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This Is What Happens When People With Diabetes Lose Medicaid – HuffPost

Posted: June 23, 2017 at 4:40 am

In 2003, Jose Sanchez was a recent graduate just starting out in the world, hustling to get his graphic design business off the ground. Then, one day, his life changed.

I went to take a nap and then I didnt wake up for two days, he said. When I woke up, I looked like the Matrix. I had all these tubes coming out of me.

Sanchez discovered he had Type 1 diabetes only after he had fallen into diabetic ketoacidosis, a life-threatening condition. His story is a reminder of what many diabetics went through in the years before the Affordable Care Act, and what many could face again if its rolled back.

Because he had very little income at the time, Sanchez was able to qualify for New York States Medicaid program. Between changing his diet and lifestyle and getting insulin and other health care through Medicaid, he managed to stay relatively healthy after the incident.

Eventually, he found stable employment and had a son. But then another disaster hit. In 2007, he learned that his jobworking nights at Abercrombie & Fitch, prepping the store for the morning crowdspaid just a little too much for him to continue to qualify for Medicaid.

Thats when I found out the true cost of being a diabetic, he said.

Without insurance, insulinrefillsalone cost him $225 every three weeks. Diapers, food and milk for his son came first, so he rationed the medication and ended up in the emergency room over and over again, racking up tens of thousands of dollars in medical bills he had no way to pay on his salary.

I would end up being in the hospital for a weeklong visit as they brought my levels back down, he said. This just became routine. Once or twice I had to have the ambulance come and get me at my house.

For a lot of people like Sanchez, the expansion of Medicaid in many states under the Affordable Care Act changed everything. The accessibility increased the chances that diabetics would be diagnosed early on before they have life-threatening emergencies. It also made it more likely that diabetics who were seeking treatment could successfully manage their disease, preventing hospital visits.

One 2009 study found that 46 percent of uninsured people with diabetes hadnt received a diagnosis, compared with 23.2 percent of insured diabetics.Medicaid expansion appears to have made a significant dent in the number of people who cant get treatment because they have never been diagnosed.

Looking at the 26 states, plus the District of Columbia, that expanded Medicaid in 2014, researchers found that new diabetes diagnoses rose 23 percent. In the other 24 states, they rose by less than half a percent.

LaShawn McIver, senior vice president of government affairs and advocacy with the American Diabetes Association (ADA), said thats really important because being aware of the condition can allow for earlier interventions to prevent complications.

That is a huge win for people with diabetes in those states, in comparison with people in states that did not expand, she said.

For people who know they have diabetes, of course, getting coverage, whether through Medicaid or other insurance, is critical to affording the treatment they need to keep their disease under control. Looking at known diabetics between 1999 and 2008, one study found people without insurance generally got less health care and had worse blood sugar levels, cholesterol, and blood pressure.

Beyond helping to pay for medication and doctors visits, state Medicaid agencies are now experimenting with new ways to help people with diabetes learn to stay as healthy as possible. For example, in 15 states Medicaid now pays for diabetes self-management classes under some circumstances. This kind of education has proved successful in helping patients keep their blood sugar down so they stay healthier.

Now, the ADA is pushing Medicaid agencies to expand this kind of approach by offering similar classes to people who are at risk of developing diabetes. Its a lifestyle intervention which gives people the skill they need to sort of take care of the behavioral changes, McIver said.

She said the program starts with classes taught by an instructor trained in a curriculum created by the Centers for Disease Control and Prevention. After that, participants meet regularly in peer groups.

Its kind of like a support group that provides these skills for lifestyle changes, she added.

Medicare will start covering this in 2018, and McIver said it only makes sense for Medicaid to do the same.

While it continues to try to make Medicaid coverage better, the ADA is now fighting to preserve coverage. Republican proposals moving through Congress now would phase out the ACAs expansion of Medicaid and also reduce funding for the core program. Under the plan passed by the House of Representatives, 14 million fewer people would receive Medicaid coverage by 2026, according to the Congressional Budget Office.The Senate version would cut Medicaid even more deeply over the long term.

At the same time, changes that reduced protections for people with preexisting conditions would quash diabetics access to private insurance on the individual market.

Diabetes is a disease that requires ongoing care, McIver said. What we worry about with any kind of repeal or replacement is that people wont have access to affordable care.

