Sex, Pregnancy and Stress

June 16, 2009

In his fourth floor laboratory at UC Berkeley, Prof. George Bentley knelt before a cabinet that reads “Caution Flammable.”  He pulled out a white plastic container and fished out a formaldehyde-preserved human brain.  It was gray and cut right down the middle revealing the remarkable inner structure that Bentley says is the seat of sex: the hypothalamus, an oval spot near the base of the cerebellum atop the pituitary gland on the brain stem.

“Here,” he says, “this peptide is produced here” he tapped a gloved finger at the dime-sized spot.  The peptide, or hormone, to which he referred, is GNIH, gonadotropin inhibitory hormone.  He and colleagues have discovered the precise, molecular activity of this previously missing piece of the puzzle about why stress causes sexual dysfunction.

“We may not be interested in sex, may have low libido, or we might have problems conceiving.  A lot of infertility is unexplained,” says Bentley.  He is a bird specialist with close-cropped blond hair and a vaguely British accent.

Bentley, UC Berkeley molecular neuroscientist Prof. Daniela Kaufer and graduate student Liz Kirby are eager to talk about their latest research published in the Proceedings of the National Academy of Sciences.  The paper shows a crucial neurochemical link between stress hormone and this inhibitory hormone, that seems to explain the mechanism behind why animals (and humans) have a difficult time with sex when they’re stressed.

“It doesn’t matter what kind of stress,” says Kaufer, who says she does yoga to reduce her stress.  “If you were about to be eaten, you wouldn’t worry about the next generation at that moment, so reproduction tends to be repressed, or shut down,” she says, explaining there’s a sound evolutionary rationale for this neuropathway.  “The problem is, we’re under stress too much of the time.”

Kirby, a chipper 25 year old researcher who sought out Kaufer’s laboratory to pursue her interest in stress effects, says this new signalling pathway could result in some significant advances for the treatment of infertility.  “To be part of this big, new discovery is very exciting.”

“All of our patients are trying to conceive, and stress seems to be a big factor,” explains Dr. Philip Chenette of Pacific Fertiltiy Center in San Francisco.  Calming piano music, soft couches and peaceful artwork greet the visitor here.  Chenette says stress affects both men and women, perhaps several million American couples who are trying in vain to have children.  “(Women who) stop ovulating and can’t possibly conceive, and men with low sperm counts.”  Chenette has five acupuncturists on duty for stress-reduction.  “At least ten percent of infertile couples suffer from stress-induced infertility, and stress contributes to many more.”

Bentley is just beginning work in human subjects, but says his immediate excitement is for endangered species.  “Animals that are captured for breeding rarely do well, because they are continually stressed,” says Bentley, a 39-year old T-shirt and sandal-wearing marathon runner.  “If (GNIH) is the mechanism, then we can (chemically) interfere with it and enable reproduction of these endangered species.”  He has already shown early success with a compound he’s given to hard-to-breed starlings, an invasive bird species.  Since the molecular mechanism appears almost identical in mammals, including humans, Bentley says it’s not far-fetched to think one day there could be a low-side effect pill that would ease the effects of stress on sex.

A worthy goal.


Not Just for Diego

June 10, 2009

Three year old Diego Sanchez pats his hand repeatedly on a wooden train on the floor of his Oakland, California, home.  His dark eyes fix on the toy.  His mother kneels next to him, calling his name as she tries to hand him a noise-making toy rocketship.  Diego doesn’t look up.

“I began to be concerned about him when he was 18 months old,” says 33 year old Maria Rodriguez, with a wide smile of effort at precise English.  “He began to lose words and stopped talking.  He didn’t walk normally.”  Doctors diagnosed Diego with autism at age two and a half.

“We are beginning to identify characteristics that begin in early infanthood,” says Dr. Pilar Bernal, a Kaiser Permanente pediatric psychiatrist and Diego’s doctor.  “Autism affects sociability, communication and behavior.  Some say it’s like being socially blind.”

Diego is one of 7400 autistic children among Northern California Kaiser patients, almost one percent of all pediatric members.  Eight years ago the number  was 2600.  What’s caused such a dramatic increase?  No one is certain.  Some suggest it is the effect of determined looking for autism and a broadened definition, but most scientists say those factors cannot explain the rise.  Kaiser Permanente researcher Lisa Croen is confident a new $16 million primarily federally-funded study will provide important answers.  She is one of its principal investigators.  “This is the best methodology to find the cause of autism,” she says.

