So when five years ago the world learned that bees in America and Canada were dying in large numbers, and hives were becoming defunct, the agricultural community and the beekeepers and just plain people became alarmed. Hives were deserted, the bees gone, presumably dead, honey production stopped, and the bee industry crippled.

The problem was called Colony Collapse Disorder, and it threatened California’s very profitable almond industry, which is dependent on bees to pollinate the trees and keep the nuts growing. And not just almonds: 130 crops in California alone depend on honey bees. Beekeepers from around the nation load their hives on trucks and bring them to California and rent them out to growers. As the disease, or whatever it is, spread, the price of renting ever-more-scarce bees went up.

Honey bee hive at UC Davis

Once the news media started reporting heavily on the plight of the bees and the beekeepers, interest soared. Researchers at universities around the country started looking into the problem; money was donated to figure out what was killing the bees. Stories appeared frequently about the scientific efforts to figure out what was causing Colony Collapse Disorder (CCD) and what would cure it. With all that attention you’d think they would have solved the problem.

But what the scientists have discovered is that they really don’t know very much about bees. They don’t have a baseline of what goes on on the microscopic level in the hives. What viruses already exist in healthy colonies? You’ve got know that before you can start to understand if a virus is normal or abnormal and may be killing bees. Scientists like Joe DeRisi at the University of California San Francisco say they’ve made great strides, even though they haven’t found a culprit.

DeRisi: “I think there’s been tremendous progress. One of the frustrating things with CCD is it doesn’t look like there’s any one single agent or culprit that you can point the finger to that’s causing all of these problems. It looks to be a confluence of things that is several different pathogens or situations or environmental conditions that are coming together to cause losses that are more than would be expected. And that’s what’s frustrating people. What has occurred because of the interest in honeybees and because of the large losses caused by CCD is people like myself and other researchers around the country applying new techniques and tools to honeybees which they normally would not have done so, and so we’ve learned an incredible amount about the ecosystem in the bee and around the bee. And what we now know is that there’s a whole host of pathogens no one knew anything about and that certain combinations of these appear to be associated with higher losses than would otherwise be expected during the season. “

DeRisi’s lab discovered four new viruses that exist in healthy hives they never knew existed before. But that didn’t solve the problem at hand.

The disease remains a serious threat, with about a third of all bee colonies affected, and no cure in sight. But many among the other two-thirds of the beekeeping community think they have it under control, because their hives are doing well. They claim they take better care of their bees, feed them better, and use various medicines and techniques to keep the hives healthy.

One technique some beekeepers swear by is splitting the hives every year or even more frequently. That means taking half the bees out, getting a new queen (you can buy queens!), and making two hives out of one. Eric Mussen, a university extension bee specialist at the University of California at Davis, thinks splitting works – up to a point:

Mussen: “When you make these splits, you more or less take the pathogen load, all the problems, you kind of split it in half and then you’ve got these little colonies that have to build up really quickly and when that happens frequently they can outrun some of the parasites. They can outrun some of the disease problems for awhile, so those colonies get up and they make it and they’re, they’re good for a season. Okay, had you not split it, it seems like in many cases the microbes and the parasites become overwhelming and the colony dies, so my terminology is starting from packages, making splits, if you could keep your colonies forever young it looks like that’s a, a way that helps deal with the problem. Nothing’s perfect.

Q: Why hasn’t that completely eradicated this problem then? Why isn’t everybody splitting?

Mussen: Well, a number of people are splitting, either by default or some by design. They’ve, they’re now understanding what the problem is and, and how this helps. But the problem is that I think some of the equipment has or whatever the CCD problem is, is kind of innate in the equipment and so it really doesn’t matter what bees you put in and how you deal with them, it’s always right there, right on the edge ready to create a real problem. So you do the best that you can to try to just stay a little bit ahead of that.”

The research goes on – and so does pollination. The almond industry is surviving, and in fact, thriving. Last year was the largest crop ever. The crisis mentality seems to have passed, but the problem remains. While beekeepers are used to cycles where their bees die off, and then come back, Colony Collapse Disorder seems to be more persistent than previous die-offs, and shows little sign of abatement. While it hasn’t been decoded nor cured, it has focused attention on a unique part of agriculture that seems to need the attention. And that’s not honey-coating the progress that has been made.

Carl Schuler is one of 10,000 vets to have donated blood samples to the Million Veteran Program.

Every year, on Veterans Day, we hear stories about bravery on the battlefield, or the challenges returning veterans face.

This story is about a different type of military service: It’s a project where veterans help scientists learn more about conditions like cancer and post-traumatic stress disorder.