If they dont have that access, many people like Sanchez will almost certainly end up in the hospital suffering from complications that medication or other interventions could have headed off. That adds up to big costs that somehow need to be covered. A study last year found that when patients with diabetes who arrived at an emergency department were referred to a diabetes center for additional support, they were much less likely to be hospitalized over the next year. The cost of institutional care also fell by $5,461 per patient.

For Sanchez, the repeated hospitalizations only ended after he missed so much work that he lost his job and ended up eligible for Medicaid again. After that, he cycled in and out of coverage. Finally, in 2014, just as other patients were getting insured under the Medicaid expansion, he got a job with the City of New York that provided good coverage.

Sanchezs life today demonstrates both the importance of strong insurance policies and the challenges that remain. He now has his disease under control, thanks to insurance that covers his medication and care. Hes able to care for his growing family(his son now has a little sister) and himself.But, because the kinds of insurance he could get on the individual market arent as good as what he has, he feels tied to his job. That means he cant go back to pursuing a career in design full-time as he always wanted.

I would love for legislation to work toward making entrepreneurs just as safe as municipal employees, he said. You shouldnt have to choose between having a job with adequate health insurance and living your dream, living your purpose.

For now, Sanchez is just working to preserve the health care expansion thats happened over the past few years, telling his story on behalf of people who are where he was 15 years agounaware that health care coverage is going to end up mattering a lot to them.

Everybodys going to have a health concern at some point or another, he said.

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Superheroes on a T1D mission! Kids with Type 1 Diabetes conquer the disease’s challenges – Fredericksburg.com

Posted: June 23, 2017 at 4:40 am

A raucous relay ball game was underway in the fellowship hall of the Presbyterian Church in downtown Fredericksburg.

Shouts, beach balls and running kids filled the room. Captain America, Spiderman and Wonder Woman were leading the activities.

"Someone's low," one child yelled.

A counselor wearing a shirt bearing the Superman logo and the words "Power of insulin" crossed the room toward a little girl in a pink dress. The counselor checked the screen of a device the girl wore on a flowered belt around her hips.

The device was a continuous glucose monitor, a tool that tracks the child's blood sugar levels all day and night to give an overall picture of how they fluctuate.

It showed that the levels were slightly down but they weren't falling. She could keep playing.

Twenty-two children between the ages of 7 and 12 gathered this week for the 11th annual Kids for a Cure Club summer camp for kids with type 1 diabetes.

KFCC is a local nonprofit organization that was founded by the Mary Washington Healthcare diabetes management staff and parents of children with type 1 diabetes to provide education and support for families living with the disease.

The summer camp, which had a superhero theme this year, aims to help kids become more proficient in managing their diabetes while letting them have fun with peers who share their daily challenges. It is sponsored by MWH and the Aquia and Fredericksburg Lions Clubs.

"The purpose is for children with diabetes to be with others who have the disease," said Lana King, a registered nurse and the camp's founder. "In their school, they might be the only diabetic child. Here, they can feel like it's a normal thing. Here, they're acting differently if they're NOT having their blood checked."

Campers are under the care of four MWH registered nurses and diabetes educators and King, who used to work for MWH and now is clinical business manager for Animas Corporation, an insulin pump company.

All the camp counselors, who are 15 and 16, and the junior counselors, who are 13 and 14, also have type 1 diabetes.

Camp activities included craftsmaking superhero capes, badges and masks, decorating flower pots and picture framesgames and special activities such as cooking classes and trips to the Farmer's Market and the pool.

The kids heard from adult guest speakersa writer and a Secret Service agentwho have diabetes. They also prepared their own diabetes-friendly snacks each day.

Regular blood sugar checks were part of the day's activities.

"I think the hardest part of this disease is that there is no break," King said. "You must get up every day and check your blood sugar 6-8 times a day or give yourself injections. You're having to be responsible."

Hence, the superhero theme. For one of the daily activities, the kids had to answer the question, "Who is your superhero and why?"

One girl answered, "My superhero is me because I have learned how to manage my diabetes."

Other kids said their parents were their superheroes for helping them with their disease.

Matthew Gomez, 13, and his sister Gianna, 11, have attended the camp for multiple years.

"I like everything about it," Matthew said. "It's definitely up there [in my list of favorite summer camps.]"

Gianna, who was diagnosed at age 6 and has a twin sister who doesn't have diabetes, wears an insulin pump which delivers insulin to her body continuously. Matthew, who was diagnosed at age 9, gives himself insulin injections and pricks his finger to check his blood sugar four or five times a day.

He said it used to hurt, but his fingers are so tough now that it doesn't bother him.

