce the risk of RA by 61 percent (11). In my clinical practice, I have seen numerous patients able to reduce their seropositive loads to normal or near-normal levels by following this type of diet.

Sugar, sugar!

At this point, we know that sugar is bad for us. But just how bad is it? When it comes to RA, results of the Nurses’ Health Study showed that sugary sodas increased the risk of developing seropositive disease by 63 percent (12). In subset data of those over age 55, the risk was even higher, 164 percent. This study involved over 100,000 women followed for 18 years.

The just plain weird – infection for the better?

Every so often we come across the surprising and the interesting. I would call it a Ripley’s Believe It or Not moment. In one study, those who had urinary tract infections, gastroenteritis or genital infections were less likely to develop RA than those who did not (13). The study did not indicate a time period or potential reasons for this decreased risk. However, I don’t think I want an infection to avoid another disease. When it comes to RA, prevention with diet is your best ally. Barring that, disease-modifying anti-rheumatic medications are important for keeping inflammation and its progression in check. However, oral steroids and NSAIDs should generally be reserved for short-term use. Before considering changing any medications, discuss it with your physician.

References: (1) J Rheumatol 2002;29(1):62. (2) uptodate.com. (3) Ann Rheum Dis 2010;69:325–331. (4) Rheumatology 2014;53(12):2143-2154. (5) Arthritis Res Ther 2011;13:R131. (6) Ann Rheum Dis 2015;74(3):480-489. (7) Rheumatology 2013;52:68-75. (8) ACR 2014: Abstract 818. (9) RMD Open 2015.  (10) Ann Rheum Dis. 2014;73(11):1914-1922. (11) Am J Clin Nutr 1999;70(6),1077–1082. (12) Am J Clin Nutr 2014;100(3):959-967. (13) Ann Rheum Dis 2015;74:904-907.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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MEET OLAF! This handsome boy is Olaf, a two-year-old medium-haired orange tabby who is currently waiting for his furever home at Kent Animal Shelter. Olaf loves to snuggle and is super mushy. He comes neutered, microchipped and up to date on all his vaccines. Won’t you stop by and say hello? Kent Animal Shelter is located at 2259 River Road in Calverton. For more information on Olaf and other adoptable pets at Kent, please call 631-727-5731 or visit www.kentanimalshelter.com.

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Michael Bernstein. Photo from SBU

By Michael A. Bernstein

From Ivy League institutions such as Harvard University to state institutions such as the University of Connecticut and several SUNY campuses, including Stony Brook, all are facing financial constraints that are prompting them to review or institute program suspensions ranging from academics to athletics. For Stony Brook, that means making difficult decisions to address budget reductions throughout all academic and administrative units.

Investments in more than 240 new faculty hires, coupled with a tuition freeze followed by a modest increase and no adjustments in state support to cover negotiated salary increases have created a structural operating deficit at Stony Brook. While we continue to work to develop new revenue sources and redouble our efforts to increase both state and philanthropic support, it is incumbent upon us to build a strong, stable foundation for continued excellence at our university.

Our budget issues are real. Strategic change is the only way to maintain our quality and offer the best and most efficient options for our students. Serious and consistent program review is necessary to ensure we are spending our scarce resources wisely, building upon our high-quality programs as well as those for which there is high student demand. This is why our program changes focus on those areas with low enrollments. In response to this, only a small number of assistant professors in the tenure track and lecturers have been directly affected.

Similar review is happening throughout West and East campuses, resulting in the suspension of admission to five programs — three in the College of Arts and Sciences and two in the School of Health Technology and Management. We have also mobilized resources to invest in areas such as Africana studies, art and creative writing and film as well as a variety of areas in the social and natural sciences.

These measures reflect our urgency to maximize our resources as we continue to support and invest in programs of excellence and impact; engage in cutting-edge research, scholarship and art-making that attract external funding and recognition; and do everything possible to empower students, meet their demands and ensure they receive an outstanding education at both the undergraduate and graduate level.

As an institution, we remain focused on our missions in education, research, scholarship, art-making, professional service and community engagement. And, as a public university with an exceptionally talented faculty and staff committed to serving a diverse student body, we must be outstanding stewards of the public’s trust and resources, constantly examining how best to invest in areas of strength, promise and need.

Michael A. Bernstein is the provost and senior vice president for academic affairs at Stony Brook University.

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The cheese has a sweet, nutty flavor with a tart aftertaste, similar to cheddar.

