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Health Costs, Health Policy, Patient Care, Research

Medicare payment reform shown to cut costs and improve patient care

Medicare payment reform shown to cut costs and improve patient care

PT got Margie practicing on crutches, including going up and down a step.A few years back, the Centers for Medicare and Medicaid Services (CMS) made a straightforward change: No longer would it pay for easily preventable conditions that develop in the hospital. A care-team fails to help ambulate a patient following a hip or knee surgery and the patient develops deep-vein thrombosis? Unfortunate for the patient and unfortunate for the hospita, which now has to absorb the cost of that care.

It seems obvious, yet slightly disturbing, that this approach would be successful. In my idealized worldview, all patients are treated the same, regardless of who’s picking up the tab.

But when you change the financial incentives, change happens. Stanford health economist Jay Bhattacharya, MD, PhD, and health economist Risha Gidwani,DrPH, who is affiliated with the VA and Stanford, found the prevalence of two preventable conditions – deep-vein thrombosis and pulmonary embolisms – for patients with a recent hip or knee surgery dropped after Medicare stopped paying. The study was published today in the Journal of General Internal Medicine.

From our press release on the work:

When CMS stopped paying for treating deep-vein thromboses and pulmonary embolisms, the incidence of those conditions after hip or knee replacement surgery dropped 35 percent in the Medicare population, Gidwani said. In the younger, non-Medicare population, the incidence of these two conditions increased, although they also decreased in the patients over age 65 who had private insurers. There are more than 1 million hip or knee replacements performed in the United States each year, and over 60 percent of them are paid for by Medicare.

“We have a win-win,” Gidwani told me. “We have patients who are avoiding adverse events while Medicare saves money.”

Previously: Beyond Berwick brouhaha: Medicare chief another step to health-care reform, Experts discuss high costs of health-care — and what it will take to change the system and Competition keeps health-care costs low, Stanford study finds
Photo by Dave & Margie Hill

Genetics, NIH, Research, Videos

DNA origami: How our genomes fold

DNA origami: How our genomes fold

Here’s an interesting factoid about our genomes: If you stretched out the DNA in a single cell, which is only a few millionths of an inch wide, it would span more than six feet. And another: DNA folding is a dynamic process that changes over time. Scientists have been trying to understand how DNA folds itself up so efficiently, and a recent post on the NIH Director’s Blog highlights new research illustrating how the human genome folds inside the cell’s nucleus, as well as how DNA folding affects gene regulation. The research team created this delightful video that demonstrates the principles involved using origami art.

Researchers have been working to determine how cells regulate gene expression for nearly as long as we’ve known about DNA. How, for example, do nerve cells know to turn off only nerve cell genes and turn off bone cell genes? DNA folding loops are part of the answer. This research team, which published their findings in a paper in Cell yesterday, found that the number of loops is much lower than expected. There are only 10,000 loops instead of the predicted millions, and they form on/off switches in DNA. As explained in the blog post:

[The] paper in Cell adds fascinating details to that map, and it confirms that DNA loops appear to play a crucial role in gene regulation. The researchers found that many stretches of DNA with the potential to fold into loops have genes located at one end and, at the other end, novel genetic switches. When a loop forms, placing a hidden switch in contact with a once-distant gene, the gene is turned on or off. In fact, the mapping work uncovered thousands of these “secret” switches within the genome—information that may provide valuable new clues for understanding cancer and many other complex, common diseases.

Previously: DNA architecture fascinates Stanford researcher – and dictates biological outcomes

Patient Care, Public Health, Research, Science

Finding cures for the most challenging diseases

640px-Drawing_Test_tubes_different_colorsThe recent Ebola outbreak and the subsequent race to find a vaccine and other treatment options has brought the topic of drug development back in the public spotlight. But despite the millions of dollars spent on these efforts and the technological advances in biomedical sciences in the last 20 years or so, the process is still time-consuming and prone to failure. A recent feature story from National Journal (which also appears on The Atlantic’s website today) describes the work of several scientists trying to find cures or treatments for some of the most challenging diseases, from infectious diseases, like AIDS and Ebola, to chronic diseases such as Alzheimer’s.

The first disease the article highlights is a rare disorder called progeria, which causes young children to age prematurely. Recent breakthroughs in treatment have come from a team led by Francis Collins, MD, PhD, who is more famous for leading the Human Genome Project and now serves as director for the National Institutes of Health. Collins worked briefly on progeria early in his career and the combination of Collins’s work and genomics made it possible for his team to crack the genetic secret of the rare disease: that it was caused by a single genetic mutation. That finding led to a treatment that extended the lives of patients with progeria by several years. But it also points to some of the overwhelming challenges of chasing down cures and treatments:

The doctors and scientists hunting for new cures and treatments work in a constant state of tension. They operate in a tremendously high-stakes environment, pouring years of their lives into research as the people who inspire them continue to suffer and even die. Drug hunters face failure after failure, almost never followed by success. Decades of work flame out. Promising ideas turn into dead ends. For every 10,000 compounds they explore, scientists wind up with just one drug approved by the Food and Drug Administration. Even when medical science moves as fast as it can—and today, it’s moving faster than ever before—it’s still an agonizingly slow process.