Trinity Riley, 10, said she was diagnosed at age 3 after she went into a diabetic coma. She doesn't remember, but her sister has shown her pictures and video of herself in the hospital.

"I looked dead, not like myself," Riley said.

She said she's the only kid in her school with diabetes and usually tries to hide what she's doing when she pricks her finger to test her blood. But at camp, she doesn't have to do that.

"It's nice not being scared," she said. "When I'm here, I'm wide open, because everyone's the same."

Jayden Britt, 12, was just diagnosed with the disease in December. She said she's loved the summer camp because it helps her "not feel so different."

For two months leading up to her diagnosis, she felt "a little weird." Her mom noticed that she had lost a lot of weight and wasn't fitting into any of her clothes and took her to be checked out. Doctors ran a urine test and found ketonesacids that remain when the body burns its own fat instead of glucose for energy. It's a common complication of diabetes.

When the doctor started to tell Britt what the diagnosis was, she saw her mom begin to tear up.

"She knew what was coming," Britt said. "My dad has type 1 and my mom was blaming herself because she hadn't noticed the symptoms."

Katlyn Agosta, a nurse and MWH diabetes educator who is in her second year with the camp, said the camp helps kids as well as parents find support in handling the disease.

Mom Karen Embrey was wearing a shirt that said, "Some people never get to meet their hero. I gave birth to mine." Her daughter, Hannah, 15, has type 1 and is a counselor at the camp.

She said the hardest part about the disease from a mother's perspective is trusting anyone other than herself to manage it.

"Letting her be away from me is hard," she said.

Embrey said Hannah has been taking care of her own diabetes for a few years and generally does a good job.

"But this camp, being responsible for other kidsit's making her more mindful," she said.

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Devin Guillory – Jackson Free Press

Posted: June 22, 2017 at 11:46 am

As a child, Devin Guillory was not interested in science, which says that she now blames on societal attitudes toward science, technology, engineering and math, or STEM, fields. At the time, she was reluctant to pursue a career in any of those areas.

"I feel like, just as a society, we are kind of trained to think that high, in-depth things like chemistry and biology are things you are supposed to not really like growing up," Guillory, a master's student in chemistry at Jackson State University, says.

Guillory wants to use scientific research to better the state and help other Mississippians learn to love science. At JSU, she spurs children's interests in science through activities such as making slime from glue. "Just little things to get them interested, where they think that science is something fun instead of something we are automatically supposed to hate," she says.

The Jackson native attended Holmes Community College from summer 2010 to December 2010 and Hinds Community College from January 2012 until that summer when she transferred to Jackson State University.

Guillory says that when she entered college, her dream career was to become a video-game developer. However, a pre-requisite chemistry class led to the realization that she really loved that subject, as well. Guillory says that even before taking the class, she always enjoyed balancing chemistry equations, which she calls "a puzzle."

Guillory received her bachelor's degree in chemistry from JSU in 2015. Her career trajectory, which she calls "somewhat medical," now involves the research behind what the clinicians are doing. Her research focuses on increasing efficiency in cancer treatment by targeting cancer cells with heat therapy. Unlike cancer treatments such as chemotherapy, which can kill both cancerous and non-cancerous cells, nanoparticles in heat therapy only target the cancerous cells.

After she graduates from JSU with a master's degree this July, Guillory will begin studying neuroscience at the University of Arkansas Medical Science Center in Little Rock for her doctorate degree. She says her ultimate goal once she completes her Ph.D. is to help Mississippians by researching both the positive and negative effects that early childhood trauma have on people later in life.

Through her research, Guillory says that she hopes to create more understanding of mental illness in society, and how things such as drug addiction, alcoholism, abuse and neglect create problems.

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Lilly Completes $90M Expansion of San Diego Biotechnology Center – Genetic Engineering & Biotechnology News

Posted: June 22, 2017 at 11:45 am

Eli Lilly has added a new state-of-the-art laboratory and 180,000 square feet of additional working space to its Biotechnology Center in San Diego, CA. Reporting completion of the $90-million expansion, Lilly said the 145% increase in working space will help to foster collaborations with external partners, and allow closer partnerships between its biotechnology, discovery chemistry, and research technology teams. The aim is to accelerate drug discovery within therapeutic areas including immunology, diabetes, oncology, neurodegeneration, and pain.

To further exploit its expertise in automated organic synthesis, and build on its Automated Synthesis Laboratory in Indianapolis, Lilly is also establishing the Lilly Life Science Studio at the San Diego site. The firm says the new facility will give researchers worldwide the ability to remotely test new ideas, and design, synthesize, and screen molecules.

