Prion diseases are neurodegenerative, attacking the brain. Could they be responsible for the recent wave of Zombie attacks across the globe? Original photo: digitalsextant. I’m a sucker for zombie movies; I’ve watched dozens of them. I am especially fond of the Resident Evil Trilogy, where the T-Viruses effectively restructure mortality and create a world of zombies. There is something incredibly satisfying with the zombie movie plot – a virus outbreak devastates a planet but a group of people are immune and fight to save humankind. Having the ultimate evil as a virus also makes it seem more plausible and compelling. Yet viruses and bacteria do not live in limbo. They are alive and under the right conditions can be killed. Which is bad news for Zombies.

But what if there existed a substance that acted like a virus or bacteria but wasn’t living? Medicine made a revolutionary leap during the time of Louis Pasteur in the mid 1800's. The inventor of food pasteurization and one of the founding fathers of microbiology – he was able to prove germ theory. Food spoiled and organisms got sick because of the growth of bacteria and viruses within them. Within sterile environments, viruses and bacteria could be killed off and food could be preserved or organisms could recover from illness or infection. Sterilization works on living micro-organisms. Prions, however, are not living organisms.

Prions are infectious proteins. For unknown reasons, these proteins refold abnormally and cause a domino effect in surrounding proteins which in turn mutate into stable structures. Prions will then cause tissue damage and cell death to surrounding areas. Prion diseases are neurodegenerative, attacking the brain and are characterized by "holes" in the tissue. The incubation time for Prion diseases is quite long. They usually surface later in life but after they surface, the diseases are rapid and fatal. Such examples of Prion diseases include Mad Cow Disease in cattle, Scrapie in sheep and Fatal Familial Insomnia in humans. FFI is a disease that literally takes away the ability to sleep and in a few months leads to death. The Book “The Family That Couldn’t Sleep” by journalist D.T. Max follows a family in Italy that passes this disease from one generation to the next over subsequent centuries.

Prions have been and still are a medical mystery. What causes them to mutate and aggressively eat away at the brain? How can they be stopped? Because they are not living they are highly resistant to sterilization methods. While viruses and bacteria can be eradicated on equipment through heat, radiation or chemical reagents, Prions are strongly immune. Maybe Zombies are not so far off after all – lurking in the shadow of medicine has been a mutation that is resistant, brain-eating and neither alive or dead. It has some serious similarities to the zombies I have watched over and over again on the big screen.

If you want to learn more about Prions and their history, check out Down to a Science’s next reading group which is focusing on the book The Family that Couldn’t Sleep or check out the book Deadly Feasts: The "Prion" Controversy and the Public's Health by Richard Rhodes. And one more thing – Happy Halloween!

David experimenting with EEGLoyal KQED blog followers have been reading of Dr. Barry Starr’s experience getting his genes tested by 23andMe. He has tested his native American ancestry and evaluated his risk for diabetes. What if Barry took even more tests, from blood toxins to more genetic tests – would that result in a clearer picture of his health? That’s exactly the premise behind David Ewing Duncan’s new book: “The Experimental Man”.

David takes “guinea pig” journalism to super size me heights. He was tested by numerous genetic sequencing companies, had dozens of brain scans, gave gallons of blood for toxicity tests, even had a virtual colonoscopy to understand what “personalized” medicine means for him. His experimentation was divided into 4 categories: genetics, environment, brain, and body.

My favorite experiment was a memory test in which David and I both participated. The study was on how normal aging changes the neural mechanisms of memory and attention; a study run by Dr. Adam Gazzaley of UCSF. His lab uses a combination of techniques including fMRI (functional magnetic resonance imaging -measures blood flow using a big magnet), EEG (electroencephalography – measures electrical signals in the brain), and TMS (transcranial magnetic stimulation – using a magnet to “scramble” regions of the brain).

In this experiment, I was getting an EEG, designed to measure electrical signals of the brain, in this case studying regions controlling memory and attention. I was fitted with a stylish red cap, my head was covered with a conductive gel, and I was seated a few feet from a computer screen. After some careful measurements of my head, I was ready to go.

