Category Archives: Seattle Science

How will health reform affect innovation and research? – CityClub event, Monday, Dec. 2nd


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Innovation & Research

2013 Health Care Series, “Health Care Reform in Puget Sound”

Research and innovation improve quality of healthcare, but also contribute to its expense.  Will the Affordable Care Act’s efforts to manage costs stifle innovation?  How can research organizations invest in developing new products that improve health and quality of life if these medications and devices are not adequately covered for consumers? How will patients be impacted? Join CityClub and a panel of experts as we learn how the Affordable Care Act will affect health care research in Puget Sound.

Panel Guests:

Dr. Jane Buckner,  Associate Director, Benaroya Research Institute
Dr. Scott Ramsey, Director, Hutchinson Institute for Cancer Outcomes Research, Fred Hutchinson Cancer Research Center
Jonathan Seib, Senior Vice President, Healthcare, Strategies 360


KING 5’s Jean Enersen  


Monday, December 2nd
Doors Open: 11:30 a.m.
Luncheon & Program: Noon – 1:30 p.m.


Washington Athletic Club | 1325 Sixth Avenue, Seattle, WA 98101

Luncheon Prices:

CityClub Members – $35 | Guests & Co-Promoters – $40 | General Public – $45
Coffee & Dessert Only Prices:
CityClub Members – $12 | Guests & Co-Promoters – $15 | General Public – $18


About the 2013 Health Care Series, “Health Care Reform in Puget Sound”

CityClub’s 2013 Health Care Series discusses preparing for the Affordable Care Act’s full implementation in 2014, narrowed to a local Puget Sound focus.  How is the Affordable Care Act affecting health care in Puget Sound? What are the emerging impacts of the law – now, in 2014, and beyond? What do “you” – individuals, providers, employers, insurers, etc. – need to do?  Individual forum topics cover 1) The consolidation and realignment of the health care system; 2) The impact on employers and small business; 3) How to navigate the care system; and 4) The impact of the Affordable Care Act on innovation and research.


Microbial molecules in our blood may influence how our cells function

David Galas

David Galas

By Klara Hanincova, Ph.D.

Scientists in Seattle have found small molecules from bacteria, fungi and other organisms in human blood that could be influencing how our bodies function.

It has been known for some time that our cells release small molecules, call microRNAs (miRNAs), that can then be taken up by other cells and influence their function by altering their protein production.

A team of researchers at Seattle’s Northwest Diabetes Research Institute led by David Galas Ph.D. was trying to better understand just how this miRNA-mediated communication between cells takes place.

As a first step, they set out to identify all the different types of miRNAs they could find circulating in human blood using a new sequencing technology.

To their surprise they found that many of the miRNAs they identified could not be matched to the human genome suggesting that they were not of a human origin.

The finding “was completely unexpected,” said Dr. Galas. “A large fraction of miRNAs that we could not map to the human genome originated from bacteria, fungi, plants and even other animal species.”

Much work remains to be done before the function of foreign miRNAs circulating in our blood is fully understood, but based on their laboratory experiments the team already has some indications.

The foreign miRNAs they found, just like those produced by our own cells, appear to be protected from degradation in the blood and are capable of influencing the behavior of human cells in culture.

“This strongly suggests that at least some of the exogenous miRNAs are functional in the human body,” said Dr. Galas.

A number of the identified foreign miRNAs seemed to come from the microorganisms that normally live in our guts, and are collectively known as the gut microbiome.

The researchers hypothesize that these microbes could be using their own miRNAs to communicate with our bodies.

“One way of thinking about this is that, if miRNAs are indeed involved in cell communication, bacteria could be using them to hack into our computer system and possibly alter its behavior” said Dr. Galas.

The delicately balanced gut microbiome is known to be important to human health and has been found to change during various diseases including obesity, diabetes and asthma.

Hence the team further speculates that the miRNAs from our gut microorganisms circulating in our blood could be a sign of disease or even be a cause of some disorders.

The discovery of miRNAs from other species in our blood opens the door to vast uncharted research territory. As for Dr. Galas and his team, the immediate next step would be to look for correlations between microbiome in the gut and miRNAs in the blood.

Their long-term objective is to understand how changes in the microbiome influence host physiology, and what role miRNAs play in this process. “It is going to be a few more years before we really figure out what is going on,” said Dr Galas.

Klara Hanincova, Ph.D. is a scientist specializing in vector-borne disease and a freelance writer based in Seattle, WA. 

IHME stats thumbnail

Americans living longer but less healthy lives, UW-led research finds

IHME stats

Change in leading cause of death in high-income North America 1990-2010

Americans are living longer lives, but we are living out these longer lives with chronic illnesses in large part due to our lifestyle choices, including eating unhealthy diets, failing to exercise, smoking, and using alcohol and drugs, according to research led by researchers at the University of Washington.

In the analysis, the researchers looked the causes of death and disability in 187 countries around the world. The study was led by the University of Washington’s Institute for Health Metrics and Evaluation (IHME) and funded by the Bill & Melinda Gates Foundation.

A live webcast will be held tomorrow, March 5 from 9 am to 10:30 am PST, in which Microsoft founder Bill Gates, UW President Michael Young, and and IHME Director Dr. Chris Murray help launch a new suite of online data visualization tools.

The webcast can be viewed at

Researchers from more than 303 institutions and 50 countries contributed to the project, called the Global Burden of Diseases, Injuries, and Risk Factors Study 2010.

US: a “mixed picture”

Analysis of the US health data revealed a “mixed picture” the researchers said: we are living longer but many of us are not enjoying a healthy old age.

The average life expectancy of American women, for example, increased from 78.6 years in 1990 to 80.5 years in 2010, yet only 69.5 of those 80.5 years were lived in good health.

