Monthly Archives: April 2014

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A World War I cannon usually resides at the memorial park in Port Jefferson, above, but is now at the local American Legion post awaiting repairs. Photo by Elana Glowatz

A cannon that saw World War I battlefields in Europe and retired to a grassy home on Port Jefferson Harbor has gone on a brief vacation, after a local veterans group took it away for repairs.

American Legion Wilson Ritch Post 432 in Port Jefferson Station maintains the war memorial at the small Brookhaven Town-owned park between Route 25A and the harbor, across from Port Jefferson Village Hall.

According to Bob Elfers, commander of the post, the memorial’s cannon is at the Legion because “the wheels are totally shot” and it needs welding work and a fresh coat of paint.

The wheels have wooden spokes and rims, with a metal hub and reinforcements.

“The wood just totally disintegrated over the years,” Elfers said. Exposure also caused rusting on the body of the cannon.

Elfers said his group is having someone repair the wheels and weld the rusted parts, and the cannon will be sanded and painted.

The cannon, which is American Legion property, is a German WWI weapon, though Elfers said he does not know its exact history or when the post acquired it, and said no one at the post is old enough to be able to speak to that.

A World War I cannon usually resides at the memorial park in Port Jefferson but is now at the local American Legion post awaiting repairs, above. Photo by Rich Acritelli
A World War I cannon usually resides at the memorial park in Port Jefferson but is now at the local American Legion post awaiting repairs, above. Photo by Rich Acritelli

According to Rich Acritelli, a Legion member as well as a military history expert and social studies teacher, the cannon was built by industrial company Friedrich Krupp AG in Essen, Germany, which is in the northwestern part of that country, close to the Netherlands.

The company built armaments as well as naval ships during that period, particularly U-boats.

Acritelli said the cannon was not a heavy artillery weapon and it could have been used in two different ways: either mounted on wheels to assist the German infantry or mounted on a ship for the navy.

Because it was used during World War I, the cannon is roughly a century old.

It is likely that an American soldier took the cannon home with him, a common practice at the time, Acritelli said. It is also likely that soldier was serving on the Western Front, because that was where most of the U.S. military went during WWI.

Aside from the cannon, the memorial park in Port Jefferson contains flags and stones that pay tribute to those who served in wars throughout the nation’s history, as well as a central WWI stone monument.

That WWI monument has a story of its own: It was unveiled on Memorial Day in 1922 and was originally located on East Main Street, on the grass in front of the former First Baptist Church of Port Jefferson.

Elfers said he is hoping the cannon will return to the park in May, in time for Memorial Day.

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When it spreads, it becomes more difficult to treat. Understanding metastatic cancer presents significant challenges to doctors and scientists in part because the disease is different in the liver than it is in the lungs.

Lloyd Trotman, an associate professor at Cold Spring Harbor Laboratory, has created a mouse model of prostate cancer that becomes metastatic. By exploring what happens to cells in different areas, Trotman hopes to get a better understanding of cancer as it spreads.

“New technology allows us to tag cells when they are at the metastatic site,” he said. He can look at “how they differ from where they started.”

When prostate cancer becomes metastatic, the cells “forget about their identity,” Trotman said. They become more like cells that are developing, which means they are not as dependent on male hormones for their survival. This change in their identity makes them difficult to treat with hormone therapy.

By developing these metastatic models of prostate cancer, Trotman has been able to do preclinical studies of drugs designed to treat the original disease and its metastatic form. He has worked with scientists from Cornell University, the Dana-Farber Cancer Institute, and the Memorial Sloan Kettering Cancer Center.

“We can ask if a drug specifically is beneficial against metastatic cancer and especially against the hormone-refractory kind,” he said.
Trotman’s research also explores how cancers that were in remission become active again. “Most [treatments] will not be curative,” he said. “Why? If it works, but then the disease comes back, what is driving the disease? What is it that the drug is doing wrong at the point that it was looking good? What limit does the drug need to push to be curative?”

With his model of the disease, he can track the changes in a living animal. He can see how the cancerous cells are glowing in areas including the liver, lymph nodes, lungs, and bone. “Our hope is that by making these things visible at a very primitive level, we can see it first, then harvest it, and read the sequencing,” he said.

Trotman’s approach has won him the admiration of other scientists. “For an early career scientist, his work stands out as particularly innovative,” said Scott Lowe, a cancer biologist and chairman of the Geoffrey Beene Cancer Research Center at Memorial Sloan Kettering.
Lowe was deputy director of the cancer center at Cold Spring Harbor Laboratory, where he was involved in recruiting Trotman to join CSHL. “His research on an important cancer gene caught our attention,” Lowe said. He described Trotman as an “enthusiastic scientist who strives to address the most important questions in his field.”

