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.

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.

Amy Miller and the two year-old twins Devon and FelixIt’s been two years since my twins, Felix and Devon were born on July 27, 2007. In that time pretty much every mother with grown children has advised me to “enjoy it while you can” because this wondrous time will seem like it flew by. “They’ll never be babies again!” they say. “Good”, I reply.

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.

Soon after Barack Obama is sworn in as President next week, he is expected to reverse George Bush’s executive order limiting embryonic stem cell research. Scientists say their research has been stifled by restricting them to existing stem cell lines. The resulting boom in this cutting-edge medical technology will benefit California's research institutes in a big way.

Researchers call stem cell technology a "revolution" in medicine, along the lines of the development of antibiotics in the 1940s, or the manufacturing of insulin and other therapies from recombinant DNA breakthroughs.

But why do stem cells offer such promise?

Robert Klein, chair of the governing board for the California Institute of Regenerative Medicine (the state stem-cell agency created by Proposition 71), says that the recombinant DNA revolution in the 1970s saved the life of his son, and that the potential for saving lives is even greater with stem cell work.

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Stem cell technology has only existed for a decade. And despite the Presidential ban on use of new lines of embryonic stem cells, the advances in research have happened quickly. And, according to Deepak Srivastava, Director of Cardiovascular Research at the UCSF Gladstone Institute, the many possible applications of stem cell work will be seen in the short term (over the next few years) and long term (regeneration of damaged organs could happen in 7 to 10 years, he says).

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Dr. Srivastava says, in the case of one of his patients, five-month-old Ryder Ortiz, stem cell technology could have been a godsend. And it might still BE a godsend, he adds. Ryder was born without a left ventricle, the heart chamber that shoots blood into the body. With stem cell technology, it may become possible to grow a new ventricle, and that would’ve been a huge boon to the infant Ryder.

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But here's the thing: Doctors jerry-rigged Ryder's circulatory system, and it's a process that works – until the patient hits his teen years. In many cases, that’s when the re-worked circulatory system fails. Now, if Dr. Srivastava's estimate is correct, and the technology develops in the next 7 to 10 years, that will be just in time for Ryder Ortiz, who will be inching nearer to adolescence at that time.

Listen to the New Life for Embryonic Stem Cell Research radio report online.

Some 30 researchers from the University of California-San Francisco and the Gladstone Institute of Virology and Immunology have come together to investigate why HIV-positive patients, who are now living longer lives thanks to anti-retroviral drugs, seem to be aging faster than their uninfected peers.

"There's a long list of concerns that people have raised about the effects of chronic HIV infection on different health outcomes," says Dr. Paul Volberding, who as a co-chair of San Francisco's Center for AIDS Research is bringing together this group of scientists. UCSF/San Francisco General Hospital cardiologist Priscilla Hsue, for example, has found that HIV-positive patients (the patients she sees in San Francisco are mostly men) have heart attacks when they're around 50 years old. That's 10 years earlier than when your average, uninfected, man has a heart attack.

Other researchers have found that HIV-infected patients develop dementia younger and kidney failure at a faster rate than their uninfected peers. Volberding says that these patients are also showing accelerated bone loss and accelerated loss of their kidney function. These are all ways in which our bodies normally decline as we age. But in patients with HIV, the decline seems to be faster.

At the beginning, researchers believed that anti-retroviral drugs were causing the aging, but as research has progressed, the thinking has shifted. "The more nuanced recognition now is that maybe some of that was from the drugs," says Volberding, "but maybe some of it was because the drugs were working and patients were living longer and allowing us to see these other effects of chronic viral infection." Even though anti-retroviral drugs can bring the amount of virus in the body down to almost undetectable levels, there is always a tiny amount of HIV replicating inside a patient's body. And Volberding and others believe that this virus could be responsible for the sped-up aging.

UCSF molecular biologist Elizabeth Blackburn, another member of this new group, has spent her life studying the tips of our chromosomes, called our telomeres (pronounced TEAL-oh-meres), and the role they play in aging. Blackburn has found that as we age, our telomeres wear away and shorten. She has studied the telomeres in patients with heart disease and cancer, and now she wants to look at HIV patients' telomeres.

Listen to the Graying of HIV radio report online.

This is the second of two stories born out of an afternoon at UCSF's Memory and Aging Center, where a team of scientists, led by Dr. Bruce Miller, is trying to tease out the differences between as many as 200 dementias that affect aging brains.

The two stories have a lot in common: Both introduce us to people who have lived with extremely difficult degenerative diseases: ALS in "Decoding the Emotional Brain," and frontotemporal dementia in this week's story. Both open up provocative questions about human nature. And neither would have happened without the generosity of a Northern California family – in this case, Cassandra Shafer, who drove down from Forestville with her daughter, Columbia, to tell me about Cassandra's husband and Columbia's father, Keith Jordan.

In these video clips, you meet Keith Jordan in the second half of his disease, after doctors at UC Davis and UCSF diagnosed him with frontotemporal dementia. The videos were taken at UCSF over the course of many hours doctors spent studying Keith and his symptoms. In them, we glimpse of two of Keith's FTD-caused obsessions: joke telling and music. (We also see one of the first symptoms to have emerged: his Jerry Garcia hairdo.)

At first glance, Keith's behavior might strike you as more eccentric than brain-damaged, which is precisely why FTD can take so long to diagnose. If you're a doctor with a 15-minute appointment slot, frontotemporal dementia might just look like a midlife crisis. What we don't see in the video clips are the five heartbreaking years that Cassandra spent trying to figure out what was happening to her husband – a search that included marriage and career counseling, the full gamut of conventional western specialists, yoga, meditation, chelation therapy, replacing every household cleaning product, every pot and pan, all the way to shamanic soul retrieval and exorcism – all while his behavior grew more erratic and difficult to be around. It's impossible to overstate the drain – both emotional and financial — that this search brought on Keith's family.