It's what brought Carl Schuler to the VA Medical Center in Palo Alto one sunny October morning.

Schuler served in the military for ten years, completing two tours in Iraq. The second tour was in Fallujah, where he oversaw a batallion of 18 soldiers.

What haunts him about his time in Iraq is the fact that he came home largely unscathed. That was not the case for his best friend, who was badly injured by an IED.

"You start thinking, well, how fair is that?" says Schuler. "Here's my friend, 88 percent burned, two people in his battalion killed. And here I am in a similar situation and we're all OK. It's a tough thing to deal with."

Back in the States, Schuler struggled with problems that will sound familiar to a lot of returning vets. He's had to tame his road rage. And sometimes, he can be a bit withdrawn.

What's gotten him through this is helping other returning soldiers. He is now a fellow for a group called The Mission Continues. His placement is with a group called USA Together, counseling Bay Area vets who are having financial problems.

It’s that same impulse — to help vets – that brought him down to the VA Medical Center in Palo Alto on a recent morning.

Schuler came to take part in something called the Million Veterans Program, or MVP. It is a project to build the largest database of medical information in the world, with both medical histories and blood samples from one million US vets. The Medical Center in Palo Alto is one of 33 VA hospitals across the country taking part, with the ultimate goal of making participation available to all veterans enrolled in the VA healthcare system. The recruitment will last between five and seven years. In 2012 alone, the program is projected to cost $19.8 million.

What makes this program possible is something that puts the VA well ahead of the curve, when it comes to health care: electronic medical records.

At a time when virtually every other sector of the economy has gone online, medicine has lagged behind. Most American doctors still carry paper files when they go into see a patient. Less than a third of hospitals have digitized records.

But VA abounds in electronic data, says the VA’s Dr. Jennifer Hoblyn. She says in addition to clinical records of its 8.6 million patients, the VA also has annual assessments that it uses to track patients, including evaluations of depression, PTSD, alcoholic substances, traumatic brain injury, and other conditions. All of the information is digitized and available to VA doctors.

"It's an amazing medical record," says Hoblyn, "and it stretches back 25 years."

Now, the VA wants to pair that information — detached from individual names — with anonymous blood samples from a million vets. It would be the biggest medical database in the world.

That's an exciting prospect for people like Robert Hiatt, who chairs the Department of Epidemiology and Biostatisticsis at UCSF.

Hiatt says when he started out in his field, researchers would send staff with clipboards from doctor’s office to doctor’s office, pulling folders from shelves and manually tallying up the data.

Electronic databases have made this type of research vastly faster and more powerful. A massive database like what the VA is building would allow Hiatt to compare thousands of anonymous medical records with just a few keystrokes.

It would help him and other researchers look for genetic explanations to the mystery of why some people get sick with diseases like lung cancer, and others don't.

"We know smoking leads to lung cancer, but not everyone who smokes gets lung cancer," says Hiatt. "And some people who get lung cancer don't smoke. Is that because of some genetic predisposition? Or some large genetic protective effect?"

Those types of questions are common in epidemiology, as well as in drug development, where researchers try and understand why some drugs work for some people, but not others.

At the VA, one major focus of research is on PTSD, which is relatively common, but hard to predict. Some soldiers suffer terribly. Others don't. To understand why, you need to look for patterns, across large numbers of vets.

Joel Kupersmith, the VA's Chief Research and Development Officer, says the MVP will allow VA researchers to compare the genes of people who have PTSD with others who don't. They’ll also take environmental factors into consideration: Where a vet lives, what other conditions he or she has, what he or she might have been exposed to in the service.

"It gets to be very complicated," says Kupersmith, "and you need large numbers to sort it out."

It's a bit like an impressionist painting that only comes into focus when you stand far away from it. The more data, says UCSF’s Robert Hiatt, the stronger your conclusions.

"Big numbers are important because effects are small. In order to see effects and have some confidence in them, you need large numbers."

Recently, the Million Veteran Project signed on its ten thousandth participant.

The VA's Kupersmith believes that in 18 months they’ll pass the half-million mark. That would put them well ahead of the other medical databases currently available to researchers, including Kaiser Permanete's biobank, which includes anonymous saliva samples — containing DNA — from 170,000 Kaiser patients, and is aiming for 500,000 participants.

To reach its goal, VA staff will have to convince hundreds of thousands of veterans to come in and donate blood. They'll also have to reassure them that the information will be kept private.

"The info is totally de-identified," says the VA's Jennifer Hoblyn. "Each sample gets a unique study info number. So actually it won’t be connected with your name whatsoever."