Trotman explained that his goal isn’t just to understand how the genome works to cause cancer, but to figure out how to cure metastatic prostate disease. He wants to see where potentially effective drugs fail and to figure out what they should be doing differently. If he develops the kind of data he hopes to explore with the mouse, he would then argue that the same kind of analysis is necessary in humans, to make sure the model and the reality in humans are aligned.

While he’s focused on prostate cancer, Trotman said he would like to find a methodology that allows him to combat and understand cancer on a broader scale.

Born in the United States, Trotman moved to Switzerland when he was 2 years old. He attended high school and received his doctorate in Switzerland. He returned to New York to do his postdoctoral work at Sloan Kettering. He became a faculty member at Cold Spring Harbor Laboratory in 2007. Trotman’s Swiss background enabled him to become fluent in English, German, French and Swedish.

A resident of Oyster Bay, Trotman lives with his wife Eva Frosch, who runs the gallery Frosch & Portmann in New York City, and their sons Liam, 8, and Finn, 5.

Trotman loves summers on Long Island, where he can surf on the south shore and head to the beaches on the North Shore.
Trotman said he hopes his mouse model of prostate cancer can help uncover how cancer progresses, becomes metastatic, and resists drug treatment.

“There are many theories about how diseases like cancer evolve,” he said. His model can “help bring [the research] down to a level where everybody can see it.”

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Goals are to relieve symptoms and slow progression

Not surprisingly, osteoarthritis is widespread. The more common joints affected are the knees, hips and hands. There are three types of treatment for this disease: surgery, involving joint replacements of the hips or knees; medications; and nonpharmacologic approaches. The most commonly used first-line medications are acetaminophen and nonsteroidal anti-inflammatory drugs, such as ibuprofen. Unfortunately, medications mostly treat the symptoms of pain and inflammation.

However, the primary objectives in treating osteoarthritis should also include improving quality of life, slowing progression of the disease process and reducing its disabling effects (1).

What are the most productive approaches to treatment? This is good time to test your knowledge. This will hopefully get you thinking and make you an active participant for the evidence to follow. There are three responses to choose from: True (T), False (F) and Unclear (U) — a new twist, because I want to keep you on your toes.

1) Dairy is effective in the treatment of osteoarthritis.

2) Low-fat and nonfat milk have potentially disease-modifying effects.

3) Vitamin D is a necessary supplement in this disease.

4) Glucosamine is an effective treatment.

5) Weight loss may provide symptom relief and disease-modifying effects.

6) Diet and exercise are more important than either alone.

So how do you think you did? The answers are as follows: 1) F, 2) U, 3) F, 4) U, 5) T and 6) T.

Let’s look at the evidence.

Dairy and milk

When we think of dairy, specifically milk, there are two distinct camps: one believes in the benefits, and the other thinks it may contribute to disease. In this case they both may be at least partly correct. In the Osteoarthritis Initiative study, an observational study of over 2,100 patients, results showed that low-fat (1 percent) and nonfat milk may slow the progression of osteoarthritis (2). The researchers looked specifically at joint space narrowing that occurs in those with affected knee joints. Radiographic imaging changes were used at baseline and then to follow the patients for up to 12 to 48 months for changes. Compared to those who did not drink milk, patients who did saw significantly less narrowing of knee joint space.

Was it a dose-dependent response? Not necessarily. Specifically, those who drank less than three glasses/week and those who drank four to six glasses/week both saw slower progression of joint space narrowing of 0.09 mm. Seven to 10 glasses/week resulted in a 0.12 mm preservation. However, those who drank more than 10 glasses/week saw less beneficial effect, 0.06 mm preservation compared to those who did not drink milk. Interestingly, there was no benefit seen in men or with the consumption of cheese or yogurt.

However, there are significant flaws with this study. First, the patients were only asked about their dietary intake of milk at baseline, therefore their consumption could have changed during the study. Second, there was a recall bias; patients were asked to recall their weekly milk consumption for the previous 12 months before the study began. I don’t know about you, but I can’t recall my intake of specific foods for the last week, let alone for the past year. Third, there could have been confounding factors, such as orange consumption.