"Investing in drug discovery and development is critical to maintaining an ecosystem that encourages and promotes innovation, commented Jan Lundberg, Ph.D., executive vice president for science and technology and president of Lilly Research Laboratories. "Expanding our presence in San Diego will not only help us discover and deliver innovative medicines faster, but will also help us achieve our goal of launching 20 new medicines in 10 years."

"This year we announced a commitment to invest $850 million in our U.S. operations based on our potential for growth and the company's long-standing investment in the U.S. market, added David A. Ricks, Lilly's chairman, president, and CEO. "This investment doesn't come without risk. America's biopharmaceutical leadership is driven by a free-market economy that rewards innovation. Today, there are multiple public policy threats to our business that would discourage or reduce our investment in the U.S. and the state. We are committed to working with policymakers and stakeholders to ensure our efforts to deliver new innovative medicines to patients are not threatened."

Lilly set up the San Diego Biotechnology Center, which is sited close to the University of California, San Diego, in 2009, having acquired Applied Molecular Evolution back in 2004.

Earlier this month Lilly reported that it will acquire a pipeline of dual amylin calcitonin receptor agonists (DACRAs) from KeyBiosciencefor the potential treatment of type 2 diabetes and other metabolic disorders.

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Epigenetic drugs set to boost immunoncology – European Biotechnology

Posted: June 22, 2017 at 11:45 am

German oncologists have unveiled that market-approved inhibitors of DNA methyltransferases (DMNTi) and histone deacetylases (HDACi) act through expression of cancer neoantigens. They already have a biomarker test to identify responders.

The findings, reported in Nature Genetics, are good news for drug developers who want to broaden the scope of current immune checkpoint modulators through combination therapies that trigger cancer cells to release immunogenic neoantigens.

Following addition of epigenetic inhibitors to cancer cell cultures thousands of atypical transcripts with altered frameshift were expressed form previously ignored endogenous promotors of retroviral origin, resulting in profound tumour cell death, group leader Plass from German Cancer Centre told European Biotechnology. His team has already a biomarker assay that could identify responders to the treatment as it measures activation of the normally silent treatment induced, not-annotated transcription start sites (TINATs).

Up to now, pharma majors such as Roche/Genentech have largely relied on combination of their checkpoint inhibitors with personalised mRNA cancer vaccines. The new findings might open the avenue to a broader activation of cancer neoantigens than these vaccinesas over 2,500 TINATs have been identified in the human genome by the researchers. The retrotransposons (elements of human endogenous retroviruses, HERVs), which are located in long terminal repeats, have entered the human genome millions of years ago.

However, application of the findings might be hampered by the fact that TINATs, so far, have only been identified in the human genome, which might complicate preclinical in-vivo testing. Its unclear if they also exist in animals, says Plass, who is currently deciphering the exact mechanism that normally stops TINATs from being activated. First findings suggest that acetylation of transcription factors might play an important role.

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AMD: Novartis challenge Regeneron – European Biotechnology

Posted: June 22, 2017 at 11:45 am

Following shrinking sales for its wet AMD drug Lucentis, Novartis is back with convincing Phase III results of its anti-VEGF-A singe chain antibody fragment brolucizumab. In two pivotal studies the drug proved to be non-inferior to Regeneron/Bayers Eylea (aflibercept).

With 25 million patients affected worldwide, age-related macular degeneration (AMD) is a highly lucrative market. For years, Novartis first-in-class drug Lucentis (ranibizumab) was dominant in the large US market, but now Regenerons competing drug Eylea (aflibercept, 2026 sales: US$3.3bn, +24%) has overtaken Lucentis (2016: US$2bn, -11%) in US sales, mostly because it is not administered once monthly as Lucentis, but once every two months and has a lower price (US$1,850 per intravitreal injection).

However, results of two pivotal Phase III studies suggest Novartis could return to its former leadership with its next generation anti-VEGF-A-antibody fragment brolucizumab, which has to be administered only once quarterly. In both trials, the HAWK and the HARRIER study, brolucizumab met the primary endpoint of non-inferiority versus aflibercept in best corrected visual acuity after 48 weeks of treatment and the secondary endpoint of mean change in visual acuity. Whats more, the two drugs had comparable side-effect profiles. Novartis plans to submit a BLA next year. Analysts say the drug could reach the market in 2019 and achieve peak sales of US$2bn if also approved in diabetic retinopathy.