The picture was the same for American men who in 2010 lived, on average, to be 75.9 years old – up from 71.7 in 1990 – but only 66.2 of those years are healthy.

Most of the illness and death in the US is caused by relatively few conditions. The top causes of death and disability were ischemic heart disease, followed by chronic obstructive pulmonary disease, low back pain, lung cancer, and major depressive disorders.

The analysis also found that the leading causes of death had changed over the past 20 years. Over those two decades,

  • ischemic heart disease, stroke, and lung cancer remained the top three causes of death;
  • chronic obstructive pulmonary disease, lower respiratory infection, and colorectal and breast cancers had moved down;
  • and diseases like diabetes, chronic kidney disease, and Alzheimer’s disease moved up.

US: Lagging behind

The study found that the US also lagged behind many wealthy and middle-income countries with Americans living shorter lives — and shorter healthy lives — than the residents of many other nations.

For example, men in 39 other countries – including Greece, Lebanon, and South Korea – live longer, and men in 30 other countries – such as Costa Rica, New Zealand, and Portugal – enjoy more years of good health.

American women fare about the same; in terms of life expectancy they are ranked 36th in the world, and in terms of healthy life expectancy they are ranked 35th, the analysis found.

We are doing so poorly because of our lifestyle choices:

  • The number one culprit: a diet that puts us at risk for such obesity-related illnesses such as heart disease and diabetes.
  • Number two: smoking, which leads to lung cancer, chronic obstructive pulmonary disorder, heart disease and stroke.

To learn more:


Seattle’s contribution to kidney-failure research reflected in one woman’s story


Nancy Spaeth at the Northwest Kidney Centers new museum explaining how this vintage dialysis machine worked when she used it in the 1960s / Photo Credit: Mali Main

By Mali Main

In 1959, Nancy Spaeth suddenly felt too tired to brush her own hair. The 12-year-old also noticed that her urine had turned a murky, mud color. Her doctor told her she had Bright’s disease, now called glomerulonephritis.

But no one told her that she had chronic kidney failure, that her kidneys were slowly deteriorating inside her, or that there was no known effective treatment.

“It was the custom in those days not to tell the patient what was going on,” recalls Spaeth, now a semi-retired nurse and teacher and grandmother of two.

It took seven years for her kidneys to completely shut down. “Kidney disease is insidious,” Spaeth says. By that time, Spaeth was a freshman at the University of Arizona. She lost her appetite, and the food she did eat would not stay down. She threw up her breakfast in the plants outside her early morning physics class. By the time the doctors sent her home to Seattle she weighed 88 pounds.

Fortunately, Spaeth returned home just when researchers in Seattle were making advances in kidney dialysis that would revolutionize the treatment of kidney failure. Many of those advances were made by researchers working at the Seattle Artificial Kidney Center, the world’s first artificial kidney clinic. The center, now known as the Northwest Kidney Centers, commemorates its 50th anniversary this year.

Spaeth would be among the first patients to be treated at the new center, and, today, she is one of the longest living chronic kidney failure patients in the world, says Christopher Blagg, former executive director of the Northwest Kidney Centers, a retired nephrologist who is writing a book on the history of the center. “She’s probably the only one who’s had every possible treatment during the course of their illness,” he adds.

Spaeth’s physician, Belding Scribner, wanted her on dialysis. Scribner had helped found the Seattle Artificial Kidney Center, but dialysis was an expensive, lifelong treatment and the Center could not accommodate more than a dozen or so patients at a time.

The Center set rigid medical guidelines for patient selection: well-adjusted adults between the ages of 18 and 45 whose kidney disease was uncomplicated by additional health problems.

But with more applicants to the Center than they could treat, anyone who wanted treatment also had to be approved by the anonymous seven-member Admissions and Policy Committee appointed by the King County Medical Society.

Spaeth, standing in the new dialysis museum at the Northwest Kidney Centers’ 700 Broadway, clinic points at a photograph on the wall. It’s a silhouette of a woman and six men sitting behind a long table, their faces obscured by shadow.

“We called them the Life & Death Committee,” Spaeth says. “They were supposed to be unbiased. But Dr. Scribner told me, years later, that he was sometimes able to get his two cents in.”

The Committee considered a variety of factors in making its life and death decision, including the applicant’s profession, whom they might leave behind and whether those left behind would be well-provided for or become a social burden.

Life Magazine and an NBC news documentary publicized their activities, inspiring the field of bioethics.

The committee sent a social worker to interview Spaeth’s family. Spaeth went through two days of psychological testing – during which she remembers they asked multiple variations of the question “Do you love your mother and father?” – before she was approved for dialysis treatment, which she began in 1966.

The Shunt

Spaeth pulls back her sleeve. Her arm is a tangle of scars from the wrist to the elbow. The divot on the inside of her left wrist is the 46-year old scar from the device that changed chronic kidney disease from a deadly illness to a treatable one: the Scribner shunt, an apparatus developed by her physician.

The scars on Nancy Spaeth’s forearm tell the evolution of dialysis technologies, how the techniques for coaxing blood from the arteries has changed over time / Photo Credit: Mali Main

The scars on Nancy Spaeth’s forearm tell the evolution of dialysis technologies, how the techniques for coaxing blood from the arteries has changed over time / Photo Credit: Mali Main

Blagg explains that before 1960 dialysis was only used to treat patients with acute, meaning temporary, kidney failure. Patients had to undergo surgery to be attached to the machine, a process that could only be done a few times. “If they had chronic kidney failure we would stop treatment there and the patient would go home and die,” Blagg says.

The shunt was a semi-permanent installation in the patient’s forearm made of three Teflon tubes.

One was inserted in an artery and the other into a vein, they were connected by a third u-shaped tube. During dialysis this u-shaped tube was removed so the arterial and venous tubes could connect to the artificial kidney.