By Bob Lipinski

Bob Lipinski

Monterey Jack, a cow’s milk cheese, was developed in the 1880s in Monterey by a Scot merchant named David Jacks. He derived the name, Monterey Jack, from the shipping point, Monterey, California, and his last name, Jacks, minus the “s.” There are, however, several other versions as to the origin of Monterey Jack cheese.

Although the cheese was first developed and sold in Monterey, it is now produced in several other states and with variations from dairy to dairy. Most Monterey Jack has an inedible rind, often black in color. The rind is sometimes coated with a mixture of oil, pepper and cocoa. It generally has a pale yellow-orange interior with numerous small holes. It is rectangular or wheel shaped, depending on the preference of the dairy.

The cheese has a sweet, nutty flavor with a tart aftertaste, similar to cheddar. When old, the taste becomes sharp and tangy. It is sometimes flavored with caraway seeds, dill, fennel or jalapeño peppers. It has a semihard texture and when labeled “Dry Jack,” it is a hard, tangy cheese suitable for grating.

Dry Jack cheese is Monterey Jack that has been aged 6 to 9 months or longer. It came into existence during World War I, when San Francisco cheese wholesaler, D.F. DeBernardi found his Monterey Jack cheese had aged too long and “gone hard.” Italian immigrants immediately found it useful because it could be grated like Parmigiano-Reggiano or pecorino.

Monterey Jack is also called Sonoma Jack (brand name), California Jack or Jack. The cheese can be paired with syrah, merlot, zinfandel, and, of course, cabernet sauvignon.

Four California wines I recently tasted would pair quite well with a wedge of Monterey Jack. My tasting notes follow:

2010 Mayacamas, “Mt. Veeder” Cabernet Sauvignon: (blend of 95 percent cabernet sauvignon, 5 percent merlot; aged 36 months in oak). Full bouquet with flavors of dried berries, herbs, black currants, dill and coffee. Full bodied, tannic and still quite youthful.

2012 Inglenook “Cask” Rutherford, Cabernet Sauvignon: (blend of 85 percent cabernet sauvignon, 12 percent cabernet franc, 3 percent merlot; aged 18 months in oak). Dark colored with a bouquet brimming with berries (blackberry and blueberry), black cherries and black currants. Layers of fruit; great depth of flavor with plenty of acidity.

2013 Hourglass “Blueline Estate” Merlot, Calistoga: (blend of 84 percent merlot, 12 percent cabernet sauvignon, 4 percent malbec; aged 2 to 3 years in oak). Deepest color, very fruity with hints of plums, chocolate and spices. Quite smooth and elegant with toasted oak on the finish.

2012 Snowden “The Ranch” Napa Valley, Cabernet Sauvignon: (blend of 75 percent cabernet sauvignon, 14 percent merlot, 8 percent cabernet franc, 3 percent petit verdot; aged 18 months in oak). Great depth of color; fruity and powerful with a certain sweetness; concentrated flavors and very complex with overtones of dark chocolate, oak and black currants.

Bob Lipinski, a local author, has written 10 books, including “101: Everything You Need to Know About Whiskey” and “Italian Wine & Cheese Made Simple,” available on Amazon.com. He conducts training seminars on wine, spirit and food and is available for speaking engagements. He can be reached at www.boblipinski.com or [email protected].

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HELLO WORLD! Maria Hoffman of Setauket was in the right place at the right time when she snapped this photo of a diamondback terrapin hatching at West Meadow Beach in Stony Brook on Aug. 20. She writes, ‘I met a young woman, Emmy Silver, who was standing watch over a diamondback terrapin nest that had begun to hatch on the side of the path to the Gamecock Cottage. She was a volunteer for Friends of Flax Pond, which monitors the turtle nesting. While I spoke with her, we watched this one egg hatch. The little turtle was only about 2 inches long. Once it broke its head out of the egg, it rested for a long while. But once it was ready to come out, it made a fast push and then all its movements were fast. It was one of the most amazing things I’ve ever seen!’

Send your Photo of the Week to [email protected].

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From left, Lisa Miller with her research team Andrew McGregor, Alvin Acerbo, Tiffany Victor, Randy Smith, Ruth Pietri, Ryan Tappero, Nadia Hameed, Tunisia Solomon, Paul Panica and Adam Lowery. Photo by Roger Stoutenburgh, BNL

By Daniel Dunaief

Most of the people at the building that cost near a billion dollars are pulled in different directions, often, seemingly, at the same time. They help others who, like them, have numerous questions about the world far smaller than the eye can see. They also have their own questions, partnering up with other researchers to divide the work.