However, both aflibercept and Lucentis are challenged by off-label use of Avastin (bevacizumab) as the full-length originator of the single chain antibodies ranabizumab and brolucizumab and competitor to Regenerons VEGF-A/PDF fusion protein has been shown to be non-inferior at a 30-fold lower price.

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Eli Lilly and Company Opens Biotechnology Center in San Diego, California – Area Development Online

Posted: June 22, 2017 at 11:45 am

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According to company officials, the center features a new technologically-advanced laboratory and an additional 180,000 square feet of working space, which is an increase of 145 percent compared to the former facility.

In addition to the center's established presence in preclinical and clinical immunology research, the new space allows for closer partnership between Lilly experts in biotechnology, discovery chemistry and research technologies while also fostering external collaborations.

Lilly's new space will help foster and accelerate the discovery of medicines within the company's core therapeutic areas of immunology, diabetes, oncology and neurodegeneration, as well as the emerging area of pain, company officials explained.

"This year we announced a commitment to invest $850 million in our U.S. operations based on our potential for growth and the company's long-standing investment in the U.S. market," said David A. Ricks, Lilly's chairman, president and chief executive officer. "Today, as part of that commitment, we are pleased to say our research footprint in San Diego has been expanded."

"Investing in drug discovery and development is critical to maintaining an ecosystem that encourages and promotes innovation. Our expansion in San Diego is a prime example of investing in a research success story," said Jan Lundberg, Ph.D., Executive Vice President for Science and Technology & President of Lilly Research Laboratories. "Expanding our presence in San Diego will not only help us discover and deliver innovative medicines faster, but will also help us achieve our goal of launching 20 new medicines in 10 years."

"Congratulations to Lilly on the expansion of its new Biotechnology Center, which will double its drug research and development in San Diego, create high-quality jobs, and encourage collaboration on groundbreaking therapies that improve patient care and lower costs," said Representative Scott Peters. "San Diego's life sciences industry is changing the face of medicine and companies like Lilly are driving this innovation."

The company said it plans an extensive investment in its U.S. Research and Development. Nearly $250 million of Lilly's $850 million capital investments will be dedicated to supporting its research and development centers around the U.S., including the center in San Diego, in 2017. Lilly's other U.S. research centers are located in Indianapolis, Indiana; Cambridge, Massachusetts; New York, New York; and Philadelphia, Pennsylvania.

In 2017, Lilly plans to spend approximately $5 billion on global R&D, nearly $4 billion of which will be invested in U.S. based programs, including projects with many of California's leading biomedical research institutions.

"This investment doesn't come without risk. America's biopharmaceutical leadership is driven by a free-market economy that rewards innovation," said Ricks. "Today, there are multiple public policy threats to our business that would discourage or reduce our investment in the U.S. and the state. We are committed to working with policymakers and stakeholders to ensure our efforts to deliver new innovative medicines to patients are not threatened."

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Ask Dr. Kevin: Understanding Sickle Cell Disease – Lasentinel

Posted: June 22, 2017 at 11:44 am

Ask Dr. Kevin: Understanding Sickle Cell Disease

Dr. Kevin Williams

Ask Dr. Kevin is a new feature brought to you by Pfizer Rare Disease in collaboration with the National Newspaper Publishers Association (NNPA) to increase understanding of sickle cell disease.

Dr. Kevin is currently the Chief Medical Officer for Rare Disease at Pfizer. He pursued medicine after being inspired by his fathers work as a general practitioner in his hometown of Baton Rouge. Dr. Kevin is passionate about raising awareness and increasing understanding of sickle cell disease in the African-American community.

What is sickle cell disease?

Sickle cell disease (SCD) is an inherited genetic disease that affects hemoglobin, the oxygen-carrying protein within red blood cells (RBC). While normal RBCs are flexible and oval-shaped, individuals with SCD have sharp, crescent-shaped RBCs that have trouble passing through the bodys blood vessels, irritating the vessels lining. This irritation leads to the production of sticky proteins that cause RBCs to clump together, along with other cells in the blood, and creates blockages in blood flow. The reduced blood flow leads to severe pain and organ damage, like the heart, brain, eyes, liver, lungs, and spleen (causing the inability to fight certain infections).

How does someone get sickle cell disease?

SCD is passed from parent to child. Everyone has two hemoglobin genes, one from each parent, and both parents must carry and pass the sickle cell gene to their child. With each pregnancy, the child has a 25% chance of having SCD if both parents have the trait.