The EARLI (Early Autism Risk Longitudinal Investigation) study hopes to enroll 1200 families with at least one autistic child for this first of its kind, real-time effort to discover what triggers the collection of symptoms known as Autism Spectrum Disorder.  Parents with an autistic child are at significantly higher risk of having another with ASD.  Scientists will use blood tests to collect genetic and biological information from parents, and, if the mother becomes pregnant again, researchers will also take samples during each trimester, at birth and then every three months thereafter. They will also vacuum families’ homes to scan for micro-contaminants, collect diet and industrial chemical exposure data.  Researchers from three other centers nationwide will do the same.

“Early stage development, we believe, is key to autism.  We also think it is a combination of genetic vulnerability and some environmental trigger, perhaps chemicals in the environment, household products, possibly something in food, in the air, the soil, or something else,” says Croen, a thin and lively, dark-haired perinatal epidemiologist who has previously studied mental disorders and genetics.  She has a 23 year old nephew with autism, whose painting of two blue fish has become the EARLI logo.

Researchers designed this study to last about eight years, but say they could have first clues in about three years.

“Diego’s father is a welder, I work in a restaurant, maybe some chemicals did this,” says Rodriguez, as Diego clutched her jacket.  “I will sign up for the study.  (It is) for all the children, not just for Diego, but for all of them.”

The Tumor Throttle

June 3, 2009

“This gene is like a cancer cell’s throttle, but it’s either full-on, or full-off.”  University of California, San Francisco Prof. Frank McCormick is talking quickly in his brand new third floor corner office of the Helen Diller Family Foundation Comprehensive Cancer Center.  He is the first Director of a dramatic $135 million, five-floor UCSF bioscience laboratory.  The view is of an impressive and growing skyline in San Francisco’s Mission Bay research park.  In ten minutes he is to give a short talk at a ribbon-cutting ceremony before two hundred international researchers, donors and media.  He patiently scans his computer desktop and opens a file.

McCormick is a wiry and shaggy-haired 57-year old British-educated genius of molecular biology.  He is an avid amateur race car driver who reminds himself of that particular adrenaline-rush with his computer screen saver.  It is a picture of him at the wheel of his 2004 Mazda-powered open-wheel racer screeching around a corner at Laguna Seca Raceway.  He uses a race-car analogy to help explain the action of an oncogene that he is studying.

The gene is called “ras ” (named, he explains, for “rat sarcoma.”)   There is actually an entire family of these genes, and McCormick is a world’s authority on what they do and how they do it.  “Ras is the on-off switch for cascades of proteins that act like the tumor cell’s accelerator.”  When ras genes are switched on, the cell rapidly divides and makes extra copies other genes that lead to cancer.  “It’s as if my gas pedal is jammed to the floorboard.”

McCormick, who has parlayed his insights and hard work into investments in the pharmaceutical industry (he founded Onyx Pharmaceuticals which sponsors his red and white race car,) now says his goal is to find the right drugs that can block the ras cascade of proteins.  On a flow chart he points to several spots where interrupting the chemical signals can stop the cancer process.  “Two major drug companies just announced a cooperative effort, one drug works here, the other here,” he taps to two junctions where the main cascades diverge.  “If these work, a combination therapy may have a major effect.”

“The trouble is, cancer cells mutate,” says Dr. Mitch Berger, in his still bare office down the hall.  Berger, a neurosurgeon and Chief of the Cancer Center’s Neurologic Oncology Program, is optimistic he and his researchers are on the path to understanding the inner mechanism of brain tumors.  Difficult to treat, in part because of the delicate and vital brain tissues they invade, brain tumors are a breed apart in the cancer wars.

Tall and tan, with gray flecked hair and dark eyes, Berger exudes confidence.  “We are very close to solving this,” he says of an especially tough brain cancer known as glioblastoma.  “Glioblastoma usually kills patients in 12-to-16 months.  It is a difficult diagnosis.  We have tried drug therapy and even vaccines to turn the body’s immune system against the tumors.”  Why any optimism?  “We now think we are on the cusp of understanding its inner mechanism.”  When I ask if he thinks it can ever be cured, Berger says flatly, “Oh yes, we will cure it in my lifetime.”

It turns out, glioblastomas are among the 25% of cancers that are triggered by the ras gene McCormick studies.  Another gene involved in glioblastoma is a called S6K1, and an international expert in that oncogene is Prof. Russ Pieper, whose office is a few paces from Berger’s.  “We are all here to share, to challenge and to inspire one another,” says Pieper, a boyish and smiling pharmacologist.  “If one of us has an experiment we’re working on, we can bounce ideas off each other.”

UCSF Chief of Urology Dr. Peter Carroll, who is among the nation’s foremost prostate cancer surgeons, has his office just down the hall from Director McCormick’s.  “We’ve been open here just about two weeks, and we’ve already had several new ideas.  This is how research and clinical work should team together.”