Lisa Miller, a senior biophysical chemist at Brookhaven National Laboratory, lives just such a multidirectional and multidimensional life. The manager for user services, communications, education and outreach at the National Synchrotron Light Source II, Miller recently joined forces with other scientists to explore the potential impact of copper on a neurodegenerative disease called cerebral amyloid angiopathy (CAA).

Miller is collaborating with Steve Smith, the director of structural biology in the Department of Biochemistry and Cell Biology at Stony Brook University and William Van Nostrand, a professor in the Department of Neurosurgery at SBU who will be moving to the University of Rhode Island. The trio is in the second year of a five-year grant from the National Institutes of Health.

Miller’s role is to image the content, distribution and oxidation state of copper in the mouse brain and vessels. Van Nostrand, whom Smith described as the “glue” that holds the group together, does the cognitive studies and Smith explores the amyloid structure.

In an email, Smith explained that Van Nostrand’s primary area of research is in CAA, while he and Miller were originally focused elsewhere.

Potentially toxic on its own, copper is transported in the body attached to a protein. When copper is in a particular ionic state — when it has two extra protons and is looking for electrons with which to reduce its positive charge — it reacts with water and oxygen, producing hydrogen peroxide, which is toxic.

Miller and her colleagues are working on a technique that will enable them to freeze the tissue and image it. Seeing the oxidation state of the metal requires that it be hydrated, or wet. The X-rays, however, react with water, causing radiation damage to the tissue.

To minimize this damage, the researchers freeze the tissue. At NSLS-II, a team of scientists are working to develop X-ray-compatible cryostages that will allow them to freeze and image the tissue.

Miller is trying to figure out where and why the copper is binding to an amyloid beta protein. This is the same protein that’s involved in plaques prevalent in the brains of people with Alzheimer’s disease.

In Alzheimer’s patients, the plaques are found in the parenchyma, or the extracellular space around the brain cells. In CAA, the deposits are attached to the surface of the blood vessels on the brain side.

Lisa Miller and her dog Dora on a recent 100-mile trek from Hiawassee, Georgia, to Fontana Dam in North Carolina Photo from Lisa Miller

The current hypothesis about how copper becomes reactive in the brain originates from work Van Nostrand and Smith published recently. They suggested that the amyloid fibrils in CAA adopt an anti-parallel orientation and the fibrils in the plaques in Alzheimer’s are in a parallel orientation. The anti-parallel structure predicts that there is a binding site for copper that, if occupied, would stabilize the structure.

“We are currently working to establish if this idea is correct,” Smith explained in an email, suggesting that the NSLS-II provides a “unique resource for addressing the role of copper in CAA. The data [Miller] is collecting are essential, key components of the puzzle.”

The NSLS-II will provide the kind of spatial resolution that allows Miller to measure how much copper is in the deposits. Ideally, she’d like to see the oxidation state of the copper to see if a reaction that’s producing hydrogen peroxide is occurring.

A challenge with peroxide is that it’s hard to find in a living tissue. It is highly reactive, which means it does its damage and then reverts to water and oxygen.

As someone with considerable responsibilities outside her own scientific pursuits, Miller said she spends about a quarter of her time on her own research. One of Miller’s jobs during the summer is to host the open house for NSLS-II, which allows members of the community to visit the facility. This year, at the end of July, she “was thrilled” to host about 1,600 members of the community.

“Most of them wanted to go on the floor and meet the scientists and walk” around the three quarters of a mile circle, she said. While they are interested in the research, the surprising mode of transportation strikes their fancy when they trek around the site.

“The thing that fascinates them when they walk in the door is the tricycles,” she said. The NSLS-II can’t take credit for being the first facility to use these adult-sized tricycles, which number over 100 at the facility. “It’s a synchrotron thing.”

The previous NSLS at BNL was too compact and had too many turns, which made the three-wheeled vehicles, which, like a truck, need a wider turning radius to maneuver on a road, impractical.

Miller, who is a part of the trike-share program, is an avid hiker. This summer, she completed a 100-mile trek from Hiawassee, Georgia, to Fontana Dam in North Carolina. This section was located in the area of totality for the solar eclipse and Miller was able to witness the astronomical phenomenon at Siler Bald in North Carolina.

A resident of Wading River, Miller, who grew up in the similarly flat terrain of Cleveland, spends considerable time walking and running with her rescue mutt Dora, who accompanied her on her recent hike.

While Miller finds the research she does with copper rewarding, she said she also appreciates the opportunities NSLS-II affords her. “Every day is different and we never know what project will show up next,” she said.

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There are many benefits to naming a minor as beneficiary of a tax-deffered retirement account.