Is sickle cell disease contagious?

No. You can only inherit it if your parents carry the sickle cell gene and pass it to you. SCD is a serious, lifelong condition that a person has from birth. You do not lose or outgrow it over time.

Are African-Americans more likely to have sickle cell disease?

SCD is more common in certain ethnic groups, especially those of African descent. It is estimated that nearly one in 14 African-American individuals carries the sickle trait and SCD occurs in one out of every 500.

What is the most common symptom for people with sickle cell disease?

Pain is the most common and difficult symptom of SCD, as it can be sudden and so severe that people need to go to the emergency room (ER) or be admitted to the hospital. This type of pain is referred to as a sickle pain crisis or vaso-occlusive crisis (as it is due to blood vessel blockage). Pain can occur anywhere blood flows, but common sites are lower back, arms, chest, stomach, and legs. Certain triggers are known to cause a pain crisis, such as dehydration, extremely hot or cold temperatures, and stress.

How can patients with sickle cell disease prevent pain?

Although you may not prevent every pain episode, avoiding triggers may reduce the occurrence and/or severity of pain crises. Its important to:

Stay hydrated to prevent dehydration. Drinking water is best.

Exercise regularly, but dont overdo it.

Avoid very hot or cold temperatures.

Manage stress to your body and mind.

Get plenty of rest.

Its also important to go for regular health checkups and talk to your doctor about managing pain episodes.

Is it possible to die from sickle cell disease?

SCD can cause a lifetime of health issues and complications that may lead to early death. In developed countries, like the United States, people with SCD often live between 40 and 60 years of age. However, in developing countries, like some countries in Africa, 90% of babies born with SCD will die before age 5.

What is the impact of sickle cell disease on the African-American community?

Severe pain crises lead to frequent ER visits and hospitalizations, which stress the patient and family, as well as the health care system. Also, those living with SCD often face disease misperceptions. For example, people with SCD are frequently believed to be drug abusers, because they have a high tolerance for pain killers. Missed days at school and work interfere with productivity and may lead to the perception that people with SCD are lazy. Studies have also shown that school-age children have a lower IQ due to effects of SCD on their developing brains.

Are there support groups for sickle cell disease?

Yes. National support groups and advocacy organizations are a great way to connect with others living with the disease. There may also be local groups in your area.

What can someone with a friend or family member who has sickle cell disease do to help?

It is important to understand and support those individuals living with SCD. As a friend, be considerate and help direct their focus away from the pain. As a family member, encourage regular checkups and help them communicate their feelings and avoid triggers that lead to a pain crisis. A knowledgeable, compassionate community can help reduce the stigma related to SCD. Stand up for those living with SCD and, now that you know more about the disease, educate others!

Stay tuned for the next Ask Dr. Kevin article, which will appear in September. Meanwhile, here are resources to find more information about sickle cell disease or the collaboration between the NNPA and Pfizer Rare Disease.

About Dr. Kevin Williams

Dr. Kevin Williams is the Chief Medical Officer (CMO) for Pfizer Rare Disease. In this role, he leads a Medical Affairs organization of approximately 150 medical colleagues around the globe supporting Pfizers efforts and portfolio in Rare Disease. Dr. Kevin joined Pfizer in January 2004 as a Director, Regional Medical & Research Specialists working in the HIV disease area.

After moving into a Team Leader position in July 2005, he has served in various leadership roles during his career at Pfizer, most recently as the Global Medical Affairs Vice President for Rare Disease in Pfizers Global Innovative Pharma business unit where he supervised a group of global colleagues providing medical leadership and strategic support for inline and pipeline assets in Endocrinology, Hematology, TTR-Amyloidosis, Gauchers Disease, and other rare diseases. Dr. Kevin moved into his current Rare Disease CMO position in May 2016.

Dr. Kevin received his medical degree from the UCLA School of Medicine and is board certified in Internal Medicine. Following a 2-year fellowship in Health Services Research at UCLA and a brief academic career as an Instructor of Medicine at the UCLA School of Medicine, he spent 8 years in private practice caring for HIV-positive patients while maintaining an academic appointment at the UCLA School of Medicine as an Assistant Clinical Professor of Medicine. In addition to his medical degree, Dr. Kevin has a Masters in Public Health from the UCLA School of Public Health and a Juris Doctorate from Harvard Law School.