“It didn’t hurt,” says Spaeth, “Not really. But it got infected a lot.” So she kept her shunt-embedded forearm wrapped in white gauze during the day while she studied for her BA in Education at Seattle University.

Then three nights a week she walked the three blocks to the Center, where the nurses unwrapped her shunt, unscrewed the u-shaped end piece, and connected her to the artificial kidney next to her bed.

While she slept, the device filtered excess salt and fluid from her blood and cleansed it of harmful wastes. In the morning, she would be disconnected and go back to school.

By 1968, Spaeth was able to have her dialysis done at home. She spent the summer of that year at the Coach House, an old motel near the campus where the University of Washington had set up a home-dialysis training program.

Nancy Spaeth on home dialysis, 1968 / Photo courtesy of Nancy Spaeth

Nancy Spaeth on home dialysis, 1968 / Photo courtesy of Nancy Spaeth

“I was always willing to try anything [the Center] was doing,” Spaeth says. “I learned how to run the machine, take it apart, clean it, and put it back together.”

Spaeth pulls back her sleeve further and slides her watch down to her palm. The scars tell the story of the changes in dialysis technology.

The different techniques for coaxing blood from her arteries is evident in the puffy overlapping grafts and the white sinusoidal scar near the soft bend in her elbow.


In 1972, Spaeth had a renal transplant, a gift from her younger brother, Charlie. “He came home from Stanford on his spring break, gave me a kidney and went back to school.”

Charlie’s kidney lasted seven years. Enough time for Spaeth to get married and have two children, a boy and a girl.

Then in 1979, she contracted an infection that caused her to lose the transplant. Her next three transplants were from strangers: a young woman who fell from the ladder of a fishing barge in Alaska, a motorcyclist who died in an accident in Bellevue, and in 2000, she received the kidney she still has today. “It was from a man who was in a car accident near Spokane,” she says.

Peritoneal Dialysis

Sometime between her third and fourth kidney transplant, Spaeth was able to try another kind of dialysis, called peritoneal dialysis, that freed her from the machine. Instead the dialysis fluid, the dialysate, runs into the abdominal cavity through a catheter implanted in her abdominal wall.

To begin the process, she only had to have a place to hang the bag of dialysate. Once connected to the catheter, the fluid from the bag would flow into her abdomen, where the water, salts and wastes would be exchanged through a thin sheet of cells, called the peritoneal lining. When it was time to drain the dialysate, she set the bag on the floor and the fluid would run out.

She lifts her shirt and points to the pinch of flesh on her lower abdomen where the catheter was installed when she switched to peritoneal dialysis. “I liked it,” she says. “It gave me a huge amount of freedom.”

“I could travel, I could do it on the airplanes,” says Spaeth. “I would just find a restaurant in the airport and they would warm [the bag of dialysate] in the microwave for me.”

“I could do it in my brother’s kitchen,” she says with a laugh. “Just hang the bag from a knob on the cabinet and sit there and have a glass of wine.

Drug trials

In the late 1980s, after Spaeth lost her second transplant, she volunteered to be part of a clinical trial of a drug that changed the lives of kidney disease patients.

She and an architect friend had just finished building her new three-story house next to a gully on Mercer Island. “I was extremely anemic,” she says. “I was crawling on my hands and knees up the stairs in that house,” she explains.

Healthy kidneys, in addition to filtering waste from the blood, also secrete the hormone erythropoietin, EPO for short.

The Northwest Kidney Centers' new Haviland Pavilion clinic at 700 Broadway houses a museum and gallery that showcase advances in kidney disease treatment.

The Northwest Kidney Centers’ new Haviland Pavilion clinic at 700 Broadway houses a museum and gallery that showcase Seattle’s contributions to kidney disease research.

“It regulates how many red blood cells we have, and therefore, how much hemoglobin we have,” says Stuart Shankland, who heads the Division of Nephrology at the University of Washington. Hemoglobin colors blood red and infuses the organs with oxygen. “So when a kidney fails, it stops making EPO and you get anemic.”

Without hemoglobin, Spaeth’s cells and tissues were essentially being starved of oxygen.

The pharmaceutical company Amgen chose the late Joseph Eschbach, a senior research advisor at the Northwest Kidney Centers, to run the first human trials of their synthetic EPO.

“Dr. Eschbach had worked on anemia in patients with kidney failure since 1963,” says Blagg. “He was Mr. EPO at that time.”

The Food and Drug Administration approved EPOGEN in 1989. “It was a miracle,” says Spaeth. “After a few weeks, I could run up those stairs.”


Today, Spaeth serves on the board of the Northwest Kidney Centers and travels around the country telling about her experience to the dialysis community. Lyle Smith, continuing education director at the Board of Nephrology Examiners Nursing and Technology, who has arranged for her to speak at professional conferences, says Spaeth is an inspiring speaker.

“In dialysis, we see so many patients who are devastated,” says Smith. “Nancy’s story gives staff hope that their patients can succeed.”

 Mali Main is studying Journalism and Quantitative Science at the University of Washington. She is the Newsletter Intern at the Division of Occupational Therapy in the UW Department of Rehabilitation Medicine and works as the Development Assistant at the St. James ESL Program. She has also covered art, astrophysics and healthcare reform.

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Globe floating in air

Chronic illness and disability becoming world’s leading health challenges – UW-led study finds


Globe 125X125By Michael McCarthy

We’re living longer, but many of us are living with chronic illnesses that significantly lower the quality of our lives, according to a new study led by researchers at the University of Washington.

The survey, called the Global Burden of Disease Study, finds that there has been a major change in the causes and impact of poor health over the past decades, with a shift away from early death to chronic illnesses and disability.

The survey found that since 1970 life expectancy has increased by 11.1 years for men and 12.1 years for women and that deaths among children under age 5 have plummeted, except in subSaharan Africa where childhood mortality remains high.