I was shown either a face or nature scene for a split second, then the screen went blank, then I was shown another face or nature scene. My task was to decide whether the two pictures were the same. Sounds exceedingly simple, but it was far from it. I left absolutely exhausted after just a few hours!

However, my results were excellent. I averaged about 95% correct over 3 hours. According to the researchers, that’s slightly better than the average 18-35 year old. David’s results were about the same, but he is more enthusiastic considering he’s closer to 50. Take a simpler version of a brain age test online.

The Experimental Man with David Ewing Duncan

Where: Atlas Cafe, 3049 20th St @ Alabama St.

When: Monday, October 19th 7-9 PM

Cost: FREE

Details: David Ewing Duncan discusses his new book “The Experimental Man”, his book exploring what cutting-edge technologies in personalized medicine can tell us about individual health and life — past, present and future: genes, environment, brain and body.

Could a genetic test have told me I was at a higher risk for developing type 2 diabetes? Image source: aldenchadwickThis sounds contrived but it isn't.  A couple of weeks ago I was diagnosed with metabolic syndrome.  Right when I am in the middle of talking about genetic testing!

Metabolic syndrome isn’t quite as scary as it sounds.  Basically I am on my way to type 2 diabetes.  But if I eat better and get off the couch, I should stave off the disease and get better.

My question, naturally, is whether or not a genetic test could have told me I was at a higher risk for developing type 2 diabetes.  And whether I would have done anything with that result.

As you know if you’ve been following my blog, I took a 23andMe genetic test and have been writing about it since.  The image below shows what the front page of my clinical report looks like (click to enlarge):

According to the DNA checked in this test, I am in the average risk range for type 2 diabetes.  This doesn’t really seem to line up with my reality.  But I might not expect it to since these genetic tests are so limited right now.

This kind of test can be informative with the yes answer—yes I carry a certain version of a gene that might lead to a disease.  But the no answer isn’t that useful.  It doesn’t mean that they've looked at all the possible genetic differences that can lead to a disease and I don’t have any of them.  Basically it means that they didn’t find the specific genetic difference they were looking for.

Now I wouldn’t necessarily have predicted that any genetic test available right now could tell me a lot more than that.  Type 2 diabetes is too complicated for that and a whole lot more research will need to be done to get a genetic test useful to lots of people.

But still, this is probably what people are looking for with these sorts of genetic tests.  Will I get cancer, type 2 diabetes, Alzheimer’s, Parkinson’s, etc.?  For most of these cases, the tests can tell you a lot about rare forms of these diseases but little about the more common forms.

So the no answer didn’t really help me much.  Here I am on my way to being a diabetic and the test said I was at average risk.  Of course, I suppose I didn’t even need to take a test… all four of my grandparents came down with type 2 diabetes.  Like lots of these complex diseases, family history is the best predictor.

The second part of my question is a hypothetical one.  Let’s say they had a perfect genetic test that said that I was at an increased risk for type 2 diabetes.  Would it have changed my behavior?  I’m not sure but probably not.

I certainly wouldn’t have changed any of my behaviors when I was young.  I was invincible, remember?

Now that I’m a bit older, such a test might have influenced my behavior a bit.  I already knew about my risk because of my grandparents but my thought has always been that maybe I got lucky and didn’t inherit their tendencies towards diabetes.  But if they were tested and we shared the same genetic differences that led to type 2 diabetes, then I might be worried enough to change what I was doing.

Most likely though, my behavior modification wouldn’t be perfect.  What I’d probably do is keep watching TV and eating Twinkies but get my blood sugar tested more often.  Once I was headed for diabetes, then I’d modify my behavior and keep it at bay.  (I’m sure doctors scream into their pillows at night because of patients like me.)

This is different than some people’s reactions to other genetic tests.  For example, some women who find out they have the version of BRCA1 that greatly increases their chances of breast and ovarian cancer have a double mastectomy and/or a hysterectomy before there are any signs of cancer.