Oddly, this was not a dose-response curve, since the most milk consumption had less beneficial effect than lower amounts. Also, why were these effects only seen in women? Finally, researchers could not explain why low-fat or nonfat milk had this potential benefit, but cheese was detrimental and yogurt did not show benefit. We are left with more questions than answers.

Would I recommend consuming low-fat or nonfat milk? Not necessarily, but I may not dissuade osteoarthritis patients from drinking it. There are very few approaches that slow the progression of joint space narrowing.

Vitamin D

Over the last five years or so, the medical community has gone from believing that vitamin D was potentially the solution to many diseases to wondering whether, in some cases, low levels were indicative of disease, but repletion was not a change-maker. Well, in a recent randomized controlled trial, the gold standard of studies, vitamin D had no beneficial symptom relief, nor any disease-modifying effects (3). This two-year study of almost 150 men and women raised blood levels of vitamin D on average to 36 ng/ml, which is considered respectable. Researchers used MRI and X-rays to track their results.

Glucosamine

There is raging debate about whether glucosamine is an effective treatment for osteoarthritis. In the latest installment, there was a RCT, the results of which showed that glucosamine hydrochloride was not effective in treating osteoarthritis (4). In the trial, 201 patients with either mild or moderate knee pain drank diet lemonade with or without 1500 mg of glucosamine hydrochloride.

There was no difference in cartilage changes in the knee nor in pain relief in those in the placebo or treatment groups over a six-month duration. Bone marrow lesions also did not improve with the glucosamine group. The researchers used 3T MRI scans (an advanced radiologic imaging technique) to follow the patients’ disease progression. This does not mean that glucosamine does not work for some patients. Different formulations, such as glucosamine sulfate, were not used in this study.

Weight

This could not be an article on osteoarthritis if I did not talk about weight. Do you remember analogies from the SATs? Well here is one for you: Weight loss, weight loss, weight loss is to osteoarthritis as location, location, location is to real estate. In a recent study involving 112 obese patients, there was not only a reduction of knee symptoms in those who lost weight, but there was also disease modification, with reduction in the loss of cartilage volume around the medial tibia (5). On the other hand, those who gained weight saw the inverse effect. A reduction of tibial cartilage is potentially associated with the need for knee replacement. The relationship was almost one-to-one; for every 1 percent of weight lost, there was a 1.2 mm3 preservation of medial tibial cartilage volume, while the exact opposite was true with weight gain.

Exercise and diet

In a recent study, diet and exercise trumped the effects of diet or exercise alone (6). Patients with osteoarthritis of the knee who lost at least 10 percent of their body weight experienced significant improvements in function and a 50 percent reduction in pain, as well as reduction in inflammation, compared to those who lost 5 to 10 percent and those who lost less than 5 percent. This study was a well-designed, randomized controlled single-blinded study with a duration of 18 months.

Researchers used a biomarker — IL6 — to measure inflammation. The diet and exercise group and the diet-only group lost significantly more weight than the exercise-only group, 23.3 pounds and 19.6 pounds versus 4 pounds. The diet portion consisted of a meal replacement shake for breakfast and lunch and then a vegetable-rich, low-fat dinner. Low-calorie meals replaced the shakes after six months. The exercise regimen included one hour of a combination of weight training and walking with alacrity three times per week.

Therefore, concentrate on lifestyle modifications if you want to see potentially disease-modifying effects. These include both exercise and diet. In terms of low-fat or nonfat milk, while the study had numerous flaws, if you drink milk, you might continue for the sake of osteoarthritis, but stay on the low end of consumption. And remember, the best potential effects shown are with weight loss and with a vegetable-rich diet.

References:

(1) uptodate.com. (2) Arthritis Care Res online. 2014 April 6. (3) JAMA. 2013;309:155-162. (4) Arthritis Rheum online. 2014 March 10. (5) Ann Rheum Dis online. 2014 Feb. 11. (6) JAMA. 2013;310:1263-1273.

•If you would like to see a specific topic covered in Medical Compass, please email info@medicalcompassmd.com.

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, go to the website medicalcompassmd.com and/or consult your personal physician.

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Paul Bingham and Zuzana Zachar, a husband-and-wife team at Stony Brook University, have spent the better part of a decade exploring a way to disrupt cancer’s energy supply line.

They have developed a compound that takes advantage of the different way cancer cells produce energy. With the help of other scientists at Stony Brook, including James Marecek in the Chemistry Department, they created another form of lipoate, called CPI-613, that doesn’t foster cancer growth.