In general, improvement in life expectancy has been steady, but it slowed in the 1990s largely due to deaths from HIV infection in sub-Saharan Africa and alcohol-related deaths in in easter Europe and central Asia.

With our longer life expectancy, the major burden caused by disease is no longer early death but instead chronic illnesses that cause pain and disability, such as arthritis, diabetes and dementia, and psychological disorders, the study concludes.

Change in the leading cause of deaths from 1990 to 2010

Change in the leading cause of deaths from 1990 to 2010 – Click on image for interactive display.

The study was led by University of Washington’s Institute for Health Metrics and Evaluation and funded by the Bill & Melinda Gates Foundation.

“We’re finding that very few people are walking around with perfect health and that, as people age, they accumulate health conditions,” said Dr. Christopher Murray, director of IHME and one of the founders of the Global Burden of Disease.

“At an individual level, this means we should recalibrate what life will be like for us in our 70s and 80s. It also has profound implications for health systems as they set priorities,” Murray said.

Dr. Paul Ramsey, chief executive officer of UW Medicine and dean of the University of Washington School of Medicine, said the study will serve as “a management tool for ministers of health and leaders of health systems to prepare for the specific health challenges coming their way.”

“At a time when world economies are struggling, it is crucial for health systems and global health funders to know where best to allocate resources,” Dr. Ramsey said.

The study found that while heart disease and stroke remained the two greatest causes of death between 1990 and 2010, all the other rankings in the top 10 causes changed.

Diseases such as diabetes, lung cancer, and chronic obstructive pulmonary disease moved up the list, and diarrhea, lower respiratory infections, and tuberculosis moved down, the researchers report.

Explore the changes with this interactive chart.

And while malnutrition used to be a major cause of illness and death, today poor diet and physical inactivity are to blame for soaring rates of obesity, diabetes, heart disease and stroke the study found.

“We have gone from a world 20 years ago where people weren’t getting enough to eat to a world now where too much food and unhealthy food – even in developing countries – is making us sick,” said Dr. Majid Ezzati, Chair in Global Environmental Health at Imperial College London and one of the study’s lead authors.

The study appears in this week’s issue of the medical journal The Lancet.

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Foldit Thumb

UW Medicine donors try their hand at protein folding


UW Medicine’s donors gathered recently to be recognized for their contributions and to match wits on the University of Washington’s online game Foldit, a interactive protein-folding game developed by UW researchers that has drawn more than 200,000 Internet gamers.

The “Tomorrow. Today” event is held each year to honor members of the Turner Society, whose donations go to support research and scholarship at UW.

This year, attendees heard a talk on the promise and challenge of protein design by David Baker, Ph.D., the newly appointed director of the UW Medicine Institute of Protein Design.

After the talk, attendees played the Foldit game, competing to see which of them could use the program to design the best protein to block the “Swine Flu” influenza virus.


Screenshot of the Foldit game


Proteins are synthesized by our cells as long chains of amino acids, but they do not become biologically active until they fold into a precise shape.

How the chain folds is determined by a number of factors, including the sequence of the amino acids in the chain, the flexibility of the bonds between them, and the almost impossibly complex interactions between electrical charges on the amino acids and those of molecules in the surrounding fluid.

An amino acid chain folds into a functioning protein spontaneously

The result is highly convoluted structure in which the simple chain is twisted into spirals, bends, sheets and other complex structures.

The interactions that drive this process is so complex that it is beyond the calculating powers of even the most powerful super computers, but the human brain cam make intuitive leaps that computers can’t, Baker said.

So working with a team at the UW department of Computer Science and Engineering, led by Professor Zoran Popovic, director of the Center for Game Science, Baker’s team created a game that would allow individuals and groups to compete online bending and twisting computer models of proteins into their most efficient conformation.

“People are smart and groups of people working together are really, really smart and groups of people competing with each other are even more powerful,” Baker said.

UW student  and Foldit expert JSnyder explains how to play the game:

The gamers, many of whom have no background in biology, have proved to be adept at solving problems that often stump the experts.

In one case, Baker’s team designed a protein catalyst to accelerate chemical reactions, but it turned out to be very slow, Baker said.

“We couldn’t make it better so we sent it out as a challenge to Foldit players to improve it,” said Baker, and they came back with a design “that when we made it in the laboratory was much, much better that what we had made ourselves.”

Learning how proteins fold is crucial to understanding how they work and how they can be used to develop new drugs, Baker said.

Most current drugs are made of small molecules that interact with a protein to either block or promote the protein’s activity.

The problem with such small molecules is they may not “fit” their target site perfectly and often interact with other proteins causing unpleasant or even harmful side effects.

Another problem is that fewer and fewer small molecules are being found that can be turned into safe and effective drugs, Baker said.

Small proteins, however, can be designed to fit the target area so precisely that it is unlikely that they would affect other targets and cause side effects.

“Now we have the potential to take all the things we’ve learned about proteins from the human genome and all the other genomes we’ve learned about and come in and design new proteins for new therapeutics, new drugs, new diagnostics, new vaccines,” Baker said.

To learn more about Foldit:

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Group Health Icon

Group Health study finds “shared decision making” may reduce medical procedures


Osteoarthritis of the knee

By Ankita Rao

While policymakers debate whether doctors should be paid by the number of services they provide or the outcomes of their treatment, shared decision could have an impact on the ground by reducing demand for medical procedures.

A new Health Affairs report about decision aids, materials given to patients to help educate them about treatment options, shows that they can help hold down costs.

“The decision aids discuss all the available treatment options equally,” said Dr. David Arterburn, an author of the study released Tuesday and investigator at Group Health Cooperative, a non-profit health system in Seattle

For example, in the aids for joint disorders, he said, “Losing weight and increasing physical activity are discussed in detail, as are anti-inflammatory medications, other over the counter medications, and prescription medications for treating osteoarthritis.”