I might react much more strongly with a valid cancer genetic test.  Cancer is scary, nasty and not really reversible.  Type 2 diabetes is different.  You can start down the road, modify your behavior and then nip it in the bud.  Carpe diem and then pay the piper.

Is corn ethanol a poor fit for future U.S. liquid fuel needs? Biofuels have received a tremendous amount of publicity lately as an alternative to gasoline and diesel. An ethanol economy based on sugarcane has helped to boost Brazil into the limelight, raising standards of living and perhaps even contributing to the country’s recent successful bid at the 2016 Olympic games. In the U.S. prospects of corn-based ethanol have piqued the interest of agriculture and oil companies alike. Such unbridled excitement has also revealed dramatic downsides. Brazilian affluence comes at the price of biodiversity as swaths of rainforest are sacrificed to plant new crop fields. Increased American deand for corn was a measurable contributing factor to the recent world food crisis.

The timing, then, was quite appropriate for a panel discussion last week organized by the Friends of Berkeley Lab at the Berkeley Repertory Theatre. Titled “Hope or Hype: What’s Next For Biofuels?” the event, hosted by KTVU’s John Fowler, featured a panel with Jay Keasling, Susanna Green Tringe, and Jim Bristow, three scientists exploring the role that synthetic biology might play in fabricating a better fuel for tomorrow’s autos. The evening consisted mainly of two themes: the relative limits of both crude oil and corn-based ethanol, and an outline of research being pursued to make new ideas practical.

Fossil fuels are unsustainable, a point that saturates public rhetoric each election cycle to the point of ad nauseum. It might be slightly more surprising to learn, however, that fuel based on ethanol (the alcohol found in all common beers, wines, and liquors) may be as bad for global warming as gasoline, perhaps even be worse. When extracted from corn, considerable energy is lost on fertilizers. If that energy was generated using a coal plant, global warming is still a problem. Additionally, ethanol is an unwieldy fuel. It is corrosive, for example, and therefore must be trucked, rather than piped, from one location to another. “I like to say that ethanol is for drinking, not for driving,” Keasling joked as he explained these faults.

The push in the American science community, then, tends to be away from corn-based ethanol and toward something called cellulosic biomass (Editor's Note: see our QUEST video "Beyond Biofuels" for more information). The idea is to make fuels not from corn, but rather from corn stover—plant leftovers after the crop has already been harvested. Alternatively, almost any other organic material ranging from wheat stover to sorghum to garbage could be used if the proper techniques are developed.

There are considerable scientific challenges. Much of the material we might like to use as fuel is tough and woody. Scientists have yet to figure out a satisfactory method for breaking this down, and a great deal of gene-sequencing effort is currently underway with the aim figuring this out. There are also challenges in terms of deciding what product will be generated from these woody materials. At least one idea is to genetically engineer an organism that can transform organic matter not into ethanol, but rather into something more amenable to transport and carbon neutrality.

What should we make of these new efforts? My own feelings are mixed. I enjoy my car, and I love road trips. As Bristow said during the panel, “The reality in the U.S. is that people are going to drive cars. We need liquid fuel.” The current push in biofuels research is tremendously important. The vast majority of energy sources are simply inadequate for powering cars to the extent that the public is accustomed to. The maximum power one could ever expect to obtain from a solar-powered car, for example, is less than 10 horsepower. Even the Geo Metro gets 55 horsepower. The new Volkswagen Beetle gets over 100 horsepower. Electric cars might hold some promise, but at this point it is impossible to tell whether batteries or biofuels will ultimately make a better alternative. These two fronts are also not necessarily exclusive, as the hybrid explosion of recent years has shown.

And yet, for all the excitement, selling the American public on biofuels feels a little like feeding methadone to a heroin addict. We believe that a shift to biofuels will assuage the continued seeping of carbon into the atmosphere. But there are a lot of side effects. The controlled production of biomass requires land, and with that allocation comes a host of ecological concerns. When it comes down to it, there will never be a substitute for good old fashioned belt-tightening.