Schuler says he knows this information isn't likely to improve his own health, or even that of the soldiers he served with. But he considers it an extension of his work to help other vets, "another piece of the puzzle," he says.

It's a way to continue his service, even now that he's back home.

Detail of the rock garden in Ruth Asawa's 'Garden of Remembrance' at UCSF. All photos by Andrew Alden.

Stone is more than the peculiar specialty of geologists. All of us have dealt with stone since our deepest ancestors' days in the African savanna, and I welcome the variety of viewpoints that center around it. The child, the builder, the fabricator, the gravestone cutter and the artist see stone in special ways. Lately I've noticed the affinity for stone that Ruth Asawa displays in her art.

Ruth Asawa has created public art in the Bay Area and elsewhere for more than 40 years. Unlike her signature woven wire pieces, Asawa's public commissions are in bronze or stone. The bronze is carefully sculpted and cast, but the stone is as nearly natural as can be. Let's look at two interesting examples in San Francisco.

The Buchanan Mall (Nihonmachi) Fountain is an installation meant for use and enjoyment as an integral part of the Japantown center. It immediately calls to mind the traditional Japanese rock garden in the streamlines of its cobblestone pavers and island stones.

Bronze sculptures, one of them a fountain, sit in two stone circles like islands or ponds. Both were inspired by origami.

Both circles include island stones and are harmoniously faced with Californian river rocks. It interests me that Japan and California, facing each other across the Pacific, both owe their geology to subduction, the plate tectonic process of clashing plates that pushes their rocks together into mountains.

The Garden of Remembrance is in a courtyard at San Francisco State University, built to commemorate the imprisonment of Japanese-Americans during World War II—a troubling act of U.S. public policy and a formative event in Asawa's life. It has two parts, a grassy square and a waterfall rock garden.

Apparently Asawa's intent for the square was to bring together rocks from each of the ten War Relocation Centers. But the first stone I approached told me immediately that geology had thwarted this purpose.

This classic peridotite, streaked blue with serpentine minerals, could not have come from California's Tule Lake or Manzanar. The first would have been black Cascades lava, the second Sierran granite or gneiss. This boulder comes from the Klamath Range. Clearly these stones were symbolic, not literal representatives of the camps. It was a relief at that point to put down my geologist's mindset, because an artwork like this should not distract anyone from its true purpose.

Later I learned that the Rohwer, Arkansas, camp where Asawa spent the war years (along with George Takei, Janice Mirikitani and more than 8,000 other American citizens) was located in a marshy lowland with no rocks at all. The same was true of the camp at Jerome, Arkansas.

While there is some color among the ten boulders, most are structureless mudstones, dark and mute. They populate their lawn in a scatter that schematically matches their pattern on the American map. (In that context, the blue peridotite represents Tule Lake and its exceptional role in the camp system. Maybe my geologist's mind has something to work on after all.) Asawa collaborated with stonesetters Isao Ogura and Shigeru Namba in selecting and placing the stones here, and in the uplifting rock garden next to the lawn.

Even at shady times of day or in the typical fog, this garden must be a bright place thanks to the light-colored Sierran boulders. On a sunny day, the combined direct and reflected light makes it almost dazzling. The top photo of this post shows a closeup. The stones themselves are luscious, coaxing even the geologist to simply stand and gaze.

Exercise prevents the shortening of telomeres caused by psychological stress. Image courtesy of mikebaird.

New research by Nobel Prize winning UCSF researcher, Elizabeth Blackburn, provides a possible mechanism by which exercise protects against stress-related chromosome aging.

The findings, presented this month at the American Association for Cancer Research 102nd Annual Meeting, were based on earlier research showing that stress accelerates telomere shortening. Telomeres are protective strands of DNA found on the end of chromosomes that protect them from degradation during cell division. Telomere length is associated with cellular health, and is a known marker of cell aging.

Shorter telomeres are associated with cell death and chromosome instability, which can lead to inflammation. In immune cells, short telomeres can predict poorer prognosis in patients with heart disease and cancer.

In a previous study by Blackburn, psychological stress was associated with shorter telomeres in the lymphocytes of caregivers of chronically ill children. This was the first demonstration that telomere length is correlated to perceived stress. In the current study, co-authored by biochemist Jue Lin, telomere length was again associated with stress levels, this time in primary caregivers looking after a family member with dementia. However when the researchers looked at the immune cells in those who exercised, there was no association between stress and telomere length.

Another study, led by Eli Puterman, examined the impact of exercise on the telomeres of healthy women who had been victims of child abuse. In this study those who exercised were protected against the effects of stress on telomere length.