“It’s like a Trojan horse,” explained Zachar, who is an assistant professor in the Department of Biochemistry and Cell Biology. “It has no catalytic ability,” which means that it looks like a key molecule for a cancer pathway in mitochondria, but doesn’t act like it.

By shutting down tumor cell mitochondria, the researchers are able to trigger several cell-death pathways selectively, explained Bingham, who is an associate professor in the same department. The scientists anticipate lower vulnerability to evolved resistance because the CPI-613 attacks two enzyme targets at the same time.

The Stony Brook team are in Phase II trials of this drug at Wake Forest University with patients who have leukemia and lymphoma.

“We saw a 38 percent response rate [among patients who were not responding to other therapies] in the first Phase I trial we completed” said Timothy Pardee, an assistant professor who conducted those trials and is performing a similar function in Phase II. While he believes the treatment has extended people’s lives, he cautioned that “it’s important to remember that these are very early results.”

The scientists have to generate significant evidence to be confident in their approach, both for basic science and for use with patients, Bingham said.

Even though the treatment has shown promise, it’s possible that cancers may respond to this approach the way they have to so many other treatments, by finding another way to avoid selective eradication. While the treatment the couple has worked on is designed to minimize this risk, they will only know whether they have been successful after extensive testing.

“Until we get more clinical experience, we can’t know that natural selection operating on cancer cells doesn’t have a diabolical trick we haven’t thought about,” Bingham said.

Robert Haltiwanger, the chairman of the Department of Biochemistry and Cell Biology, said scientists had known since the 1930’s that the metabolism of cancer cells is different from that of normal cells. Bingham and Zachar have developed a compound that “seems to have an effect,” which means it has potential in a “wide variety of cancers.” In addition to contributing to cancer research, Bingham is also a “very popular lecturer,” said Haltiwanger.

Bingham and Zachar, who had done extensive work on the fruit fly Drosophila, began looking at cancer metabolism in the late 1990’s as a “side project.” That showed enough promise for them to transform it into a full-time pursuit.

Bingham grew up in the rural Midwest, attending high school in a small town in a farming area of central Illinois that produces corn and soybeans. He received his doctorate from Harvard University in the Department of Biochemistry and Molecular Biology.

Zachar was born in what is now the Czech Republic. She moved to Ghana, West Africa when she was 10 and emigrated to the United States in 1968, settling near Chicago, Ill. She was at the University of North Carolina, Chapel Hill and Bingham was at the National Institute of Environmental Health Sciences in North Carolina when they met.

“We didn’t grow up as clinical researchers,” Bingham said. “We came up as basic, fundamental” scientists who were “drawn later in our careers into clinical work. When I was told we were going to work with people, my first reaction was anxiety for fear of doing harm.”

The researchers, who are residents of South Setauket and have lived on Long Island for 32 years, love the hiking trails.

They expressed satisfaction at the prospect of contributing to an effort that might aid in cancer treatment. Bingham said the research has particular meaning for him.

His mother, Doris Rorhman Bingham, died of cancer when he was 16. “Had she lived another 10 or 20 years, my life would have been completely different,” he said. “I still think of her almost every day.”

Zachar said the couple feel fortunate to be able to do this kind of work., “Saving other families from what [Bingham’s] family went through would be supremely fulfilling,” she said.

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By Linda M. Toga, Esq.

The Facts: I heard that the New York’s estate tax laws changed and that the value of an estate that can pass estate tax-free was increased.

The Question: Is that true? If so, what is the current NYS estate tax exemption?

The Answer: Fortunately for New Yorkers, the tax laws have changed and the tax exemption or so called “exclusion amount” was increased significantly for the first time in many years. As of April 1, 2014, individuals whose estates would have been subject to state estate tax if the value of assets passing to a non-spouse exceeded $1,000,000, can now pass on assets valued at up to $2,062,500 estate tax-free to any beneficiary. The new laws did not change the unlimited marital deduction so individuals can still pass all of their assets to a surviving spouse estate tax-free, regardless of their value. Since New York recognizes same-sex marriages, same-sex couples can take advantage of the unlimited marital deduction on both their New York and their Federal estate tax returns.

Not only has the NYS exclusion amount increased significantly as a result of the new law, but it will continue to increase at a rate of $1,062,500 per year until 2017 when it will be $5,250,000. Another increase will take effect on January 1, 2019 at which time the NYS exemption amount will equal the Federal exemption amount.