This is the idea behind this impressive travertine and aluminum building, with its soaring interior atrium, glass panel walls and joined laboratories.  Ideas and insights from different specialties converge and focus here; face-to-face discussions and informal talks, in a way no email, phone call or text message could ever do, spark the flashes of brilliance that may one day indeed cure cancer.

You might think of it as the hotrod racer on a fast track, with a daring driver at the wheel.  We all could be the winners.

Inside the Cancer Cell

May 28, 2009

The American Cancer Society says deaths from all cancers is dramatically declining.  Death rates are down 19% for men and 11% for women over the most recent 15 years for which data are available.  The biggest reasons are stopping smoking and earlier detection of colorectal and breast cancer.  Better diets and exercise likely also play a role.  So do much improved anti-cancer drugs.

During a visit to Joe Gray’s laboratory in Berkeley, California, managed by the Lawrence Berkeley National Laboratory, I saw young men and women scientists busily working on a fabulously intricate analysis of breast cancer tumors.

“Each tumor is unique, actually molecularly different from every other,” Gray explained.  He is a quick-smiling bear of a man who started his professional life as a nuclear physicist.  It was the death of his father from lung cancer that set him on the path to uncovering the mysteries of cancer cells.

“We now can peer deep into the inner workings of the cancer cell in exquisite detail.  We can then determine which drug therapies will work best and, in essence, create the ultimate in personalized medicine: the most effective anti-tumor molecule with the least effect on normal tissues.”  Gray walked me around his lab, gently insisting I wear protective eyewear.

Gray’s research includes discovering why some tumors become resistant to first-line drugs.  His latest work is on HER2-receptor positive breast cancer tumors.  This type represents about a quarter of all breast cancers, and usually is discovered much too far-advanced in younger women.  This is the type for which drugs such as herceptin and lopatinib were designed.  It is the aggressive kind of cancer that killed my good friend and colleague, Faith Fancher, several years ago.  Ironically, Faith’s stepson, Sean Drummond, accompanied me on this day, videotaping a news story.

Gray discovered that one of the reasons this particular cancer is so aggressive and difficult to treat is that the tumor cell makes thousands of extra copies of HER2 genes that help the cell survive.  There are about 30,000 genes in a cancer cell, he says, and maybe 15% of them go haywire, either over-expreessing or under-expressing and dysfuntional.  Then, the tumor often becomes resistant to the drugs, much like bacteria become resistant to anti-biotics.  Gray says he’s discovering the molecular trick that allows the tumors to become resistant.  He plans to publish a study shortly that may help researchers find a new way to kill the tumor cells.  That will be a big step toward better treatment for breast cancer.

Gray, in collaboration with colleagues at UC San Francisco, across the bay, has just won a several million dollar award from the Stand Up 2 Cancer Foundation, to pursue exactly this strategy.

Driven first by a family tragedy, now by his curious intellect, Joe Gray can see into the heart of a killer, and knows its weaknesses.  It’s knowledge that may save your life, or that of someone you care for.

Vaccine Choice and Risking Lives

May 26, 2009

Lifestyle and choices are key California concepts.  Parents who eat only organic vegetables, wear clothing from recycled hemp and refuse to vaccinate their children, are not hip.  They’re risking their kids’ lives and are putting at risk children around them, say pediatricians.

“Celebrities get media attention, and unfortunately some of them are saying ‘don’t vaccinate,'” says Rina Shah, the Walnut Creek, California, mother of 15 month old Dia.  Shah is a working mom, a pediatrician in private practice.  “This is a dangerous message for their children and mine, because pertussis (whooping cough) is still very much a problem.  We live in a diverse and well-traveled community and this disease is with us.”

In the 2007, the most recent year for which figures are available, more than 10,000 children nationwide had confirmed pertussis, and ten died.  The bacterial infection hospitalizes hundreds every year in ICU’s.  “I think I may have caught it myself,” Dr. Shah said, “I worked in a (San Francisco Bay Area) clinic where there were several cases.”  Immunity sometimes wears off even after vaccination.  For Shah, it was a couple of months of chronic coughing.

A new Kaiser Permanente study in the journal Pediatrics suggests that parents who decline routine DPT vaccines put their children at a 23 times greater risk for pertussis.  Refusal raised risk from about 1-in-500 to 1-in-20.  In the Kaiser study, 92% of children who got pertussis were not vaccinated.  A recent study in the New England Journal of Medicine revealed a similar risk for measles.  Vaccines have controlled or eliminated polio, smallpox, mumps, measles and rubella.