“We saw a relationship between childhood trauma and short telomere length but the relationship seems to go away in people who exercise vigorously at least three times a week,” said Lin in a press release.

Exercise is known to beneficially impact immune function and several other aspects of health. This new research illuminates on one possible mechanism by which physical activity exerts its helpful effects.

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UCSF bioengineering graduate student Alvin Tamsir places E.coli bacteria onto a petri dish in the lab. (Credit: Susan Merrell, UCSF)

Reported for KQEDnews.org.

Researchers at the University of California-San Francisco have hacked into the genetic wiring of billions of individual bacteria and outfitted them with the kind of on/off switches normally found in computer chips, not living organisms.

The switches, which are built out of genes, allow the bacteria to listen for chemical signals and respond, much like computer chips that can perform powerful tasks.

The switches may one day help the development of biofuels that are cheaper and more powerful than gasoline, or a new suite of pharmaceuticals that could more effectively target and kill tumor cells with fewer side effects.

“Scientists have been trying to engineer bacteria to be more programmable, to do various things, but biology is hard to program” said Alvin Tamsir a doctoral student at UCSF. “I want to generate the technology so that bacteria can be more programmable in a more predictable way.”

Tasmir was the lead author of a study on the subject that was published last week in the journal, Nature.

UCSF bioengineering graduate student Alvin Tamsir. (Credit: Susan Merrell, UCSF)

By building new molecular circuits into bacteria, Tamsir and his team can now make the bacteria perform specific tasks, much like the millions of wires which comprise the electrical circuitry of a modern computer chip enable the dizzying array of complex calculations and tasks a computer can do in micro-seconds.

It’s all part of the new field of synthetic biology, where principles from computer science, electrical engineering and genetics, along with other sciences, mix together to reveal the tools and strategies for reprogramming the cellular machinery of living organisms like bacteria and yeast. Scientists and companies in the Bay Area and elsewhere, working on other synthetic biology project, already are developing a new generation of drugs and biofuels with bionic bacteria and yeast.

“Some of these drugs that we are working on right now require 40 genes. And you have to control when those genes turn on and for how long and in what order, and for all that, you need a circuit,” said Christopher Voigt, an associate professor at UCSF’s Department of Pharmaceutical Chemistry and the senior author of the study.

Tamsir and Voigt looked to the world of electrical engineering, where circuits bring the necessary level of control to millions of precisely timed calculations that a computer chip must complete to execute any task, like spellchecking a document or surfing the web.

To do these tasks, microscopic switches called “logic gates” are etched into the silicon of computer chips. The logic gates function according to a set of rules and are connected with wires that make up a circuit on the chip. Each of these logic gates receives an input, such as an electrical current, from the wires, and responds based on the kind of gate it is. For example, if it’s an “AND” gate, it will turn on and send its output of an electrical signal to the gate next to it, but only if it is getting inputs from the two wires that feed into it. If it’s an “OR” gate, it will turn on even if it is getting a signal from just one of the wires connected to it.

“In computers, complex tasks like opening a document or performing a calculation can be boiled down to simpler calculations performed by these logic gates,” said Tamsir. A modern Pentium chip can have more than a million logic gates, each one performing a tiny piece of the calculation or task at hand.

“But you don't have an engineer at Intel that is choosing exactly where each wire goes,” said Voigt. Instead, programming languages have automated the process, quickly and reliably reproducing on the computer chip the precise circuits of logic gates needed to carry out functions specified by a computer engineer.

“We are trying to create a programming language for cells,” Voigt added, “and ultimately have it so you can take any function you can imagine and convert that into a DNA sequence that carries out that function.”

Four colonies of E. coli bacteria cells plated onto a petri dish. Each colony contains a billion cells. (Credit: Susan Merrell, UCSF)

But scientists can’t exactly take the hardware of tiny gates and wires on computer chips and insert them into living bacteria like E. coli. So Tamsir and his team had to engineer genes that would reprogram the DNA of E. coli, instructing it to make logic gates out of proteins that would help the bacteria perform more like a computer to carry out a specific task – in this case, to make a fluorescent yellow protein.

In computer chips, the metal wires that feed into a logic gate are physically separated so that the inputs going into one logic gate don’t cross with the wires of a nearby logic gate. But this isn’t the case with living bacteria. “Every gate is a molecule and they're all being run based on molecules and they're all crammed together in the bag that is the cell,” Voigt said.

Although the scientists created eight different colonies of bacteria, each with their own discrete logic gate, only four colonies were used at a time to see if they could link up to form a circuit that would yield the fluorescent protein.