Decision aids can be used for a variety of medical issues, from cardiovascular health to hip replacements. They are delivered in the form of DVDs or printed guides, and are usually provided before a patient visits a specialist.

Researchers conducted randomized trials in Washington state with patients who suffered from knee and hip osteoarthritis, the most common joint disorders in the U.S. They sent aids to 332 patients with hip osteoarthritis and 978 to patients with knee osteoarthritis. The treatments and outcomes were then tracked and compared to a control group that did not receive the aids.

After six months, researchers found that among patients with knee problems who received aids, 38 percent fewer chose to have elective knee replacement surgery than the control group.

Among patients with hip problems, 26 percent fewer opted for hip replacement surgery.

Patients who received aids also had slightly fewer visits to primary care and specialty care doctors.

Overall treatment costs were lower among patients who received aids. For those with hip osteoarthritis, the average total cost of treatment was $13,489 after the use of decision aids, compared to $16,557 for the control group. In the knee osteoarthritis groups those with aids spent $8,041 compared to $10,040 in the control group.

Many states see promise in the shared decision model, and are taking early steps to encourage its use.  Minnesota, for example, outlines the need for a physician to discuss health care options in a shared decision making process in its rules for medical homes.

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John Wecker

Pacific Northwest Diabetes Research Institute appoints John Wecker president and CEO.


John Wecker

Pacific Northwest Diabetes Research Institute (PNDRI) announced today that John Wecker, PhD has been appointed president and CEO.

Dr. Wecker was most recently Global Program Leader, Vaccine Access and Delivery at PATH.

PNDRI is an independent non-profit biomedical and clinical research center that focuses on eliminating diabetes and its complications.

The Institute, which has a team of 85 physicians, scientists and technical staff, was founded in Seattle in 1956 by Dr. William Hutchinson, Sr., who also founded the Fred Hutchinson Cancer Research Center.

Before he joined PATH, Dr. Wecker worked for Boehringer Ingelheim, a global pharmaceutical company, where he led pharmaceutical product development teams and championed the company’s efforts to expand access to treatments for HIV/AIDS in the developing world.

During this time he established a program to provide medication for the prevention of mother-child transmission of HIV/AIDS, free of charge to over 120 countries around the world.

Dr. Wecker received his doctorate in Biological Psychology from the University of Rochester, Rochester, NY.

Dr. Wecker succeeds Dr. Jack Faris, who has been serving as acting CEO during the past eighteen months. Dr. Faris will remain part of the PNDRI team as a strategic advisor.

Dr. Wecker will begin at PNDRI on April 23rd.

To learn more:

  • For more information about PNDRI, visit or call (206) 726-1200.

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Dr. Larry Corey

Hutchinson Center President Larry Corey Elected American Academy of Art and Sciences Fellow


Dr. Larry Corey

Dr. Larry Corey, M.D., president and director of Fred Hutchinson Cancer Research Center, has been elected to membership in the American Academy of Arts and Sciences.

The Academy is one of the nation’s oldest and most prestigious honorary societies and independent policy-research centers.

The current membership includes more than 250 Nobel laureates and more than 60 Pulitzer Prize winners.

Dr. Corey has led the Hutchinson Center since January 2011 and has held other leadership positions there since 1996, first as head of infectious disease sciences in the Clinical Research Division and later as senior vice president and co-director of the Center’s Vaccine and Infectious Disease Division.

Dr. Corey is an expert in virology, immunology and vaccine development. His research has focused on herpes viruses, HIV and other viral infections, particularly those associated with cancer.

He also is principal investigator of the Hutchinson Center-based HIV Vaccine Trials Network, an international collaboration of scientists and institutions that combines clinical trials and laboratory-based studies to accelerate the development of HIV vaccines.

Dr. Corey is a professor of laboratory medicine and medicine, adjunct professor of pediatrics and microbiology, and holder of the Lawrence Corey Endowed Chair in Medical Virology at the University of Washington. He is also an infectious disease physician at Seattle Cancer Care Alliance.

Dr. Corey is the Hutchinson Center’s second president to be elected to the Academy. Yeast geneticist Lee Hartwell, Ph.D., a 2001 Nobel laureate, was elected in 1998. He led the Center from 1997 until 2010.

Corey is among 220 leaders in the sciences, social sciences, humanities, arts, business and public affairs who have been elected to the American Academy of Arts and Sciences 2012 class of fellows.

Since its founding in 1780, the Academy fellows have included: George Washington and Benjamin Franklin in the eighteenth century, Daniel Webster and Ralph Waldo Emerson in the nineteenth, and Albert Einstein and Winston Churchill in the twentieth.

The new class will be inducted at a ceremony Oct. 6 at the Academy’s headquarters in Cambridge, Mass.

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Paul Allen donates $300 million to Allen Institute for Brain Science


Billionaire philanthropist and Microsoft co-founder Paul Allen will donate an additional $300 million to the Allen Institute for Brain Science, raising his total contribution to the non-profit research center he founded to $500 million.

Purkinje cells (red, yellow, and green dots) in a region of the cerebellum.

Purkinje cells (red, yellow, and green dots) in a region of the cerebellum.

The new funds will support the first four years of a 10-year plan that will double the Institute’s staff to 350 and launch three new scientific initiatives.

These projects will seek to answer three key, related questions:

  • How does the brain store, encode and process information?
  • What are the cellular building blocks that underlie all brain function, and are often targets of disease?
  • How do those cells develop, and then create the circuits that drive behavior, thought and brain dysfunction?

The the stated goal of the Institute is to accelerate brain research by providing researchers with the most detailed information possible about the brain’s anatomy, genetics and biochemistry.