Many New Yorkers are under the impression that the new tax laws will have no effect on their estates. However, since estate tax liability is calculated based upon the value of assets owned by or controlled by a person at the time of death, even the estates of people of relatively modest means often incurred a tax liability under the old laws. That is because the estate tax calculation starts with the value of a person’s gross taxable estate and is not limited to the value of the assets that pass under a person’s Will. Rather, the value of assets such as jointly held property and bank accounts, life insurance proceeds and funds held in an IRA or 401(k), for example, are also part of a person’s gross taxable estate and may be taken into consideration when calculating an estate’s tax liability. If the gross value of an estate exceeds the exclusion amount, an estate tax return must be filed even if allowable estate tax deductions reduce the net value of the estate below the exemption amount and no tax is due.

While New Yorkers should welcome the new tax laws, they are complex and it is advisable to seek professional assistance when dealing with estate tax questions.

Linda M. Toga, Esq. provides legal services in the areas of litigation, estate planning and real estate from her East Setauket office.

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The human body not only defends itself against bacteria and viruses, but it also has a system to suppress or prevent tumors. Cancers, however, weaken this defense.

Sumita Bhaduri-McIntosh, an assistant professor in the Department of Pediatrics and in the Department of Molecular Genetics and Microbiology at Stony Brook University, has recently discovered a step cells take to weaken the cell’s defenses and become cancerous.

Using the Epstein-Barr virus, which causes mononucleosis and which more than 90 percent of people carry, Bhaduri-McIntosh has been able to turn healthy cells into those that divide and grow uncontrollably.

“If we take B cells (a part of the immune system) from healthy individuals and isolate those cells, we can infect them with EBV in the lab, where the virus expresses its own cancer,” she said. “This allows us to systematically examine a variety of cellular events, from minute one until we have these proliferating cells.”

Human cells have a defense called DNA damage response. This system is a set of mechanisms operating in every dividing cell that finds damage or defects in the genetic code and slows down or pauses the process of copying DNA and promotes repair of the damaged code, Bhaduri-McIntosh explained.

The virus she inserted triggered the activation and increased production of the cellular protein STAT3. Scientists knew this protein could drive gene expression and was an important ingredient in many human cancers. What they didn’t know, however, was that it also muted DNA damage response.

The results of these experiments were recently published in the journal the Proceedings of the National Academy of Sciences of the United States of America.

This finding “reveals a novel mechanism for development of cancer,” said Ayman El-Guindy, an assistant professor in the Division of Pediatric Infectious Diseases at Yale School of Medicine, where Bhaduri-McIntosh was a postdoctoral fellow and an assistant professor. Disruption of these pathways can “lead to accumulation of mutations in our genome that can ultimately cause cancer.”

El-Guindy suggested the kind of work Bhaduri-McIntosh is doing, while filled with the potential to help people, faces financial obstacles.

“While it is unfortunate that basic research is increasingly underfunded and has suffered multiple budget cuts in recent years, Dr. Bhaduri-Mcintosh’s discovery highlights the importance of basic research to develop new remedies against cancer,” El-Guindy said.

While a majority of people have the EBV, Bhaduri-McIntosh reassured people that it is extremely rare for it to become cancerous, especially in North America.

“There are EBV-related cancers that occur and are quite prevalent in other parts of the world,” including endemic Burkitt lymphoma in equatorial Africa, nasopharyngeal cell carcinoma in Southeast Asia and AIDS lymphomas.

Cancers caused by EBV can occur in as many as one in five solid-organ transplant recipients, triggered by the immunity-suppressing drugs that keep the recipient from rejecting the new organ.

A native of India, Bhaduri-McIntosh has a medical degree and a Ph.D. She sees patients as an attending physician at Stony Brook Children’s Hospital, although she spends most of her time doing research.

“When I was going through medical school in India, infectious disease is an even bigger scourge than in the western world,” she said. “You see it all around you, with tuberculosis, leprosy and parasitic diseases.” Studying infectious disease was “a very natural connection.”

Becoming an infectious disease expert “fed the detective urge,” she said, as symptoms don’t necessarily point to a specific diagnosis.

In one case when she was at Yale, she worked with a 10-year-old boy with multiorgan failure, while his bone marrow was making blood cells that were being destroyed. In an investigation of family members, she helped discover that some of them had a mutation.

The boy had a bone marrow transplant and, from the last she heard, “is doing rather well.”

Bhaduri-McIntosh credits her success to her parents in India and to her Wading River-based family. She and her husband, Michael McIntosh, the science adviser to the Foreign Animal Disease Diagnostic Laboratory on Plum Island, have a 14-year-old son, Rohin, and a 12-year-old daughter, Uma. She called the three of them “absolutely, veritable rocks.” She is also grateful for the support of the Pediatrics and Molecular Genetics departments.