“As much as we say that failure is part of what we do—if you’re not failing, you’re probably not doing science that’s very interesting—it still hurts,” Collins says. “It is frustrating, because you want to come up with the answer. You want to save lives. That’s what we all get into this medical research area to try to achieve, and yet the challenges are immense. And we make progress, oftentimes, in very small baby steps, even though what we’re hoping for are big leaps.”

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Chronic Disease, Neuroscience, Parenting, Pediatrics, Research

High blood sugar linked to reduced brain growth in children with Type 1 diabetes

High blood sugar linked to reduced brain growth in children with Type 1 diabetes

Some areas of the brain grow more slowly in children with Type 1 diabetes than those without, according to findings published this week in Diabetes. Researchers also found that children with the highest and most variable blood sugar levels had the slowest brain growth.

Glucose, the main form of sugar in our blood, is the brain’s primary fuel, and in Type 1 diabetes, the body loses the ability to produce a key hormone needed to regulate blood sugar levels. Type 1 diabetes treatment for children has often focused on making sure their glucose levels don’t get too low, since very low glucose can quickly put someone into a coma. But it’s emerging that chronically-high sugar is also bad for the brain.

The better the glucose control, the more likely that a child’s brain development will be unimpeded.

The new study, conducted at Stanford and four other universities, tracked brain structure and cognitive function in 144 young children with Type 1 diabetes and a comparison group of 72 children without diabetes over 18 months. MRI scans showed that the brains of both groups of kids were growing, but gray- and white-matter growth was slower in several areas of the brain in the diabetic children.

“These studies provide strong evidence that the developing brain is a vulnerable target for diabetes complications,” the researchers wrote. The affected brain areas have a variety of roles, including visual-spatial processing; auditory, language and object processing; executive function; spatial and working memory; and integration of information from sensory systems.

I asked two of the paper’s Stanford authors for more thoughts about what they found.

“The magnitude of the group differences in brain growth over time was surprising,” said Allan Reiss, MD, the study’s senior author. “I actually thought these differences would be more subtle — they were not.”

Past studies have found cognitive and brain-structure changes associated with diabetes in older patients, but this research stands out because the kids included were so young — at the start of the study, their ages ranged from 4 to just under 10, with an average age of 7 — and because the study had a prospective design, following children forward in time. In addition to examining brain structure, the researchers also tested the kids’ cognitive function with standard tests of IQ, learning and memory, and mood and behavior, among others. They saw no significant differences in cognitive function between the two groups, a finding Reiss said did not surprise him.

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Biomed Bites, Research, Videos

Using organic chemistry to decipher embryogenesis

Using organic chemistry to decipher embryogenesis

Here’s this week’s Biomed Bites, a weekly feature that highlights some of Stanford’s most innovative research and introduces Scope readers to scientists in a variety of biomedical disciplines. 

For decades, scientists were stumped by a tricky puzzle: How does a fertilized egg cell, nearly uniform, developed into an organism, with specialized cells and a vertical and horizontal axis?

Many experiments demonstrated that several signaling pathways — including one known as the Hedgehog pathway — establish gradients of certain chemicals in a developing organism, allowing cells to differentiate.

Puzzles remain, however. Is it possible to intervene in development gone awry? And, a more recent discovery showed the Hedgehog pathway is active in some cancers. Can that be reversed?

Stanford biochemist James Chen, PhD, uses the magic of organic chemistry to examine developmental pathways. Here’s Chen in the video above:

(We’re) trying to understand the molecular mechanisms that underlie embryogenesis. We view this through the lens of organic chemistry, meaning that we use small molecules that we synthesize to try to understand the processes that control the patterning of different parts of your body…

Using these tools we can figure out what genes are doing at what time to control the formation of complex structures.

The discoveries made by Chen’s team can then be used to develop therapies for a variety of disorders.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: Zebrafish: A must-have for biomedical labs, Viva la hedgehog! Signaling protein also shown to be important in prostate growth and Another blow to the Hedgehog pathway? New hope for patients with drug-resistant cancers

Big data, Cancer, Cardiovascular Medicine, Fertility, Men's Health, Research, Stanford News

Male infertility can be warning of hypertension, Stanford study finds

Male infertility can be warning of hypertension, Stanford study finds

sperm graffitiA study of more than 9,000 men with fertility problems links poor semen quality to a higher chance of having hypertension and other health conditions. The findings suggest that more-comprehensive examinations of men undergoing treatment for infertility would be a smart idea.