Keith died in May and Cassandra is still, she says, "inching her way" out of the "foreign land" that FTD plunged her into. As unlikely as it sounds, I think she takes some comfort in the fact that Keith's illness also gave doctors a chance to explore profound questions about human nature and the extent to which the structure of our brains determines who we are.

FTD can turn Democrats into Republicans, and vice versa. People with no interest in art begin to paint obsessively. As the neurons in Keith's right frontotemporal lobe (just behind the right eyebrow) died, his taste in music, his sense of humor, his relationships with his family members and friends changed completely. Our self, in other words, may owe much more to the way our brains are built than we'd care to acknowledge.

And what to make of the fact that this same part of the brain that shapes personality is also responsible for reading other people's reactions? People with some forms of FTD can't empathize with others (hear more about this in our slide show about FTD and art) or read the emotion on another person's face. Not only do they experience radical personality changes, but they lose the ability to sense others' reactions to them. In other words, how we define ourselves – whether we consider ourselves funny, smart, ambitious — seems to have everything to do with how others define us. We are all, in other words, people people.

Which begs the question: What about people raised in isolation, without the critical feedback loop of social interaction? What does FTD tell us, for example, about children who have been deeply neglected in orphanages? Or – taking another angle entirely — autistic people, who have trouble empathizing with others? What does self-perception look like in those who can’t perceive those around them?

If all this is giving you a headache, you might spend some time exploring the web extras we've produced for these two stories. Here, Bruce Miller explains why frontotemporal dementia can bring with it an artistic renaissance. And here, we introduce you to Matt Cheney and find out what his compulsive laughing and crying jags might reveal about emotion and the human brain.

Then use our blog, below, to let us know what you think.

Listen to the Beyond Alzheimer's radio report online, and watch our Web Extra: Dementia and Artistic Renaissance slideshow.

Being a neurologist in the era of fMRI scanners must feel like being a kid in a candy shop. What's going in there while we're, say, shopping? How about reading? Watching campaign ads? Now that we have a way to take real-time images of the brain at work, the scientific possibilities are endless.

On the surface, the experiment at the heart of this story might seem pretty narrow. It focuses on a rare disorder called pseudobulbar affect, which afflicts only people with ALS, or Lou Gehrig's disease — a far cry from the universal rites of shopping or reading. But what’s fascinating about pseudobulbar is the light it might shed on all of us, and one of the most primal and mysterious human experiences of all: emotion.

People with pseudobulbar get happy and sad, just like the rest of us. They laugh and cry like the rest of us too. But then sometimes, something else happens: They keep going. And going. In this video, you can see how what looks like a laughing fit morphs into something else entirely. It’s as if the laughing and crying mechanisms have become detached from whatever part of the brain triggered the emotion in the first place. Maybe – and this is the hope of scientists Howard Rosen and Robert Levenson – by seeing that disconnect take place in real time through the fMRI, we’ll understand, for the first time, how emotion plays out in people without pseudobulbar affect.

(And it doesn’t stop there. Listen to the radio piece to hear Rosen's theory about what PBA might mean for depression, obsessive compulsive disorder, and, particularly, PTSD.)

Finally, a note about Matt Chaney. As Rosen and Levenson remarked many times, science can't happen without people like Chaney. While the rest of us sat comfortably in front of the fMRI monitors, Chaney spent an hour and a half lying in the cramped quarters of an MRI tube, watching highly emotional videos designed to make him sad. Moving his head by a millimeter would blur the image, so not only is Chaney being taken on an emotional roller coaster, he's doing it without moving a muscle – a lot to ask from anyone, let alone someone with a degenerative muscular disease like ALS.

Journalism is a little less demanding (at least I hope so) but Chaney added to an already long day by spending time in an interview with me. He and his wife, Liz, were also extremely generous in allowing us to share videos of them, which illustrate pseudobulbar far more movingly and effectively than anything I could have written.

Listen to the Decoding the Emotional Brain radio report online, and watch our Web Extra: Emotions from the Inside and Out video.

There is a lot we don't know about our DNA and how it works. While there seems to be news every week about genetics, scientists are still in the early stages of finding out what effect our genes have on us (check out this post from another QUEST blogger, Dr. Barry Starr). That's what the researchers at the Canine Behavioral Genetics Project are doing. But in this case, they're looking at dog DNA.

It turns out that human intervention in the form of hundreds of years of dog breeding has created a unique genetic experiment. Because purebred dogs are in essence closed gene pools, it's much easier for scientists to compare of DNA of dogs within a breed. The Canine Behavioral Genetics Project is doing this to find the genes that are associated with behavioral disorders, like anxiety and fear. They also hope to use that information to find the genes in humans that are associated with similar disorders.

Millions of problematic dogs are given up each year in the U.S. And while the UCSF team definitely believes that training is a huge part of dealing with dog behavioral disorders, they're also hoping to understand the genetic influences. Many owners are starting to use medications to help treat these problems, like doggie Prozac. But Melanie Chang, a member of the UCSF team, made a good point to me. Owners tend to think their dog's problems are the owner's fault. Sometimes there are other forces at work.

Listen to "Doggie DNA: Human Genetics through Dogs" online, as well as find additional links and resources. Also, check out the photo set with behind-the-scenes photos.

Lauren Sommer is an Associate Media Producer for QUEST.