Are they related to me? I still don't know…When last I left you, I was searching for my great-great grandmother’s DNA in my own DNA.  Remember, legend has it she was Cherokee and I wanted to confirm the legend with a genetic test from a company called 23andMe.

In my last blog post, I showed how the two most powerful ancestry tests, mitochondrial DNA (mtDNA) and Y chromosome, were useless to me in my hunt. Now I want look at the rest of my DNA.  So here we go!

The Y chromosome and mtDNA are a small fraction of my DNA—something like 0.8% of the total DNA in one of my cells.  But they are incredibly useful because they change very little from generation to generation.  The mtDNA I got from my mom is probably exactly like hers.  Same with most of the Y I got from my dad.

The other 99.2% of my DNA is a lot trickier to look at from an ancestry perspective because it has changed a lot from generation to generation over time.  For example, the chromosomes I inherited from my parents are not the same as the ones they have.  I got a mix of their chromosomes

For example, my mom had two copies of chromosome 1 (and two copies of her other 22 chromosomes too).   As you know, she passed one chromosome 1 to me (my dad gave me my other one).  But, through a process called recombination, her two copies of chromosome 1 swapped DNA so that I got a hybrid of her two copies.  I inherited a unique chromosome never before seen.

This is all well and good from a survival of the species point of view, but it is a problem for ancestry testing.  Imagine that instead of my mom, we look at my Cherokee great-great grandmother.  She has just had a child who inherited a mix of her chromosome 1’s.  This chromosome will look Native American and the child would appear half Native American.

Actually, the test isn’t perfect yet and so there isn’t yet a “Native American” set per se.  Instead, here is how 23andMe describes Native American DNA in their tests:

“…people who identify themselves as Native American exhibit fairly consistent Ancestry Painting proportions of about 75% Asian and 25% European, plus or minus 10%.”

This means the chromosomes the child got from his or her mom won’t look Native American but instead will look 75% Asian and 25% European.  (See a realted post of mine elsewhere for why it looks like this.) Now imagine that this half Native American child grows up and has my grandfather as his or her son.

My grandpa will inherit a mix of his parents’ DNA too.  In this case the Native American DNA will mix with the European DNA to create a hybrid.  On average, you would now see something along the lines of 37.5% Asian (this is a simplification but it gets us into the ballpark of the number we might expect).

Each generation would see, on average, a continued dilution of this Asian part.  My dad would have 18% Asian, I would have 9%, etc.  Here are my ancestry results (click the image to enlarge):

Not a hint of Asian.  Looks like my great-great grandma wasn't Cherokee.  Or was she?

There are lots of ways she could still be Cherokee.  First off, I don’t know how solid the 75% number is for all Native Americans.  I don’t know how many Native Americans are in their database.  I also don’t know how much variation there will be tribe to tribe.

Secondly, you may have noticed that I was very careful to always say, “on average.”  This is because the recombinations don’t have to be a 50-50 swap.  It is true that if you look at a large number of recombination events, the average will be 50%.  But individual recombination events can be biased towards one or more chromosomes.  Occasionally you’ll get mostly one chromosome and sometimes mostly the other.

Sort of like flipping a coin—do it enough and you’ll get pretty close to half heads and half tails.  But if you flip a coin twice, you might get one head and one tail.  And you might not.  Half the time you’ll get two heads or two tails.

This is less a problem than you might think with our chromosomes since the recombination is spread over 23 pairs with each pair being independent of the others.  But it can still throw a monkey wrench into the works.  23andMe actually has a nice chart that hints at this by giving the most likely range of possibilities.  Unfortunately, this chart didn’t come up with my results and I had to stumble on it while I was playing around.

Using the chart, I can see that the bottom end of my expected results in 0.24% “Native American” (if I am reading the chart correctly).  That is pretty low and it seems like a pretty minor mistaken assumption at the beginning might knock this down to zero.

So where am I after this?  Still in the dark.  This is actually how many genetic tests end up.