About a quarter of the adults in the United States (and in the entire world) have hypertension, or high blood pressure. Although it’s the most important preventable risk factor for premature death worldwide, hypertension often goes undiagnosed.

In a study published today in Fertility and Sterility, Stanford urologist Mike Eisenberg, MD, PhD, and his colleagues analyzed the medical records of 9,387 men, mostly between 30 and 50 years old, who had provided semen samples in the course of being evaluated at Stanford to determine the cause of their infertility. The researchers found a substantial link between poor semen quality and specific diseases of the circulatory system, notably hypertension, vascular disease and heart disease.

“To the best of my knowledge, there’s never been a study showing this association before,” Eisenberg told me when I interviewed him for a press release about the findings. “There are a lot of men who have hypertension, so understanding that correlation is of huge interest to us.”

In the past few years, Eisenberg has used similar big data techniques to discover links between male infertility and cancer and heightened overall mortality, as well as between childlessness and death rates in married heterosexual men.

Eisenberg sums it all up and proposes a way forward in the release:

Infertility is a warning: Problems with reproduction may mean problems with overall health … That visit to a fertility clinic represents a big opportunity to improve their treatment for other conditions, which we now suspect could actually help resolve the infertility they came in for in the first place.

Previously: Poor semen quality linked to heightened mortality rate in men, Men with kids are at lower risk of dying from cardiovascular disease than their childless counterparts and Low sperm count can mean increased cancer risk
Photo by Grace Hebert

Aging, Cancer, Genetics, Research

Telomeres tell all about longevity and health

Telomeres tell all about longevity and health

10085714333_d8367dbe2a_oIf I were to go back to school for a PhD, I think I’d study telomeres. Telomeres, the protective caps at the end of each chromosome, shrink with aging and other stressors leaving an organism vulnerable to a various disorders and cancer.

So, telomere fan that I am, I was thrilled to sit in on a recent Psychiatry & Behavior Sciences Grand Rounds talk at Stanford featuring Elizabeth Blackburn, PhD. A professor of biology and physiology at the University of California, San Francisco,  Blackburn won the Nobel Prize in 2009 for her work on telomeres.

During the event, she gave the packed auditorium a whirlwind overview of telomere biology. Blackburn explained to attendees that telomere length is affected by both genes and the environment, and that some folks just start out with longer ones. Telomeres are maintained by an enzyme called telomerase. Slashing the amount of telomerase can cause early, immune dysfunction, cancer and diabetes. Some genetic telomere troubles manifest as disorders such as aplastic anemia or pulmonary fibrosis.

In general, telomere length correlates with what Blackburn called a “health span,” or duration of time someone stays healthy.

Recently she and colleagues measured telomere length in 100,000 people of all ages, a project they needed to develop a special robot to complete. They found that length of telomeres decreases into age 75. Then, it curves up to 95, accounting for the longevity of individuals with long telomeres. And yes, older women tend to have longer telomeres than older men.

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Health Costs, Health Policy, Patient Care, Research

Spotting stellar primary care practices, Stanford study identifies 10 practices that lead to excellence

Spotting stellar primary care practices, Stanford study identifies 10 practices that lead to excellence

crutches-538883_1280Many of us know first-hand that expensive, substandard health care abounds in America. The problem has been analyzed and bemoaned, measured and critiqued. Solutions, bright spots and success stories are less abundant—in fact they are downright rare. That’s why recent findings from a partnership between Stanford’s Clinical Excellence Research Center and the Peterson Center on Healthcare, a new organization that aims to improve health care in the United States, are so exciting. Bucking current theories, researchers found that independent, primary care medical practices can provide superior care while saving money. And, they identified 10 principles these practices embrace, which distinguish them from their peers.

I had the chance to speak with CERC Director Arnold Milstein, MD, about the Stanford-based project:

What exactly did you do?

We examined the performance of more than 15,000 primary care practices looking for “positive outliers” or practices that provide excellent care at a lower cost. This is the first  systematic comparison of its kind and we weren’t sure we’d be able to discern any differences. But we did. We found a substantial difference in measures of quality and the total annual amount of health care spending between sites. Then, we arranged for  observers (independent physicians) to visit these offices to understand what was different about care delivery at sites associated with less spending and high quality scores.  They discovered 10 distinguishing features of successful health-care practices that were present much more frequently in these positive outlier practices than in other offices. There are some major differences in how they deliver care.

What were some these features? Did any surprise you?

About two-thirds align with current national initiatives such as Choosing Wisely and the Patient Centered Medical Home, but about one-third are new ideas.