One logic gate in one of the bacteria colonies may need two inputs, like a sugar and an antibiotic, to release its molecular output, such as an enzyme, that would then act as an input for a second set of logic gates. But this next set of logic gates may have been designed so that it produces its own molecular output only if it doesn’t receive the sugar and antibiotic inputs that triggered the activity of the first logic gate.

“It’s by combining multiple gates together that you get different behavior. And that's how electrical circuits behave – they use a lot of logic gates and combine them in various ways to get various functions,” said Tamsir. Similarly, the scientists were able to modify the behavior of their bacterial circuits by simply moving the location of the bacteria colonies in the petri dish, since each colony operated with its own set of logical rules for responding to the chemical inputs feeding into it.

An illustrated wiring diagram showing two different kinds of logic gates (NOR and Buffer) operating in four bacteria colonies on a petri dish. The last bacteria colony, indicated in brown, completes the circuit to make fluorescent yellow protein. (Credit: Alvin Tamsir, UCSF)

Tamsir built 16 different kinds of genetic logic gates to program the bacterial 'computers'. Each one successfully suppressed or promoted the production of the fluorescent yellow protein depending on how it was linked together in the bacteria.

“The hard part,” said Tamsir, who has worked for more than two years on this research, “was combining different genetic parts so that when they are put together, they function as you want them to.”

Other researchers are taking note.

“They have begun the process of creating a characterized library of elements which can be used by other labs to build more complex systems,” said Douglas Densmore, an assistant professor of computer and electrical engineering at Boston University who read the Nature paper describing the UCSF team’s research.

Tamsir and his team now want to increase the complexity of their bacterial circuits by building even more sophisticated logic gates.

Voigt added that there are roughly 200 to 300 circuits that regulate different biological activities in E. coli bacteria.

“And that’s the good news – that it’s not millions,” he said. Unlike a computer chip, “the bacteria don’t require a lot of gates and if we had 100 gates, we could do some pretty amazing things,” Voigt said.

By designing more complex gates and more of them, he said a scientist could be “in full control of programming bacteria.” This arsenal of expanded logic gates could then coax the bacteria to produce more than just a biofuel or a low-cost malaria drug, like the one developed using synthetic biology by Amyris Biotechnologies in Emeryville.

“Everything you see in biology — such as a corn plant growing — those complex processes are being implemented by natural circuitry,” said Voigt. “And one of the reasons that we can't access those functions is because we don't have that refined level of control.”

With the new system of logic gates snapping together to form synthetic circuits, the UCSF scientists have expanded that level of control and consequently, what bacteria or yeast could be programmed to do, like some day make synthetic wood, silk or antibiotics.

UCSF bioengineering graduate student Alvin Tamsir handles test tubes containing E. coli bacteria. (Credit: Susan Merrell, UCSF)

Life Technologies, a biotech firm based in Carlsbad, has partnered with Voigt’s lab to generate a software package that would allow other scientists to specify the kind of logic gates they want to run in the bacteria being used in their experiments. After a few keystrokes and some processing by the computer, the scientists would receive a recipe for making those logic gates, which could then be sequenced from the sugars and phosphates which make up genes, and inserted into their bacteria.

For Tamsir, the research is incredibly challenging but also extremely rewarding, a vital part of his doctorate degree in bioengineering which he hopes to complete in May. The 26 year-old scientist grew up tinkering with circuit boards and even derived programming inspiration from Lego Mindstorms, a line of robotic toys.

“I found out about the field of synthetic biology through Chris Voigt's lab. Right then, I knew that this was the right field of study for me,” he said. “It combines my love for computer programming with my love for biology.”

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There is one thing that aging experts say can stave off the effects of aging on the brain: exercise.

Last year, Americans spent $300 million dollars on products intended to improve their short-term memories, or to help them concentrate better at work. Do these products work?

A couple years ago, Alvaro Fernandez’s wife, Lisa, had a baby. She took six months off, then she went back to work. Fernandez says it was a tough adjustment. “Obviously she would have loved to have a brain bootcamp to go back to her job.”

A bootcamp, for the brain. Fernandez, who is an analyst with the market research company Sharp Brains, says 20 years ago baby boomers were discovering aerobics. Pretty soon he believes they'll be hiring personal brain fitness trainers. Today, he says, Americans spend $300 million on brain fitness games. “We predict that by the year 2015, the industry may grow to between two billion to eight billion dollars.”

Right now, the industry mostly consists of video games. They cost anywhere from 50 to 400 dollars. They're also popular thank you gifts for public media station fund drives, including KQED. Examples include Lumosity, Cognifit, and Happy Neuron.