The Institute gathers this information by adapting highly automated “high-throughput” industrial production techniques to perform laboratory work that would take years, if not decades, for university researchers to complete using standard techniques.

The Institute then makes its data available on huge searchable, online databases for free at the Allen Brain Atlas data portal at

To guide these and other initiatives, the Institute had been recruiting new talent including.  Christof Koch, Ph.D. from Caltech, R. Clay Reid, M.D., Ph.D. from Harvard Medical School, and Ricardo Dolmetsch, Ph.D. from Stanford.

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Hutch researchers identify barrier that blocks pancreatic cancer drugs


Pancreas (head, body, and tail of the pancreas, and the pancreatic duct) and nearby organs and structures (duodenum, common bile duct, and small intestine). - Don Blis/NCI

From the NCI Cancer Bulletin

Researchers have discovered a physical mechanism that prevents chemotherapy from reaching pancreatic cancer cells, as well as a way to reverse that mechanism.

Dr. Sunil Hingorani of the Fred Hutchinson Cancer Research Center and his colleagues reported their results March 19 in Cancer Cell.

Pancreatic adenocarcinoma, the most common type of pancreatic cancer, is notoriously resistant to chemotherapy and radiation therapy, leading to an overall 5-year relative survival rate of less than 5 percent.

Using mice with tumors that are genetically similar to human pancreatic adenocarcinomas, the researchers found that, as the tumors grow, a thick matrix develops and surrounds the tumors’ cells.

The matrix exerts tremendous pressure on the tumors—pressure that greatly exceeds the normal pressure found within blood vessels—causing the tumors’ blood vessels to collapse.

This collapse prevents chemotherapy drugs in the blood stream from reaching the tumor cells.

Dr. Hingorani and his colleagues identified a substance called hyaluronic acid that forms a large part of this pressurized matrix.

When they treated the mice with an enzyme called PEGPH20, which breaks down hyaluronic acid, the pressure within the tumors returned to normal, and the blood vessels regained their normal shape and function.

When the researchers treated mice with a combination of PEGPH20 and the chemotherapy drug gemcitabine, 83 percent of tumors within the pancreas shrank after only one cycle of treatment, and all tumors shrank after three cycles.

Similar responses were seen in metastatic tumors. Mice that received the combination therapy survived almost twice as long as mice that received PEGPH20 plus a placebo.

“When able to penetrate the tumor bed, gemcitabine can indeed be an effective agent against this disease,” wrote the authors. An early phase clinical trial is testing the combination of PEGPH20 and gemcitabine in people with metastatic pancreatic cancer.

To learn more about pancreatic cancer read the NCI pamphlet What You Need to Know About Cancer of the Pancreas.

The NCI Cancer Bulletin is an award-winning biweekly online newsletter designed to provide useful, timely information about cancer research to the cancer community. The newsletter is published approximately 24 times per year by the National Cancer Institute (NCI), with day-to-day operational oversight conducted by federal and contract staff in the NCI Office of Communications and Education. The material is entirely in the public domain and can be repurposed or reproduced without permission. Citation of the source is appreciated.

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Seattle Children’s opens biobank for pregnancy research


Blood, placenta tissue and other specimens will be saved.

A Seattle Children’s project to reduce premature births and still births opens a new facility today to store tissue from pregnant women that researchers from around the world can use to study both normal and abnormal pregnancies.

The biorepository will be run by the medical center’s Global Alliance to Prevent Prematurity and Stillbrith (GAPPS).

Specimens stored at the facility will include maternal blood and urine, cervical vaginal swabs, placenta tissue, and cord blood.

Samples will are collected from the first trimester through the postpartum period.

The specimens will be linked with information about the mothers’ preconception history, course of her current pregnancy, environmental exposures, medical and reproductive history, mental health, nutritional intake, and behaviors.

Participation is voluntary, and the identity of participating mothers is kept confidential with the specimens being identified only by number.

“While pregnancy specimen biobanks have been developed before, this is the first time that specimens paired with information about mothers and their pregnancies have been made widely accessible,” said Dr. Craig Rubens, executive director of GAPPS.

The repository currently has more than 8,000 individual specimens available to scientists, with 800-900 specimens being added each month.

The collection includes contributions from women representing a wide range of racial, ethnic, regional, and socioeconomic backgrounds.

Among the goasl of the GAPPS Repository project are to:

  • Help researchers discover biomarkers and create screening tools to identify women and babies at risk for preterm birth and stillbirth
  • Use those findings to develop diagnostic tests, treatments, and prevention strategies
  • And to support research to identify the causes of poor birth outcomes and the fetal origin of adult diseases in the hope of developing cures.

“Many adult health problems can be traced to fetal development,” Dr. Rubens said. “With these specimens, researchers can begin to understand what causes adverse pregnancy outcomes, and develop novel interventions to prevent them.”

To learn more:

  • Go to the GAPPS Flickr page to see more photos of the repository.
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Brain changes linked autism start early in life — UW study


Changes in the brains of children at high-risk for developing autism who later go on to develop the condition can be detected as early as six months of age, long before any signs of autistic behavior appear, according to a new study by University of Washington researchers.

The changes, detected in white matter of the infants’  brains, were widespread and would likely have a profound effect on brain development, said Annette Estes, PhD, research associate professor of speech and hearing sciences at the UW and a co-author of the study.

The findings also suggest that autism does not develop suddenly but involves a long process that begins early in life, Estes said.

A tensor diffusion MR image showing the white matter tracts of the brain

A tensor diffusion image showing the white matter tracts of the brain

Individuals with autism typically have difficulty with social interaction, interpersonal communication and may engage in repetitive behaviors. Symptoms can range from mild to severely disabling.