By Nancy Burner, ESQ.

Nancy Burner, Esq.

Many of our clients have retirement assets held in a traditional IRA, 401K, 403(b) or other similar plan. It is important to periodically review the beneficiary designations on these types of plans. A review should confirm that the institution still has the proper designations on file, the clients’ wishes are being followed, the designations fit into the larger estate plan of the client and that the best interests of the beneficiaries are taken into account. This is of special concern if the beneficiaries are grandchildren or other minors.

There are certain benefits to leaving retirement assets to a minor who is a much younger beneficiary than the original account holder. When you leave retirement assets to a nonspouse, the beneficiary has the right to take it in an “inherited IRA.”

The beneficiary of an inherited IRA must start taking distributions the year after the death of the original account holder. These distributions are taken as a “stretch,” meaning they are determined by the life expectancy of the new IRA beneficiary. In that case, the account can grow tax deferred over a much longer life expectancy.

The rule of thumb is that the account will be worth approximately 30 times its value if distributions are taken over the life expectancy of a grandchild. For example, suppose you name your grandchild as beneficiary of an IRA account with a $100,000 balance. If your grandchild takes distributions based upon her life expectancy each year, then the account could be worth $3,000,000 over her lifetime. This is one of the great benefits of naming a minor as beneficiary of a tax-deferred retirement account.

The problem is that you cannot achieve the benefit of the stretch if you name a minor directly as the beneficiary of any account — you must name a trust for the benefit of the minor.

Since she is not an adult, the minor will be unable to take the distributions as required beginning the year after your death. The only way to access the account is for the court to appoint a guardian for the property of the child, usually the parent. First, this will be a costly and unnecessary proceeding. But the result is even worse.

The court will direct the guardian to distribute the entire IRA and pay the income tax. The income tax will be based upon the parents’ income if the child is under 14 years of age, also known as the “kiddie tax.”

In addition, the monies that are left after paying the income tax will be deposited in a bank account earning very little interest. If that isn’t bad enough, the account will be turned over to the child upon attaining the age of 18. This will obviously impact the child’s financial aid when he or she applies for college. This is a financial disaster. In addition to retirement accounts, you do not want to name minors directly as beneficiaries on IRA accounts, annuities, insurance policies, bank accounts or any other account. Any and all distributions for a minor should be distributed to a trust that is drafted for the benefit of the child.

The trust should be created as part of the estate plan, either through a last will and testament or in an inter vivos trust. Providing for the beneficiary’s share to go into a trust will ensure the benefits of inheriting a retirement asset are received.

The beneficiary can get the stretch on the account and the asset will not need to be held by the court. However, be certain that the trust you are naming for the benefit of the minor is drafted for the purpose of receiving retirement accounts; all trusts are not created equal in this respect. A trust must be properly drafted and meet certain requirements set by the IRS in order to accept the IRA distribution and receive the benefits described above.

Before naming a beneficiary on an account, one should check with the institution holding the account. Each plan has its own individual rules regarding the designation of beneficiaries. For example, the New York State Teacher’s Retirement system has certain benefits for which you can name a trust as beneficiary, while other benefits, including pensions, do not allow this type of beneficiary. Retirement savings can be the largest asset one leaves behind. Being sure it is properly designated can protect the best interests of your beneficiaries long after you are gone.

Nancy Burner, Esq. practices elder law and estate planning from her East Setauket office.

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People who are considered metabolically healthy may still have a higher risk of developing heart problems if they are obese.
Obesity still increases risks of many chronic diseases

By David Dunaief, M.D.

Have we entered a fourth dimension where it’s possible to be obese and healthy? Hold on to your seats for this wild ride. This would be a big relief, since more than one-third of Americans are obese, another third are overweight and the numbers are on the rise (1). In one analysis referenced by the Centers for Disease Control and Prevention (CDC), the average medical cost for obesity alone is 41.5 percent higher than for those of normal weight, based on 2006 numbers (2). Still, there are several studies that suggest it’s possible to be metabolically healthy and still be obese.

What does metabolically healthy mean? It is defined as having no increased risk of diabetes or cardiovascular disease (heart disease and stroke) because blood pressure, cholesterol levels and inflammatory biomarkers remain within normal limits.

However, read on before thinking that obesity can be equated with health. Though several studies may suggest metabolic health with obesity, there is a caveat: Some of these obese patients will go on to become metabolically unhealthy; but even more importantly, obesity will increase their risk significantly for a number of other chronic diseases. These include osteoarthritis, diverticulitis, rheumatoid arthritis and migraine. There is also a higher rate of premature mortality, or death, associated with obesity. In other words, the short answer is that obesity is NOT healthy.