One game, made by the San Francisco-based company Posit Science, involves listening carefully to short blasts of sound, and determining whether the pitch goes up or down. The general idea is that by doing a series of basic and repetitive tasks, which get harder over time, you’re actually changing your brain structure. Over time, the manufacturers claim, you can train an old brain to behave like a new one.

“All of the physical, functional, and chemical functions that contrast the old versus young brain — and I mean all — appear to be reversible,” says Mike Merzenich, the Chief Scientific Officer of Posit Science and a retired professor of neuroscience at UCSF.

But many scientists who study aging are skeptical.

“I think most of the claims they make are exaggerated,” says Murali Doraiswamy , who teaches psychiatry and geriatrics at Duke University Medical Center, and has researched these games.

Doraiswamy is not entirely critical of brain fitness games; in fact, he believes some of the research on them is promising. But he says there hasn’t been nearly enough of it.

“Because they can sell these products without FDA approval,” he said, “there’s not a lot of incentive to do the kinds of large clinical trials. And unfortunately because of that, the evidence is still weak.”

Take, for example, an issue scientists call "transfer."

Say you start getting higher scores on a brain fitness game. Is that all that's changed? Several game manufacturers have studied this, and the manufacturers say the skills do carry over to the rest of your life.

Laura Carstensen, who directs the Center for Longevity at Stanford University, disagrees. “It's the difference between I can teach you something, or I can make you smarter.”

“Can you improve your brain so that it's faster, more adept, more vital? That's what the claims are, and I don’t think there’s really any evidence for that.”

There is one thing, however, that Carstensen and other aging experts say can stave off the effects of aging on the brain: exercise.

“I think that the research such far demonstrates a much clearer link between exercise and brain health,” says Joel Kramer, a neuropsychologist at UCSF's Memory and Aging Center.

When asked his advice on how to improve brain functioning, Kramer’s advice was simple: “Head to the gym and start getting some aerobic exercise.”

Of course, it isn’t just the fear of normal aging that has people buying brain fitness programs.

In his office, Kramer showed me a video of a medical screening he’d done on a patent. Kramer read the man a list of words, and then, seconds later, asked the patient to repeat them. “Can’t remember a single one,” said the patient.

This is not normal aging. This is Alzheimer’s disease. Asked whether brain fitness programs could have helped Joel Kramer’s patient, Stanford's Laura Carstensen was unequivocal. “No evidence. No evidence. None. Zero. That these games could prevent Alzheimer’s disease.”

At this point, nothing has been shown to prevent Alzheimer's. Not crossword puzzles, not Sudoku, not exercise. But that doesn’t mean Carstensen won't give advice to people who worry about becoming forgetful as they age:

“Continue to be involved in the community, with kids, with schools, with work.”

Studies have shown that in addition to exercise people who do things like teach kids to read, or take dancing lessons, seem to stay sharp, longer. Scientists aren't sure why that is, exactly, but they say it’s not a bad program to follow.

Says Duke’s Murali Doriswamy, “my recommendation is whatever it is that they find novel, they find challenging, and to stick with it.”

Listen to When Brains Hit the Gym radio report online.

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By Deirdre Kennedy.

It is well known that strokes can happen in the elderly. But what many people don't know is that babies suffer strokes. So an entire month, May, has been dedicated to childhood stroke awareness. Infants often don't show the same symptoms as adults and because babies can't tell us when they're having problems moving or thinking. There is just a lot less known about infant strokes.

A stroke happens when the blood supply is cut off from a part of the brain or a blood vessel bursts and causes a build up of pressure in the brain. Doctors can tell that a child has had at stroke as an infant by taking an MRI of the brain. Researchers at UCSF Children's Hospital are working to develop early treatments for babies who suffer from stroke before it causes long-term brain problems. Donna Ferreiro, Chief of Child Neurology at UCSF and one of the nation's leading experts on neurological complications in babies, says a baby with a stroke can look completely normal.

"Often those strokes get missed in the nursery because these are babies who generally look well, they're cherubic, they weigh the right amount, they feed ok…It's not until they're older and then all of a sudden the parents notice that they're only reaching with one hand, and not both hands like they should, or that when they try to stand up and walk they topple to one side".

A stroke can continue to cause brain problems over time. It may cause seizures, which researchers believe, can damage the brain further. Like strokes, seizures are also hard to notice with the naked eye. Babies don't have big shaking movements like adults. They may have a subtle eye or head movement, some lip smacking or bicycling movement of the legs, says Ferreiro. By monitoring the brain waves of babies who have had birth problems or are born premature, doctors can intervene with drugs and other therapies. Both strokes and seizures can also happen in utero but there are no established treatments for newborn or fetal strokes yet.