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Aging-related mutations in blood cells represent major new risk factor for cardiovascular disease – Medical Xpress

Posted: June 22, 2017 at 11:44 am

June 22, 2017 Credit : Susanna M. Hamilton, Broad Communications

Scientists at the Broad Institute of MIT and Harvard have found that a set of genetic mutations in blood cells that arises during aging may be a major new risk factor for cardiovascular disease. In contrast to inherited genetic predispositions and traditional lifestyle risk factors, such as smoking or an unhealthy diet, the new mutations are "somatic mutations" that originate in stem cells in the bone marrow as people age.

Because the mutations are relatively common in older people (over 10% of people over the age of 70 harbor at least one of these mutations), potential future efforts to screen for the mutations in blood cells, identify people at increased risk for coronary heart disease, and reduce risk in those individuals through lifestyle changes or therapeutic interventions could have a significant clinical impact, according to the researchers.

"There is more work to be done, but these results demonstrate that pre-malignant mutations in blood cells are a major cause of cardiovascular disease that in the future may be treatable either with standard therapies or new therapeutic strategies based on these findings," said Benjamin Ebert, a co-senior author of the new study, an institute member at the Broad, a professor of medicine at Harvard Medical School, and a hematologist at Brigham and Women's Hospital.

Featured in the New England Journal of Medicine, the work also contributes to the broader understanding of pathogenesis in coronary heart disease by supporting the hypothesis that inflammation, in addition to elevated cholesterol levels, plays an important role in this illness and potentially other diseases of aging.

"A key finding from this study is that somatic mutations are actually modulating risk for a common disease, something we haven't seen other than in cancer," said first author Siddhartha Jaiswal, a pathologist at Massachusetts General Hospital and researcher in the Ebert lab. "It opens up interesting questions about other diseases of aging in which acquired mutations, in addition to lifestyle and inherited factors, could modulate disease risk."

Previous research led by Ebert and Jaiswal revealed that some somatic mutations that are able to confer a selective advantage to blood stem cells become much more frequent with aging. They named this condition "clonal hematopoiesis of indeterminate potential," (CHIP), and found that it increases the risk of developing a blood cancer more than 10-fold and it appeared to increase mortality from heart attacks or stroke. In the new study, the researchers analyzed data from four case-control studies on more than 8,000 people and found that having one of the CHIP-related mutations nearly doubled the risk for coronary heart disease, with the mutations conferring an even greater risk in people who have previously had a heart attack before age 50.

While the human genetics data showed a strong association between CHIP and coronary heart disease, the team hoped to uncover the underlying biology. Using a mouse model prone to developing atherosclerosis, the scientists showed that loss of one of the CHIP-mutated genes, Tet2, in bone marrow cells leads to larger atherosclerotic plaques in blood vessels, evidence that this mutation can accelerate atherosclerosis in mice.

Atherosclerosis is believed to be a disease of chronic inflammation that can arise in response to excess cholesterol in the vessel wall. To examine this on a cellular level the team turned to the macrophage, an immune cell found in atherosclerotic plaques that can develop from CHIP stem cells and carry the same mutations. Because Tet2 and other CHIP-related mutations are known to be so-called "epigenetic regulators" that can alter the activity of other genes, the team examined gene expression levels in the Tet2-mutated macrophages from mice. They found that the mutated cells appear to be "hyper-inflammatory" with increased expression of inflammatory molecules that contribute to atherosclerosis. In support of this finding, humans with TET2 mutations also had higher levels of one of these molecules, IL-8, in their blood.

The work demonstrates that CHIP associates with coronary heart disease in humans, that mutation of the CHIP-related gene Tet2 causes atherosclerosis in mice, and that an inflammatory mechanism likely underlies the process. More work is needed to show whether other genes that are mutated in CHIP also lead to increased inflammation. The team is also exploring whether interventions such as cholesterol lowering therapy or anti-inflammatory drugs might have benefit in people with CHIP.

Inflammation is also thought to modulate several other diseases of aging besides cardiovascular disease, such as autoimmune disorders and neurodegenerative disease. Because CHIP also increases in frequency with age, somatic mutations that alter inflammatory processes could influence several diseases of aging, though more work is needed to test this possibility.

"By combining genetic analysis on large cohorts with disease model and gene expression studies, we've been able to confirm the earlier hints of CHIP's surprising role in cardiovascular disease," said co-senior author Sekar Kathiresan, director of the Broad's Cardiovascular Disease Initiative, associate professor of medicine at Harvard Medical School, and director of the Center for Genomic Medicine at Massachusetts General Hospital. "Beyond the mutations that you inherit from your parents, this work reveals a new genetic mechanism for atherosclerosismutations in blood stem cells that arise with aging."