Metabolically healthy obesity

Several published studies imply that there is such a thing as “metabolically healthy obesity,” or MHO. In the Cork and Kerry Diabetes and Heart Disease Phase 2 Study, results show that approximately one-third of obese patients may fall into the category of metabolically “healthy” (3). This means that they are not at increased risk of cardiovascular disease, based on five metabolic parameters, including LDL “bad” cholesterol, HDL “good” cholesterol, triglycerides, fasting plasma glucose and insulin resistance. The researchers compared three groups: MHO, metabolically unhealthy obese and nonobese participants. Both the MHO participants and the nonobese patients demonstrated these positive results.

There were over 2,000 participants involved in this study, with an equal proportion of men and women ranging in age from 45 to 75. The researchers believe that a beneficial inflammation profile, including a lower C-reactive protein and a lower white blood cell count, may be at the root of these results.

In the North West Adelaide Health Study, a prospective (forward-looking) study, the results show that one-third of obese patients may be metabolically healthy, but it goes further to say that this occurs in mostly younger patients, those less than 40 years old, and those with a lower waist circumference and more fat in the legs (4). The reason for the positive effects may have to do with how fat is transported through the body.

In metabolically unhealthy obese patients, fat is deposited in the organs, such as the liver and heart, potentially leading to cardiovascular disease and type 2 diabetes. A theory is that mitochondria, the cells’ energy source, are disrupted, potentially increasing inflammation.

However, the results also showed that over a 10-year period, one-third of “healthy” obese patients transitioned into the unhealthy category. Over a longer period of time, this number may increase.

Premature mortality

To hammer the nail into the coffin, so to speak, obesity may be associated with premature mortality. In one study, about 20 percent of American patient deaths were associated with being obese or overweight (5). The rates were highest among white men, white women and black women. The researchers found this statistic surprising; previous estimates were far lower. Researchers reviewed a registry of 19 consecutive National Health Interview Surveys, from 1986 to 2004, including more than 500,000 patients with ages ranging from 40 to 84.9 years old.

Interestingly, obesity seems to have more of an effect on mortality as we age: obesity raised mortality risk 100 percent in those who were 65 and over, compared to a 25 percent increased risk in those who were 45.

Osteoarthritis

It is unlikely that any group of obese patients would be able to avoid pressure on their joints. In an Australian study, those who were obese had a greater than two times increased risk of developing osteoarthritis of the hip and a greater than seven times increased risk of developing osteoarthritis of the knee (6). If this weren’t bad enough, obese patients complained of increased pain and stiffness, as well as decreased functioning, in the hip and knee joints. There were over 1,000 adults involved in this study. Patients who were 39 years or older demonstrated that obesity’s impact on osteoarthritis can affect those who are relatively young.

There is a solution to obesity and its impact on osteoarthritis of the knees and hips. In a randomized controlled trial of 454 patients over 18 months, those who lost just 10 percent of their body weight saw significant improvement in function and knee joint pain, compared to those who lost less than 10 percent of their body weight (7). So, if you are 200 pounds, this would mean you would experience benefits after losing only 20 pounds.

When diet and exercise together were utilized, patients saw the best outcomes, with reduced pain and inflammation and increased mobility, compared to diet or exercise alone. However, diet was superior to exercise in improving knee joint pressure. Also, inflammatory biomarkers were reduced significantly more in the combined diet and exercise group and in the diet alone group, compared to the exercise alone group.

The diet was composed of two shakes and a dinner that was vegetable rich and low in fat. The exercise component involved both walking with alacrity plus resistance training for a modest frequency of three times a week for one hour each time. Thus, if you were considering losing weight and did not want to start both exercise and diet regimens at once, focusing on a vegetable-rich diet may be most productive.

While it is interesting that some obese patients are metabolically healthy, this does not necessarily last, and there are a number of chronic diseases involved with increased weight. Though we should not be prejudiced or judgmental of obese patients, this disease needs to be treated to avoid increased risk of mortality and increased risk of developing other diseases.

References: (1) CDC.gov. (2) Health Aff. September/October 2009;vol. 28 no. 5 w822-w831. (3) J Clin Endocrinol Metab online. 2013 Aug. 26. (4) Diabetes Care. 2013;36:2388-2394. (5) Am J Public Health online. 2013 Aug. 15. (6) BMC Musculoskelet Disord. 2012;13:254. (7) JAMA. 2013;310:1263-1273.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.

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