The positive result tells you a lot.  Had there been Native American DNA, that would have been a slam dunk.  (This isn’t always the case with genetic tests but it would be here.)  But there wasn’t.  Which means, given that I was on the edge of detection, that she may or may not have been Cherokee.

Now, this isn’t 23andMe’s fault.  The test itself couldn’t be conclusive given how far back we need to go and the DNA tests that 23andMe offers.  In fact, 23andMe does an excellent job of presenting the data.  There are pretty chromosome paintings, graphs superimposed on world maps, etc.  All very nice.

I am still worried that the explanations that go along with these images assume an awful lot of knowledge that most people might not have.  Without that knowledge, it can be hard to assess the significance of a certain result.  Next blog that’ll become even more important as I tackle health conditions.

Zoloft is a popular drug used for the treatment of depression symptoms.

Depression is hardly new. The Roman physician Galen, in the second century A.D., expounded on the prevailing medical view that four bodily fluids, or humors, existed within all people but that the unique variation of these humors within people resulted in individual differences among people in their behavior and temperament. An excess of black bile, for example, indicated a melancholic personality.

Fortunately, a lot of scientific progress has been made since then in understanding depression to be an organic, brain-based medical condition that afflicts millions. In fact, an individual has a ten to fifteen percent lifetime risk of developing a major depressive episode. But as Dr. Karl Deisseroth, a Stanford neuroscientist and psychiatrist, told me during our interview for “Illuminating Depression”, “Diagnosis is a big challenge because in psychiatry, we don’t have a lab test. There’s not a blood draw that you can do as you might to check how your liver is doing or how your thyroid function is doing.” So given that the diagnosis of depression is based on clinical observation (most often done by a primary care physician), one can’t help feel that hard, empirical understanding of depression is somewhat lacking, especially when compared to diseases of other organs like the heart and lungs where tests do exist to gauge the presence of pulmonary and cardiovascular diseases.

This was the most interesting observation for me when working on this story. Imagine a medical disease that afflicts eighteen million people in the U.S. (26 million if you include Bipolar Disorder), for which more than 160 million prescriptions were filled in 2008, that is one of the leading causes of disability in the U.S., but a disease for which no definitive medical model of pathology exists. Increasingly, doctors are prescribing antidepressants to treat not just depression but a host of other medical conditions, including chronic pain and insomnia, some of which can co-occur with depression. Sure, we’ve made strides since the time of Galen’s bodily humors and the Freudian view of misplaced hostility and mourning to explain depression, but in some respects, we’re still in the dark about why some people get depression while others don’t, why some people respond to one treatment and not another, or why one person will suffer from a form of depression that is less or more severe than another person. This lack of clear, empirical understanding comes at an awful price to victims of depression, as they encounter remarks from people that tell them to “snap out of it”, implying that they somehow can control the emotional crumbling and dark ideations that accompany the disease.

The consequence of all this is that it’s incredibly tough to create effective, lasting treatments for the disease if we can’t exactly track how the disease affects not only specific regions of the brain but the activity among individual brain cells in regions that may not have even been known to play an integral role in the disease. My layperson’s view is that treating depression currently is a bit like bringing in a car to the mechanic and telling him to fix it but there’s a catch – the mechanic can’t get under the hood to observe directly what’s wrong with the car. We suspect that the problem is with the engine but good luck with opening it up and peering into its pistons. So the mechanic attempts to work on the engine but indirectly, and whatever repairs are attempted may affect the engine but they may also have unwanted effects on the car’s transmission, muffler, timing belt, etc.

Fortunately, advances in imaging techniques like two-photon microscopy and fMRI are elucidating the activity of the depressed brain, allowing the previously impenetrable forest of billions of neurons to be explored, to see their pathways altered, their branches pruned by the disease. And scientists like Philippe Goldin and Kelly Werner are compiling biomarkers like DNA and brain blood flow activity to see if those biomarkers can help predict if people suffering from anxiety and/or depression will respond more favorably to cognitive behavioral therapy than to mindfulness meditation, for example. Dr. Deisseroth is using genetically engineered, photosensitive proteins implanted into rodents’ brains to control brain activity at the level of individual neurons.