The U.S. Centers for Disease Control and Prevention estimates that 1 in 110 U.S. children is affected by the disorder. The condition is usually detected in the second year of life after a seemingly normal infancy.

Although the cause of autism is unknown, recent research suggests that abnormalities in the brain’s white matter are involved.

White matter: the brain’s wiring

White matter is made up of bundles of millions of nerve fibers that create the “wiring” through which nerve cells communicate with each other. These nerve fibers are sheathed in a fatty insulating material, called myelin, that gives these areas of the brain a whitish appearance.

It is thought that abnormalities in white matter not only disrupt communication within the brain but also impair normal brain development, Estes said.

In the study, the UW researchers, working with collaborators from across the country, studied the brains 92 infants with a technique called diffusion tensor imaging that allowed them to track the development of the infants’ white matter,

The infants all came from families that already had one child with autism, which meant the infants were at high-risk of developing the condition as well.

Each infant had diffusion tensor imaging study at six months followed by a behavioral assessment at the age of two. Most also had follow-up scans at at one and two years of age.

The  researchers found that at the age of two, 28, or 30 percent, of the children had symptoms of autism while 64, or 70 percent, did not.

Comparing the brain imaging studies of the two groups revealed significant differences in the development of 12 of the brain’s 15 major white matter tracts.

That so many white matter tracks are involved suggests that at this stage autism is a “a whole-brain phenomenon not isolated to any particular brain region at this early stage of development,” said said Dr. Stephen R. Dager, M.D., UW professor of radiology and principal investigator of the University of Washington team.

The study’s findings are preliminary and diffusion tensor imaging is not ready to be used to diagnose autism in infants, Estes said, but the technique should help researchers better understand the cause of the condition and hopefully develop better interventions.

Autism and childrearing

In the past, it was commonly held that autism was the result of the failure on the part of parents to be sufficiently nurturing to their infants,  but the findings of this study suggest autism involves abnormal brain development that begins very early in life, Estes said.

Many parents wrongly blame themselves when their child develops autism, Estes said, but these findings indicate they “did nothing wrong” to cause the condition.

Future research will include looking at changes in the white matter development in infants younger than six months of age and tracking those changes as children age, Estes said.

The study, published online by the American Journal of Psychiatry, was the result of a collaboration with the Infant Brain Imaging Study (IBIS) Network funded by the National Institutes of Health and headquartered at the University of North Carolina at Chapel Hill.

Dr. Joseph Piven, professor of psychiatry at University of North Carolina at Chapel Hill and director of UNC’s Carolina Institute for Developmental Disabilities, was the senior author of the study.

Other institutions that took part in the study include the University of Utah, Washington University in St. Louis, McGill University, Children’s Hospital of Philadelphia and the University of Alberta.

To learn more:

  • UW Autism Center’s IBIS page.
Geyser rimmed with the growth of orange-colored extremophile organisms.

Strange organisms shed light on how living things evolve



Researchers at Seattle’s Institute for Systems Biology (ISB) have discovered how a group of organisms that thrive in places with conditions that would kill most living things —such as hot springs, geysers, and salt ponds — rapidly adapt to changing conditions.

The trick, the researchers report, is the organisms’ ability to alter the activity of a group of proteins that, in turn, rapidly reset many of the organisms’ functions simultaneously.

These proteins, called general transcription factors, have long been thought to operate primarily in the background, playing a quiet, supporting role in the process of gene expression.

But new findings suggest these factors play a more important regulatory function than previously though and a fundamental role in evolution, says Nitin Baliga, Ph.D., director of Integrative Biology at the institute, who led the research team.

The paper was published online by the journal Molecular Systems Biology.

The findings not only shed light on how living things evolve, they may also help increase our understanding of the role that the human counterparts of these factors play in human health and disease, says the paper’s lead author ISB research scientist Serdar Turkarslan.

Extremophiles can thrive in geysers and hot springs.

The focus of the Seattle team’s study was Halobacterium salinarum, a microscopic, single-celled organism that can thrive in super-salty environments like the the Great Salt Lake and the Dead Sea and even in salt evaporation ponds. These are the organisms that give such high-salt waters their sometimes pinkish tinge.

H salinarum belong to a group of organisms often called extremophiles (extreme + loving), because members of this group are found  living in extreme environments.

Indeed, these organisms can live in water ten-times saltier than the sea, in temperatures as high as 235 degrees F (113 C), and in highly acidic conditions with a pH as low as zero.They are also found in oxygen-poor environments such as deep-sea sediments — and the human gut.


Halobacterium salinarum are from a group of extremophiles called archaea.

Although the archaea were first discovered in the 1970s in extreme environments, they have been found in many environments, and it is estimated that they make up about 20 percent of the earth’s biomass.

The archaea were originally grouped with the bacteria, but now are considered to be their own unique group because they have a different evolutionary history and a unique biochemistry.

Like bacteria, they lack nuclei, but the way they process the genetic information encoded in their DNA more closely resembles the processes seen in eukaryotes, including humans. “They look like bacteria,” says Baliga, “but they are in many ways simplified eukaryotic cells”

This makes them interesting organisms to study, Baliga says: because they are simple, they are easy to grow and tinker with; but because their molecular machinery more closely resembles that of eukaryotes, studying them can provide better insights into the molecular biology of eukaryotic, including human, cells.

Transcription Factor B

The proteins in these cells Baliga and his team were interested are a group of proteins called general transcription factors, in particular transcription factor B, or TFB.

These factors affect the activity of hundreds, even thousands of other genes, so a change in their function can have a widespread effect throughout a cell.

What was particularly interesting to the ISB researchers was that the archaea had so many copies of TFB genes, up to eleven. “Researchers wondered if only one copy was necessary, what are the other copies doing?’ Baliga said.