UCSF is heading up an international consortium to test new drugs for babies. One involves using a growth factor called erythropoietin that promotes the formation of new blood cells. Ferreiro says it has been shown in the lab to make new neurons grow. You can find out much more about current treatments being used on newborns with brain defects, by listening to our Quest radio report, Baby Brain Development.

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The last time we reported on Swine flu, or 2009 H1N1 virus, the Centers for Disease Control and Prevention was considering whether or not to invest in a vaccine for the new influenza strain.

Now, after several delays, the first batches of vaccines — first, a nasal spray version, then an injectible vaccine — is due to hit hospitals and clinics across the country (and around the world) in the first weeks of October. It's up to each state to decide which groups to prioritize, but pregnant women, young children, and those with certain preexisting conditions such as asthma may be considered priorities. Over the following weeks, the flow of vaccines, produced at five different labs across the country, will steadily increase until, officials hope, any American who chooses to be vaccinated has access to a dose.

To learn more about where to get the vaccine, call: (800) CDC-INFO (800 232-4636) or visit www.cdc.gov/flu.

Here's another good resource for basic H1N1 vaccine info.

In this piece, we profile work taking place at the University of California, San Francisco's Viral Diagnostics and Discovery Center. This lab is home to the ViroChip – a powerful viral diagnostic tool that won its inventor, Joseph DeRisi, a MacArthur "Genius" Grant back in 2004. TheViroChip and other tools are critical to the fight against 2009 H1N1 . Among other things, they may be the first to alert us should the virus mutate into a form that's resistant to the leading antiviral drug, Tamiflu. (Several cases of Tamiflu-resistant 2009 H1N1 have already been reported, but so far they appear to be isolated incidents.)

They'll be looking out for another important mutation too: That's if 2009 H1N1 changes enough so that the current vaccine for it — the one coming out in October — no longer works. (This kind of subtle virus mutation is the reason we need new flu vaccines every year.) So far, this does not seem to be the case.

Listen to the Predicting Swine Flu radio report online.

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You've probably heard about some of the breakthroughs in personal genome sequencing, where companies take a look at your DNA and send back your risk profile. That can be confusing information to have (check out this post from Quest blogger Dr. Barry Starr for his take on it). But there's a flip side to all this genetic research that doesn't have to do with risk: personalized medicine. That's where doctors can customize medical treatments to fit your genetic profile.

Right now, there are only a handful of drugs that are labeled with genetic information, so doctors can take it into consideration. (Here's an article from the New York Times that gives an overview).  But that doesn't mean existing medications are left out.  I spent some time with Deanna Kroetz in this story, who studies pharmacogenomics at UC San Francisco.  She explained that differences in our DNA can cause some of us to process drugs at different rates. We all metabolize drugs with enzymes in the liver, but based on expression of our DNA, we may have different levels of enzymes or our enzymes may not function as well.

There are plenty of other things that affect how we process drugs, like our diet or other drugs we're taking. But these genetic differences mean some people metabolize drugs quickly and others metabolize them slowly. One example that many people are familiar with is codeine.  Codeine is converted into morphine by our bodies and it's the morphine that actually has an effect — but that conversion depends on a particular enzyme. Some people have very low levels of the enzyme that's needed, so codeine doesn't do much for them.

They're also studying another drug response mechanism at UCSF and it has to do with our cells. Many drugs have to go inside our cells in order to have an effect, but if you think back to high school biology, you might remember that cells are protected by membranes.  It takes transporters – those special gatekeepers sitting on the cell membranes — to allow things in.  They also can spit things out of cells.

I spent some time in the lab with Rachel LaFond, a graduate student at UCSF.  She was running experiments on one particular transporter known as ABCG2. This transporter is particularly good at spitting things out of cells. Normally its job is to kick toxins out, but some cancers have been able to hijack this machinery.  Cancer cells with an over expression of this transporter can spit out chemotherapy drugs, which means they aren't helping the patient.  LaFond is working to understand this variation better, so they could one day develop a genetic test for it.

Listen to the Personalized Medicine radio report online.

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Amy Miller and the two year-old twins Devon and Felix

I wish I could say that the time has flown by but the fact is that the first year and a half were pretty challenging for us as first-time parents. Don’t get me wrong. I count my blessings every minute of every day. I have two beautiful, healthy, happy little boys. But it’s only been recently that Alex and I feel that we’ve found a rhythm with them and we’re starting to actually have fun. They are talking, singing, dancing, running and just recently, interacting and playing more with each other. They make us laugh all the time. Who knew that toddlers had such a sense of humor?