When she’s not in the lab or helping patients, Bhaduri-McIntosh likes to sing. She was trained in Indian classical music. Nowadays, she sings Indian contemporary, as well as Western, music.

As for her career, working with patients and in research makes her better in both arenas, she said.

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Incidence of melanoma has increased significantly

Longer days are here again, and you can feel the jubilance of people coming out of hibernation after a long, hard winter. Summer weather will be here before you know it, and millions will be heading to the beaches. What could possibly be wrong with this picture? With all of these benefits, you need to be cognizant of cutaneous (skin) melanoma. It is small in frequency, compared to basal cell and squamous cell carcinomas, responsible for only about 5 percent of skin cancers; however, it is much more deadly.

Statistics

Unfortunately, melanoma is on the rise. Over the last 40 years from 1970 to 2009, its incidence has increased by 800 percent in young women and by 400 percent in young men (1). These were patients diagnosed for the first time between 18 and 39 years old. Overall, the risk is greater in men, with 1 in 37 afflicted by this disease in their lifetimes. The rate among women is 1 in 56. It is predicted that in 2014, there will be over 76,000 cases, with over 12 percent of these resulting in death (2).

Melanoma risk involves genetic  and environmental factors. These include sun exposure that is intense, but intermittent; tanning beds; UVA radiation used for the treatment of psoriasis; the number of nevi (moles); Parkinson’s disease; prostate cancer; family history; and personal history. Many of these risk factors are modifiable (3).

Presentation

Fortunately, melanoma is mostly preventable. What should you look for to detect melanoma at its earliest stages? In medicine, we use the mnemonic “ABCDE” to recall key factors to look for when examining moles. This stands for asymmetric borders (change in shape); border irregularities; color change; diameter increase (size change); and evolution or enlargement of diameter, color or symptoms, such as inflammation, bleeding and crustiness (4). Asymmetry, color and diameter are most important, according to guidelines developed in England (5).

It is important to look over your skin completely, not just partially, and have a dermatologist screen for potential melanoma. Screening skin for melanomas has shown a six-times greater chance of detecting them. Skin areas exposed to the sun have the highest probability of developing the disease. Men are more likely to have melanoma tumors on the back, while women are more likely to have melanoma on the lower legs, but they can develop anywhere (6).

In addition, most important to the physician, especially the dermatologist, is the thickness of melanoma. This may determine its probability to metastasize. In a recent retrospective (backward-looking) study, the results suggest that melanoma of >0.75 mm needs to not only be excised, or removed, but also have the sentinel lymph node (the closest node) biopsied to determine risk of metastases (7). A positive sentinel node biopsy occurred in 6.23 percent of those with thickness >0.75 mm, which was significantly greater than in those with thinner melanomas. When the sentinel node biopsy is positive, there is a greater than twofold increase in the risk of metastases. On the plus side, having a negative sentinel node helps relieve the stress and anxiety that the melanoma tumor has spread.

Prevention

The two most valuable types of prevention are clothing and sunscreen. Let’s look at these in more detail.

Clothing can play a key role in reducing melanoma risk. The rating system for clothing protection is ultraviolet protection factor. The Skin Cancer Foundation provides a list of which laundry additives, clothing and cosmetics protect against the sun (8). Clothing that has a UPF rating between 15 and 24 is considered good, 25 to 39 is very good and 40 to 50 is excellent. The ratings assess tightness of weave, color (the darker the better), type of yarn, finishing, response to moisture, stretch and condition. The most important of these is the weave tightness (9).

Interestingly, The New York Times wrote about how major companies are producing sun-protective clothing lines that are fashionable and lighter in weight. The article is entitled “Fashionable options reshape sun-protective clothing” (10).

We have always known that sunscreen is valuable. But just how effective is it? In an Australian prospective (forward-looking) study, those who were instructed to use sun protective factor 16 sunscreen lotion on a daily basis had significantly fewer incidences of melanoma compared to the control group members, who used their own sunscreen and were allowed to apply it at their discretion (11). The number of melanomas in the treatment group was half that of the control group’s over a 10-year period. But even more significant was a 73 percent reduction in the risk of advanced-stage melanoma in the treatment group. Daily application of sunscreen was critical.