Dr. M. Bret Schneider told me during our interview, “A real cure for depression is gonna involve being able to selectively affect those portions of the brain which don’t function properly in depression… But fathoming the huge number of possibilities in each brain with every brain being a little bit different than every other one, is gonna require individualized solutions and will be a scientific feat.” I suppose that with a disease as complex as depression, where one’s individual genetic makeup can influence the kinds of side effects one may experience with an antidepressant, it’s apropos that the future of treating and eventually curing it will entail personalized medicine. Until then, let’s hope that more people bring psychiatry into the research lab to study illnesses like depression, for it’s only through the methodical rigor of science that we have the best hope for curing depression.

Watch the Illuminating Depression television story online.

An image of a bioreactor being developed by OriginOil scientists.

Today’s episode of QUEST features our 10-minute TV story about efforts to produce biofuels from algae. In 1996, when the U.S. Department of Energy concluded its 25-year research project into the potential of algae as biofuels, its report concluded that the most cost-effective way to grow algae was in open ponds. With climate change and geopolitics prompting new research into the algae-as-fuel question, some companies are pursuing the open pond route, while others are looking into closed systems such as bioreactors. In our TV story we profile OriginOil, a Los Angeles-based company developing a bioreactor that looks like a miniature Christmas tree, complete with bright, colored lights. And we interview the CEO of Aurora Biofuels, a company based in the Bay Area city of Alameda, which is re-imagining open ponds, as well as trying to create strains of algae that are ideal for fuel production. Before becoming the CEO of Aurora Biofuels, Bob Walsh worked at the oil company Shell for 25 years. Here’s an excerpt of QUEST’s March, 2009, interview with Walsh, most of which didn't make it into the TV segment.

QUEST: What excited you about algae?

BOB WALSH: I ran oil products businesses for many years and understand the cost-competitiveness and the commodity basis of it. And what excited me about algae was, A, it’s renewable. B, you're using a feed stock of carbon dioxide, which is basically free. And finally, what excited me about this company, Aurora Biofuels, was the aspect of solving it end to end, not just the biotech (end of things), but also the engineering aspects.

Q: What has algae been grown for in ponds in the past?

WALSH: Algae’s been grown in open ponds for decades. And typically it’s been done with nutraceuticals – spirulina, which many people use as a protein pill. That is grown in open ponds, but not very cost-effectively because they haven’t had to be very cost-effective. They can charge $10 per pound.

Q: What would be the difference that you would be looking for in terms of cost-effectiveness, compared to what’s been done already?

WALSH: Historically, algae were just grown in an open pond and captured carbon dioxide (CO2) from the atmosphere and the sun. What we’re actually doing is injecting the CO2 we recover from a steel mill or power plant, to give the algae food. And we’ve engineered it to get better mixing, so it grows more quickly. And then finally, rather than drying the algae out, we actually do a wet extraction of the oil, which is much more cost-effective than drying it as they have historically done for proteins.

Q: So what price would you be aiming for, and what price can the algae be grown for now?

WALSH: Oil today has been around $50 per barrel. We believe we need to be competitive in the $50-60 range. And that’s what our final target is. I think oil will be $60-100 over the next 10 to 15 years.

Q: What would the algae biofuels facility of the future look like?

WALSH: You’ll situate it very close to a CO2 source – a steel mill or a power plant. It will encompass several thousand acres of barren land – because you want dry, barren land – and use salt water. And it would produce roughly 120 million gallons a year of useable fuel into the existing infrastructure.

Q: Can algae fuel actually make a contribution to our transportation needs?

WALSH: Algae can be a player. It’s going to take a lot of different solutions because of the different climates and things that you need for it. It’s also a trillion-gallon market. And so it’s not going to happen tomorrow. But certainly algae can be a 5- to 10-percent player in ten years, in the marketplace.

Watch the Algae Power television story online.