In addition, not only were the curiously large number of TFB genes, there also seemed to be a clear pattern to their evolution: Archaea that live in high temperature environments, for example, appeared to develop one set or “lineage” of TFBs , while those that are able to live in low oxygen environments another, and those that live in saline environments yet another.

It appeared that in Archaea, at least, TFBs doing more than just playing a quiet, supporting role in the background. “It was an observation that was hard to ignore,” says Baliga.

ISB researchers Baliga and Turkarslan


By tracing the family tree of the archaea, researchers have worked out that the organisms had accumulated TFB genes through a process called duplication.

Duplication is a common way cells create new genes. Indeed, about 90 percent of the genes in our chromosomes arose through duplication.

In this process, an organism makes an extra copy of a gene. Now, with two copies of the gene, it is possible for one of the copies to mutate without harming the cell.

The cell survives because, as one copy mutates, the other copy continues to do the gene’s original job. With time and chance the mutating gene can evolve to a new form that gives the organism a new ability.

“For some period of time, the genes would have the same function,” says Baliga. “But one gene can mutate as long as there is a second copy that continues to do the gene’s original tasked function. And, voila, eventually you have two genes that came from the same original gene that now have two functions.”

If that new function allows the cell to adapt to a change in the environment, say it allows the cell to handle higher temperatures, the organism now has an advantage over cells that do not have the new gene and is more likely to survive in a hotter environment.

What is Systems Biology?

Systems biology is the study of an organism, viewed as an integrated and interacting network of genes, proteins and biochemical reactions which give rise to life. Instead of analyzing individual components or aspects of the organism, such as sugar metabolism or a cell nucleus, systems biologists focus on all the components and the interactions among them, all as part of one system.”

From the ISB Intro to Systems Biology more…

In the new study, Baliga and his colleague wanted to find out what role the different TFB genes might play in helping in H salinarum adapt to different environments.

So what they did was grow the cells in different conditions, varying the temperature, salinity and concentration of copper, a potentially toxic element in high enough concentrations.

Cells that grew better in one environment were deemed to be more “fit” for that environment than those that did not.

Then, using the systems biology approach, the team measured the activity of the different TFB genes in the different conditions and the effect they had on other genes and proteins throughout the cell.

They also tinkered with the cells, sometimes removing the genes for different TFBs, sometimes inserting genes, and repeating the experiments to see what effect the loss or addition of a particular TFB had on the cell’s “fitness”.

All in all they ran nearly 2,500 experiments, generating millions of data points on gene expression, protein activity and other factors, which they then analyzed using powerful computer algorithms.

What they found was that the different TFBs, either alone or in combination, did, indeed, allow the cells to better survive in radically different environments. In some environments, one TFB or a combination of TFBs, was crucial. In other environments, and another set of factors was important.

Expanded genetic “toolbox”

The findings suggest that by having several types of TFBs, the archaea have on hand in their genetic “toolbox” the means to quickly adjust to a variety of new conditions.

“The result is a simple, efficient way for these cells to rapidly acclimate to a changing environment,” says Baliga. “It gives them the flexibility to adapt.”

In nature, this means in a population of archaea living in a salt pond that suddenly begins to dry up and become more salty, some of the cells are more likely to have a mutated version of a TFB on hand that will allow the cells to adjust and survive in the new environment. Subsequent generations would then be able to evolve even more to be even better adapted to the new environment.

The findings not only shed light on a “fundamental mechanism of evolution”, says Baliga, it gives us insight into the biology of a the archaea, a class of organisms that makes up a substantial, if little understood part of life on earth.

Baliga says that one of the first practical uses of the research may be to engineer artificial TFBs that would make it possible for archaea to survive in highly toxic environments, such as that created by a toxic spill, where the organisms could break down the toxins and render them harmless.

The archaea could also be used as models in research into the roles TFBs play in a wide variety of human diseases, including heart disease, cancer, and a number of inherited conditions, Baliga said.

To learn more:

  • Visit the Institute for Systems Biology’s website.
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Hutch hosts lecture series for the public next month


Next month, Fred Hutchinson Cancer Research Center offers its annual “Science for Life” series in which the center’s top researchers will explain the latest science. The promise “a fun and informal atmosphere.”

The talks will be held 7 p.m. to 8:30 p.m. every Thursday of the month.

What’s Stress Got to Do with It? — February 2

Dr. Bonnie McGregor is a behavioral medicine pioneer interested in how psychological factors affect the health of our bodies and our minds. Hear how stress influences our vulnerability to disease, and how stress management techniques can help you reduce your own disease risk.

Stem-cell Therapy: The Hope, the Hype and the Real Potential — February 9

Join Drs. Beverly Torok-Storb, Tony Blau, Phil Horner and Chuck Murry in a discussion of stem-cell research. Learn about the different types of stem cells, common misunderstandings about stem-cell work, clinical therapies being explored and what these researchers envision for the future.

Cancer and Infectious Diseases: Making a Global Impact — February 16

Did you know that nearly a quarter of cancers around the world are infection caused or related? Meet Dr. Corey Casper, the force behind the Hutchinson Center’s research on infection-related cancers in Uganda. By focusing efforts in a country with a higher disease burden, we hope to understand how chronic infections lead to cancer, including why this happens in some of us and not in others.

Influenza: A Study in Evolution — February 23

Soon personal genomic sequences will be cheaper than personal computers. But genomic sequences don’t come with instruction manuals, so revealing what they tell us about evolution and disease remains a challenge. Dr. Jesse Bloom will take us on a journey along the evolutionary path followed by one influenza gene over the last 40 years, and reveal the obstacles and forces that shape genetic change as we attempt to understand evolution at the molecular level.


February 2-23
7-8:30 pm


Fred Hutchinson Cancer Research Center
1100 Fairview Ave. N., Seattle
Thomas Building
Pelton Auditorium

To Register go HERE.