The recommendations after this study, and others like it, is that an SPF of 15 should be used daily by those who are consistently exposed to the sun and/or are at high risk for melanoma according to the American Academy of Dermatology (12). The amount used per application should be about one ounce. However, since people don’t use as much sunscreen as they should, the academy recommends an SPF of 30 or higher. Note that SPF 30 is not double the protection of SPF 15. The UVB protection of SPFs 15, 30 and 50 are 93 percent, 97 percent and 98 percent, respectively.

The problem is that SPF is a number that registers mostly the blocking of UVB, but not so much the blocking of UVA1 or UVA2 rays. However, 95 percent the sun’s rays that reach sea level are UVA. So what to do?

Sunscreens come in a variety of UV filters that are either organic filters (chemical sunscreens) or inorganic filters (physical sunscreens). The FDA now requires broad spectrum sunscreens pass a test showing they block both UVB and UVA radiation. Broad spectrum sunscreens must be least SPF 15 to decrease the risk of skin cancer and prevent premature skin aging caused by the sun. Anything over the level of SPF 50 should be referred to as 50+ (3).

The FDA also has done away with the term “waterproof.” Instead, sunscreens can be either water-resistant or very water-resistant if they provide 40 and 80 minutes of protection, respectively. This means you should reapply sunscreen if you are out in the sun for more than 80 minutes, even with the most protective sunscreen (3). Look for sunscreens that have zinc oxide, avobenzone or titanium oxide; these are the only ones that provide UVA1 protection in addition to UVA2 and UVB protection.

In conclusion, to reduce the risk of melanoma, proper clothing with tight weaving and/or sunscreen should be used. The best sunscreens are broad spectrum, as defined by the FDA, and should contain zinc oxide, avobenzone or titanium oxide to make sure the formulation not only blocks UVA2 but also UVA1 rays. It is best to reapply sunscreen every 40 to 80 minutes, depending on its rating. We can reduce the risk of melanoma occurrence significantly with these very simple steps.

References:

(1) Mayo Clin Proc. 2012; 87:328–334. (2) CA Cancer J Clin. 2014;64:9-29. (3) uptodate.com. (4) JAMA. 2004;292:2771-2776. (5) Br J Dermatol. 1994;130:48-50. (6) Langley R. G. et al. Clinical characteristics. In: Cutaneous Melanoma, Third Edition. St. Louis, Mo., Quality Medical Publishing Inc. 1998. p. 81. (7) J Clin Oncol. 2013;31:4385-4386. (8) skincancer.org. (9) Photodermatol Photoimmunol Photomed. 2007;23:264-274. (10) nytimes.com. 2013 July 17. (11) J Clin Oncol. 2011;29:257-263. 12 aad.org.

*If you would like to see a specific topic covered in Medical Compass, please email  info@medicalcompassmd.com.

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, go to the website medicalcompassmd.com and/or consult your personal physician.

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From left, Daniel Henshall as Caleb Brewster, Jamie Bell as Abraham Woodhull, Heather Lind as Anna Strong and Seth Numrich as Benjamin Tallmadge. Photo from AMC Networks

The history of the Culper Spy Ring is nothing new to Setauket and North Shore of Long Island residents. This Sunday, April 6, thanks to the new AMC show “Turn,” Setauket and some of its most legendary residents will become household names throughout the country.

Based on Alexander Rose’s 2006 book, “Washington’s Spies,” the show stars Jamie Bell as Abraham Woodhull, the Setauket farmer turned spy for Gen. George Washington’s Continental Army during the Revolutionary War. Enlisted in 1778 by Major Benjamin Tallmadge (Seth Numrich), Woodhull along with Caleb Brewster (Daniel Henshall) and Anna Strong (Heather Lind), among others, worked together to send messages — often in code — about the British troops to Washington.

In a telephone interview, show runner and executive producer, Craig Silverstein — responsible for The CW Television Network series, “Nikita” — said he had heard about the Culper ring before, but didn’t know exactly what they had done until fellow executive producer, Barry Josephson, introduced him to Rose’s book in 2008 while they were working together on Fox’s “Bones.” He thought it would make a great show. “They were very good at what they did,” Silverstein said of the spy ring.

Silverstein, who admitted to not being much of a history buff prior to working on the show, described the show as “a spy thriller,” with a great international cast. He said one of the most surprising things to learn about was how intimately connected the characters were to George Washington.

“There weren’t a ton of layers,” Silverstein said. “[That] brought him more down to earth.”