The 10 features are not abstract ideas, they are tangible and therefore more easily transferable. For example, the higher-performing sites are ‘always on’ — patients can reach the care team quickly 24/7. I use the word ‘care teams’ because I’m not referring to physicians only. These teams include nurses, nurse practitioners, medical assistants and/or office managers, developed  to the highest of their abilities. These teams often treat conditions in a gray zone between primary care and specialist care. They follow up with their patients when a case is referred to a specialist. They check in with patients to ensure they are able to follow self-care recommendations.  Their work station is shared, so they can learn from each other. These teams adhere to systems to deliver care — choosing individual tests and treatments carefully. Distribution of revenues among physicians is not  solely based on service volume. Finally, these practices invest much less in office rent and costly testing hardware.

 

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Immunology, Neuroscience, Research, Stanford News

Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice

Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice

brain in motionAttention, nerve cells: It’s not all about you.

As a new study in the Journal of Clinical Investigation led by Stanford neuroscientist Kati Andreasson, MD, shows, blocking the action of a single molecule situated on the surfaces of entirely different brain cells reversed memory loss and a bunch of other Alzheimer’s-like features in experimental mice.

The very term “neuroscience” strongly suggests that nerve cells, a.k.a. neurons, are the Big Enchilada in brain research – and, let’s face it, you wouldn’t want to leave home without them. But they’re far from the entire picture. In fact, neurons account for a mere 10 percent of all the cells in the brain. It may be that the mass die-off of nerve cells in the brains of people with Alzheimer’s disease may largely occur because, during the course of aging, another set of key players ensconced in that mysterious organ inside our skull and  known collectively as microglia begin to fall down on the job.

In  a release I wrote to explain the study’s findings in lay terms, I described microglia as the brain’s very own, dedicated immune cells:

A microglial cell serves as a front-line sentry, monitoring its surroundings for suspicious activities and materials by probing its local environment. If it spots trouble, it releases substances that recruit other microglia to the scene … Microglia are tough cops, protecting the brain against invading bacteria and viruses by gobbling them up. They are adept at calming things down, too, clamping down on inflammation if it gets out of hand. They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells – including clusters of a protein called A-beta, notorious for aggregating into gummy deposits called Alzheimer’s plaques, the disease’s hallmark anatomical feature. … A-beta, produced throughout the body, is as natural as it is ubiquitous. But when it clumps into soluble clusters consisting of a few molecules, it’s highly toxic to nerve cells. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing A-beta, as well as keeping a lid on inflammation,” Andreasson told me. If their job performance heads downhill – as seems to occur during the aging process – things get out of control. A-beta builds up in the brain, inducing toxic inflammation.

But by blocking the activity of a single molecule – a receptor protein on microglial cells’ surfaces  – Andreasson’s team got those microglia back on the job. They resumed chewing up A-beta, quashing runaway neuro-inflammation, squirting out neuron-nurturing chemicals. Bottom line: the Alzheimer’s-prone experimental animals’ IQs (as measured by mousey memory tests) rose dramatically.

Aspirin and similar drugs also tend to shut down the activity of this microglial receptor, which may or may not explain why their use seems to stave off the onset of Alzheimer’s in people who start using them regularly (typically for unrelated reasons) before this memory-stealing syndrome’s symptoms show up. But aspirin et al. do lots of other things, too – some good, some bad. The new findings suggest a compound carefully tailored to block this receptor and do nothing else might be a weapon in the anti-Alzheimer’s arsenal.

Previously: Another big step toward building a better aspirin tablet, Untangling the inflammation/Alzheimer’s connection and Study could lead to new class of stroke drugs
Photo by Henry Markham

Mental Health, Research, Technology

Reducing your stress level could be as simple as checking email less frequently

Reducing your stress level could be as simple as checking email less frequently

4329363938_26522735d1_zAs the end of 2014 approaches, many of us are thinking about what changes we’re going to make come Jan. 1 to be healthier and happier. Those looking for ways to reduce their stress level in 2015 may want to consider adopting a New Year’s resolution to limit how often they check their email throughout the day.

A study (subscription required) recently published in Computers in Human Behavior suggests that there are psychological benefits to easing up on the number of times you click your inbox. For the experiment, researchers at the University of British Columbia instructed half the participants to read emails no more than three times a day for a week, while a second group was allowed to check their inbox as often as they wished. The groups’ instructions were then reversed the following week. New York Magazine reports:

Overall, “limiting the number of times people checked their email per day lessened tension during a particularly important activity and lowered overall day-to-day stress,” the researchers write, and was associated with various other positive measures of psychological well-being. Those who checked their email a lot also didn’t perceive themselves as any more productive than those who were on an email diet.

…This study, combined with a lot of prior research into things like the distractions imposed by task-switching, paint a pretty clear picture: Ceaselessly checking your email probably isn’t making you more productive, and it probably is making you more stressed.

Previously: What email does to your brain
Photo by Ian Lamont

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