As a result of the QUEST story, my pregnancy became more of a public event than I expected it to be. Naturally, after the boys were born, there were several inquiries as to our well-being. Here’s what happened:

After lying in bed at California Pacific Medical Center in San Francisco for 30 days, I was very close to the end of my rope. Bed rest is infinitely more difficult that I could have ever imagined. When I was 34 weeks and 5 days pregnant, after an evening of crying to Alex that I couldn’t take much more of it, I decided to wind down and go to sleep. Normally, Alex would drive back to Oakland, where we lived at the time. But it was 1AM and even though he had to be at work at 6AM, he was too tired to go home. We asked a nurse to bring him a cot to sleep on in my room. Thank goodness we did. About 10 minutes after we turned off the lights, I felt my water break. If he’d gone back across the Bay Bridge, he would have missed the birth. We called the nurses and doctors and they decided to deliver the boys via caesarian section. Devon, or “baby A” as he was called at that time, was still breech and doctors will not deliver twins vaginally if the first baby is breech.

By 3:30AM, I had two little pink, wrinkly babies. Baby A was 4lbs. 12 oz., Baby B was 4 lbs., 6 oz. They stayed in the Neonatal Intensive Care Unit for 2 weeks then we took them home. They were perfectly healthy but just needed to gain a bit of weight and be able to keep their temperatures up without the help of an incubator. The rest, as they say, is history. They are now developing normally; growing and learning new things every hour, it seems. Life is good.

I’m also very happy to report that the other two families in the QUEST story are doing very well, too. Trynne Miller and David Prince’s identical twin daughters, Kate and Charlotte, were born at 28 weeks and 5 days gestation. Average gestation for twins is 35-36 weeks. For a singleton, it’s approximately 40 weeks. Kate weighed 2 lbs. 8 oz., Charlotte was 2 lbs., 5 oz. They were in the NICU for 8 weeks before going home. Today, according to father, David:

Kate and Charlotte Miller-Prince

"They have 'caught up to their age' in terms of their height and weight, and I suspect also
their skills, as they're dancing and talking up a storm. Charlotte (aka Charlie) is speaking in complete, well-formed paragraphs… but we can only understand a few of the words of them."

Josephine Tooley Boyd at age 2

The other child in the story, Josephine Tooley Boyd was born at 28 weeks, 2 days. She was 2 lbs., 12 oz. at birth. She spent 55 days in the hospital before going home at 4 lbs., 6oz. Mother Sarah and her husband moved the family to Oregon in early 2009. According to Sarah, Josephine is “doing great” and quite a big girl. She’s already in the 99th percentile for height and weight for her actual age, not even her “adjusted” age, which is a common parameter for preemies. She’s a talker, speaking in three word sentences and seemingly possesses above average motor skills. She loves playing outdoors and especially loves tractors.

All three children were enrolled in UCSF’s longitudinal MRI study to monitor development of preemies through the first couple of years of their lives. No problems were ever detected with any of these children. But they were the lucky ones. In our society today, preterm birth affects more than 530,000 children and the numbers continues to rise.

In November 2008, the March of Dimes released a “report card” for the nation on prematurely, which assigns grades to both the nation overall as well as to states which are based on how well they address the issue of prematurity.

The U.S. earned a “D” and not a single state received and “A”. The only state to earn a "B" was Vermont. Eight others earned a "C," 23 states earned a "D," and 18 states plus Puerto Rico and the District of Columbia got failing grades of "F."

There’s lots of good research being done but we still have a long way to go before we understand enough about why prematurity occurs that we can prevent it. Until then, visit the March of Dimes website for important information for all pregnant women that will help them recognize the early signs of preterm labor and possible risks for premature birth.

Sometimes, I think back to those thirty days when I was hospitalized prior to their birth and I remember all the things that I was fretting about. Would the boys be healthy? Will I be a good mother? Will our relationship weather the turmoil of two newborns? Will I love them? Will they love me? How will we be able to afford two children? How can we manage to both work full-time when I go back to QUEST in a few months? Believe me, if there was an issue to worry about, I did it. I think that’s pretty normal for first time mothers but lying in a hospital bed with nothing else to do immediately prior to being forced to deal with these issues really amplified those concerns for me.

Now that I’m an old hand at motherhood, I can look back and realize that many of these issues have a way of working themselves out. We figure things out as we go. We adjust to the changes that come along with parenthood because we have no choice but to do so. And thankfully, we did not have any short or long-term health issues to deal with as a result of their premature birth.

Watch the Born Too Soon: Pre-term Births on the Rise television story online.

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