Genetic tests often don’t give as much information as you might think.In a previous blog I talked about getting my DNA tested with 23andMe.  Well, I got the email the other day saying that my results were ready.  So I logged on and up popped this screen pictured to the left.

All sorts of goodies to try out!  I feel like a kid at Christmas.

The first thing I thought I’d do is check out my ancestry.  My grandfather’s grandmother was supposedly Native American and so I wanted to find out if I could see that in my DNA.  (This relates to my supposed relationship with the outlaw Sam Starr but that is a different story.)

23andMe has this Native American testing app in their 23andMe Labs section.  I clicked on my data and up popped this result:

Recent Native American ancestry is unlikely

Has it all been lies?  My great, great grandma wasn’t Native American?  Not so fast…

A “no” answer on a genetics test doesn’t necessarily tell you a lot.  (And sometimes, the “yes” answer isn’t so helpful either!)   Now as a geneticist, I know the drawbacks of ancestry tests like these.  What I wanted to see was if 23andMe did a good job of explaining them.

I first checked out my mitochondrial DNA (mtDNA) and my Y chromosome data.  These DNA don’t change a lot from generation to generation and so are really good at tracing ancestry many generations back.  Their downside for me is how they are passed down.

The Y chromosome passes from father to sons.  My great, great grandma didn’t have a Y to pass on so of course my Y chromosome data wouldn’t show that she was Native American.

mtDNA passes from mom to her children.  At first this sounds promising since we are talking about my great, great grandma until we realize that I am related to this woman through my grandfather.  His mtDNA died with him (except for his female relatives and their descendants) so that is lost to me as well.

Here is what 23andMe has written under interpretation of my mtDNA and Y chromosome results:

This mitochondrial DNA haplogroup is inconsistent with Native American ancestry along the maternal (mother's mother's mother's …) line.

This Y chromosome haplogroup is inconsistent with Native American ancestry along the paternal (father's father's father's …) line.

I suppose this says what I just said but I am not sure how many people would really appreciate the limitations of mtDNA and Y chromosome data from this explanation.  There wasn’t a link to a more explicit discussion of the limitations of this sort of testing and there wasn’t anything I could see from a quick glance at the ancestry part of the site either.  An explicit explanation would be good or maybe a figure like this one:

To me, this drives home the point that there is a whole lot of missing ancestry.  It might help if they had some sort of family tree app where you could indicate as much as you know about family relationships.  Once you’ve inputted the data, it would spit out what tests results would be useful to look at.

So the mtDNA and Y chromosome test results are of little use to me in this quest.  (And of little use to me in general as it confirms my pasty whiteness.)  Next blog I’ll deal with the rest of my DNA and what that can and can’t tell me about my great, great grandma.

Every fall, 30,000 raptors and hawks migrate across the Bay Area in a fantastic display.Every fall, 30,000 raptors and hawks migrate across the Bay Area in a fantastic display. Most stop for a quick snack in the Marin Headlands before moving on to their winter homes. Bay Area scientists and volunteers have been using the opportunity to conduct counts, as raptors have long been seen as indicators for ecosystem health. The Golden Gate Raptor Observatory, now a program of the Golden Gate Parks Conservancy, was set up 25 years ago as the first bird monitoring system in California. Anyone that visits “Hawk Hill” during this time can attest to mass migration; Upwards of 1000 birds are seen per day during the peak. To my amazement, the observatory is almost fully run by volunteers; there are only 3 full time employees compared to over 300 volunteers. Clearly, this is one of the most successful citizen science projects in the Bay Area.

In celebration of the 25^th anniversary, there are a number of interactive events and talks scheduled over the next month.

Hawk Talk and Banding Demo

Where: Hawk Hill

When: Sat 9/12, Sun 9/13, Sat 9/19, Sun 9/20, Sat 9/26 12 Noon – 2 PM

Cost: Free

Details: At these Hawk Talks, a GGRO volunteer gives an hour-long talk about hawk monitoring, migration, and identification using photos and other props. Then at 1 PM a newly banded wild hawk is shown to the crowd, a volunteer talks about GGRO's banding program, and the hawk is released.