Interestingly enough, Bev Tyler, the historian for the Three Village Historical Society who runs the SPIES! exhibit at the society’s headquarters, agreed often times films and shows based on the American Revolution make Washington the opposite of what Silverstein described. “They can’t do it without deifying him, without making him larger than life,” Tyler said.

Silverstein said he found it interesting how few American Revolution-based films and television shows exist. He said much of what is out there is “very ‘Schoolhouse Rock!’” referring to children’s-type programming. “The real truth is much more complicated,” he added.

While maintaining historical accuracy was important, Silverstein said writers could take some creative license because a lot of what the spies did is still unknown.

However, in an effort to get the facts right, Rose is working as a consultant on the show. Silverstein said some the crew visited Setauket; Tyler, who said he would definitely be watching on Sunday, took one of the show’s writers on a society walking tour.

Silverstein said he thinks everyone, even those who aren’t history buffs, will enjoy the series as it is an exciting depiction of the American Revolution. “It’s only a world that you thought you knew,” he said.

“Turn” premiers with a special 90-minute episode on Sunday on AMC Networks, Optimum channel 43, at 9 pm.

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They know it works, but they’re not exactly sure how. They mix ingredients with something that helps make everything happen and, like a magician, wave their wand and get the rabbit, or in this case, the clean hydrogen, they were trying to produce. Except that, in their world, nature is the one whose slight of hand remains a mystery.

That’s where Argentinian-born Dario Stacchiola and his Brookhaven National Laboratory team of two postdoctoral researchers and one graduate student come in. An associate chemist, Stacchiola is trying to figure out the small steps in between the beginning of a reaction and the creation of this form of hydrogen, which is suitable for fuel cells in cars and industrial chemical processing.

While Stacchiola recognizes the possibility of a commercial use of his analysis down the road, he emphasizes that he is on a basic scientific mission. “Our end goal is not to get a commercial catalyst,” he said. “We are a step removed from that transition. We are really trying to look at the atomic level.”

Stacchiola’s curiosity about catalysts has earned him the admiration of his colleagues and coworkers. He is “well-respected not only across the lab, but also in our field,” said Ashleigh Baber, a postdoctoral researcher who has worked in his lab for three years.

His “knowledge of catalysis, coupled with his strength in experimental physical chemistry give him a unique perspective on how to approach and tackle important issues and holes in the field.”
Indeed, one of those many holes is understanding the intermediate reactions in the water-gas shift reaction, which is used to purify hydrogen and remove carbon monoxide.

“There are at least four different mechanisms proposed” for that reaction, Stacchiola said, with each one involving between five and 10 steps. His experiments helped to “narrow it down to two probable mechanisms.”

One of the big problems for scientists looking for these intermediate steps is that these reactions are easiest to see under cold, high-vacuum conditions, where the scientists don’t have to worry about interactions between the reactions they’re testing and atoms in the air. In those conditions, some of the intermediate chemicals generated during the reaction don’t form.

Using the latest technology, including near-ambient X-ray photoelectron spectroscopy, near-ambient pressure infrared reflection absorption spectroscopy, density functional theory computational analysis and scanning tunneling microscope, they were able to look behind the curtain in some of these steps at more everyday temperatures and pressures.

“We are now starting to see processes happen that we couldn’t see at lower pressures,” he said. He sees the stabilization of weak intermediates at the interface of oxide and metal nanoparticles in catalysts.

Scientists had predicted that the reactions Stacchiola studies would involve a carboxyl group, which is present in most organic acids and is made up of carbon, two oxygen atoms and hydrogen. These groups hadn’t been found on metal or oxide surfaces in this process. His research detected a product derived from the carboxyl group that was attached to the metal oxide interface of nanoparticles.

Scientists had predicted the likelihood of this carboxyl group for about a decade. The discovery of this combination of atoms was the closest thing to a “Eureka” moment he has had, Stacchiola said.

At conferences, Stacchiola has met with people who are trying to improve the efficiency of these reactions and who are looking to optimize the perimeter of oxide-metal interfaces.

Baber explained that “even small increases in catalytic efficiency extrapolate to huge savings in large-scale industrial processes.”
A resident of South Setauket, Stacchiola lives with his wife, Zulema Cabail, who does research and teaches microbiology at Stony Brook, and their 11-year-old daughter, Sofia, whose name, he said, is easy to reproduce in any language, which is helpful for a couple from Argentina who have lived in South America, Europe and North America.

As for his work, Stacchiola said he is driven by some of the same curiosities he had as a child, where he needed to understand how things worked. “I never felt very comfortable with black boxes,” he said.

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