Explore further: A role for mutated blood cells in heart disease?

More information: Siddhartha Jaiswal et al. Clonal Hematopoiesis and Risk of Atherosclerotic Cardiovascular Disease, New England Journal of Medicine (2017). DOI: 10.1056/NEJMoa1701719

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Aging-related mutations in blood cells represent major new risk factor for cardiovascular disease - Medical Xpress

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Light-scattering tool peers into pancreas to find cancer – Phys.Org

Posted: June 22, 2017 at 11:44 am

June 22, 2017 by Sarah Bates NSF-funded researchers have developed a technique that is based on the physical principles of light scattering to non-invasively determine the properties of subcellular structures (such as cell nuclei) in organs, providing physicians with more diagnostic information. Credit: Lev T. Perelman, Beth Israel Deaconess Medical Center and Harvard University

Pancreatic cancer is difficult to detect early because the pancreas is deep inside the abdomen, making potentially cancerous cells hard to reach and identify without surgery.

Researchers funded by the National Science Foundation (NSF) developed a new light-based technique that can identify precancerous and cancerous cystssmall, fluid-filled cavities in the bodyby piggybacking on a standard diagnostic procedure.

"This approach can be called a virtual biopsy, as it does not collect any tissue," said Lev Perelman, professor at Harvard University and director of the Center for Advanced Biomedical Imaging and Photonics at Beth Israel Deaconess Medical Center, whose team developed the tool with the support of the NSF Directorate for Engineering Biophotonics program.

One-fifth of pancreatic cancers come from cysts. While magnetic resonance imaging and other non-invasive imaging techniques in use today can scan for cysts, they have limited accuracy in determining which cysts are malignant and which are benign.

The best available diagnostic approach involves inserting a thin tube called an endoscopic ultrasound through a person's mouth into the stomach and the first part of the small intestine. There, a small needle is inserted through stomach wall or intestine into the pancreas, where it can puncture a cyst. Medical personnel then collect and analyze cyst tissue. But lab results take time and are often inconclusive.

Perelman, who explores the ways in which light interacts with biological tissue, thought that a technique based on the physical principles of light scattering would be able to non-invasively determine the properties of subcellular structures (such as cell nuclei) in organs, providing physicians with diagnostic information.

Imagine a cell or a cellular nucleus, a small ball with a diameter of a fraction of the width of a hair, Perelman explains. If you shine white light on that ball, only part of that light will be reflected back at you and it will come back changed. Certain wavelengths will also be absorbed depending on the ball's composition. The vast majority of cells in the human body only reflect visible light, though some, such as red blood cells, also absorb it.

His team applied light-scattering spectroscopy to several organs before discovering its potential to help overcome the unique challenges posed by the pancreas.

"Pancreatic cysts are a major clinical problem for gastroenterologists," said Douglas Pleskow, clinical chief in the division of gastroenterology at Beth Israel Deaconess Medical Center and associate professor of medicine at Harvard Medical School, who collaborates with Perelman. "We need better tools, and that's where the spectroscopy comes into play. The question is: Can this be used as a reliable tool to tell us whether a cyst is cancerous or not?"

Applying the basic premise about light scattering, the researchers inserted a tiny fiber optic probe connected to a broadband light source into the needle used to collect fluid samples in pancreatic cysts. They gathered the photons reflected from a cyst's surface and then used an algorithm to process the data, providing an immediate result.

"The goal is to make this a real-time diagnosis, and eventually avoid having to puncture the cyst at all," Pleskow said, emphasizing that the tool is still in the research stage. "We anticipate this could replace everything, but medicine takes a long time to change."

In a study published in the journal Nature Biomedical Engineering, the team reported they accurately identified 95 percent of cysts in 25 patients.

"What makes NSF grants so valuable," Perelman said, "is that they provide seed money to figure out basic principles about how stuff works before applying for larger funding needed to advance technology toward making it clinically available. The NSF Biophotonics program, directed by Leon Esterowitz, played an especially critical role in its long-term support for the light-scattering spectroscopy research."

Explore further: Light scattering spectroscopy helps doctors identify early pancreatic cancer

More information: Lei Zhang et al. Light scattering spectroscopy identifies the malignant potential of pancreatic cysts during endoscopy, Nature Biomedical Engineering (2017). DOI: 10.1038/s41551-017-0040

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Light-scattering tool peers into pancreas to find cancer - Phys.Org

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