GGRO Open House and Raptor Fest!

Where: Ft Cronkhite at Rodeo Beach

When: October 24^th and 25^th, 10 AM-4 PM

Cost: Free

Details: Scientific Displays, Radiotelemetry Demonstrations, Live Non-releasable Raptors, Kid Crafts, GGRO 25th Anniversary Product Sales, Visits to Hawk Hill, Banding Demonstrations, and Raptor Art. On Sunday only – Speakers from UC Davis, SF State University, UC Berkeley presenting results of their research with GGRO.

Celebrate Raptors—A Series of Raptor Biology Talks

Satellite-Tracking Peregrines throughout the Americas

Where: San Francisco Zoo

When: Thursday, September 10^th 7-9 PM

Cost: $3-$5 suggested donation

Falconiformes Discovery: Field, Lab, and Conservation

Where: California Academy of Science’s Nightlife

When: Thursday, October 15^th 7-9 PM

Cost: $12

Eagle Quest:  To See All the World’s Eagles

Where: Mission Blue Chapel, Cavallo Point

When: Wednesday, November 18^h 7-9 PM

Cost: $3-$5 suggested donation

Hmmm… I think I 'm a monkey… but how do I know for sure?? Image credit:

Monkeys have tails. Monkeys have tails. Monkeys have tails. If you leave the zoo learning one thing about primates, learn that monkeys have tails and apes do not. This is one zoo science standard that we try to teach all visiting school children, even the kindergarteners. They are quick to learn, and teach others. They do not hesitate to correct a parent who is pointing to our tail-free chimpanzees saying, "Look at the monkey". Makes me proud.

In preparation for our upcoming Conservation Speaker Series presenter, Noel Rowe, Founder of Primate Conservation, Inc, I decided to delve further into understanding primates by picking up his book, The Pictorial Guide to the Living Primates. After being in the zoo industry for eight years, I figured I knew quite a bit, but I opened up the book with some of my most experienced and knowledgeable co-workers and we were all awe-struck.

Let's begin by getting clear that a primate is a monkey, ape or prosimian. A monkey has a tail, an ape does not and a prosimian is like a lemur or bush baby. The word "prosimian" means "before apes" and is still not recognized by spell check who insists I must mean "promising." Let's hope that is the case for all primates. My hope for this blog is to expose my top 4 new favorite primates.

Western Tarsier -These little guys have gigantic eyes, are carnivorous and have a long, grooming claw on the third toe. They can rotate their heads 180 degrees, like an owl as they leap around trees in Indonesia, Borneo and Sumatra. Prosimian.

Pygmy Marmoset - This animal makes me want to say the C-word. The one we are not supposed to use to describe fuzzy, furry, tiny, big-eyed animals. Only 14-16 cm in length, they are the smallest true monkey. Also called a Dwarf Monkey, they live in the rainforest canopies in Brazil, Peru, Ecuador and Colombia. Tail = monkey.

Gelada Baboon – This is an old world monkey with a unique hour glass-shaped area of naked, bright pink skin on the chest. It is this area that becomes swollen to signal estrus. Various bands can form a herd of up to 600 baboons, traveling throughout the high plateaus of Ethiopia, where they sleep on cliffs.  Tail = monkey.

Mountain Gorilla – OK. This is not a new favorite, but the book reminded me of how much I truly am in awe of these creatures. From the majesty of the silverback to the playfulness of the juveniles, I will always list this mostly leaf, shoot and stem eating animal as a favorite (connect other blog). No tail = ape.

If I open this book again tomorrow, I will have 4 new favorites and on and on until I cover all 250 or so primate species. It is indeed a wondrous world of animals.

To quote Jane Goodall in the book's forward, "without our help, many monkeys, apes and prosimians will vanish." You can begin helping by attending Noel Rowe's lecture at the Oakland Zoo on September 23^rd where he will introduce us to the 25 most endangered primates. The lecture and silent auction are an annual benefit for The Budongo Snare Removal Project in Uganda.

PS.  Monkeys have tails.