All U.S. states require childhood immunizations before children can attend school, but permit medical exemptions from school immunization requirements.  48 states allow religious exemptions, and 21 states allow exemptions based on philosophical or personal beliefs.  In California, parents need only “submit a letter or affidavit stating the immunization is contrary to his or her beliefs.”

“Bad public health policy,” says Dr. Randy Bergen, a Kaiser pediatrician and infectious disease specialist.  Bergen, who’s worked overseas in Liberia, India and Thailand, knows first-hand the risks of third-world medicine.  “Modern vaccines save lives, are safe and should not be refused by parents without medical counseling.  Refusals put children at serious risk.  I support strengthening the exemption law.”

“I’m a mother and I want to be able to make choices for my children,” says Shah.  “I completely support that concept.”  While we talked, little Dia squealed and giggled while chasing bubbles in the backyard.  Dia has had her immunizations. “But, before granting a vaccine exemption, schools should require parents get at least some minimum vaccine education.  Without knowledge, ‘personal belief’ has no value.”

A Different Yosemite

May 23, 2009

The spectacular big trees that so define Yosemite National Park in California’s central Sierra Nevada are dying faster than young trees can replace them.  About a quarter of the biggest trees have disappeared, compared to a detailed survey done in the 1930’s.  Researchers say global climate change is responsible.

Rapid recent changes in temperature appear to have caused an unexpected unbalancing of the web of life that sustained the forests for millennia.

“We expect more intense fires,” says UC Berkeley Forestry Specialist Bill Stewart, who studies the ecology of forests.  “Those fires will in turn kill more trees.  Dense stands of big trees in Yosemite and Sequoia National Forests will thin out,” he says explaining fewer young “recruits” have grown in the vacant spots.   “Expect to see a lot more sunlight in those forests.”

It’s just one snapshot of a much bigger problem: a Western US-wide die off of large diameter trees, reported earlier in Science.  Forest scientist John Byrne of the USDA Forest Service and colleagues discovered larger trees are dying twice as fast as just 25 years ago.  Climate change disproportionately favors insects and diseases, such as fungi, which can move with the wind.  Trees do not have that adaptation for rapid acclimatization.

Temperature is a key driver of ecological balance.  Pine bark beetles, for instance, are devastating western forests.  Normally, the beetle dies when temperatures under the bark cool to about 25F.  A few years ago, they began to live through winters when the low temperature rose just one degree warmer.  Now in many parts in the Rocky Mountains, temperatures drift above the kill temperature all winter long.

The key tree species in Yosemite that are dying off are white fire, lodgepole and Jeffrey pines.  So far researchers have not identified as hard hit the iconic Giant Sequoia and redwoods.  Those big trees appear hardier, but require abundant water to survive.  Drought is stalking the Sierra for a third straight year, and experts say there is significant risk as well to the signature specimens that survived two thousand years before the burning of fossil fuels.

Know the consequences of driving your SUV.

Tahoe Temblors and Seche

May 16, 2009

California’s stunning Lake Tahoe straddles three earthquake faults, in a 6,000 foot high section of the seismically active Sierra Nevada mountains.  Two studies from Scripps Institution suggest a magnitude 7 quake there is long overdue.

“A large earthquake could set off an underwater landslide,” said UC Davis physics and geology professor John Rundle, the Director of the California Institute for Hazard Research.  “A large landslide could trigger a seche, which is what we call a tsunami in a lake.  It could send a 30 to 40-foot high wall of water across Tahoe shoreline communities,” he said.  “Local officials are not taking this risk very seriously.”  Rundle is also advising the Undersea Voyager project which has a small submersible in Lake Tahoe, looking for bottom clues to previous earthquakes.

“We’re trying to find indicators of past quakes, to help us figure out how often they’ve happened,” said Bob Oberta, an engineer with the project.  The submarine is now transecting three faults that lie at the bottom of 1,645 feet of still-amazingly clear water.

What’s most troubling about the research is that sonar profiles of the lake sediment reveal a clear history of big quakes, averaging one every two to three thousand years.  The most recent large quake was 4100 to 4500 years ago, along the West Tahoe Fault, according to the sediment records.

“The next large quake could happen any time.  We put the probability of a magnitude 7 quake at Lake Tahoe at between 2 and 3 percent per year,” said Rundle as he showed me his research laboratory, a collection of earnest grad students and post docs at double-wide computer screens.  “That means it’s likely in the next forty years or so.  The probability changes daily,” he went on, because of other seismic events nearby relieving or increasing strain on the faults, or other factors including plate movement, which at Tahoe includes a steady shearing and pulling apart of about a millimeter per year.  “That’s why there’s such interest in quake forecasting.”

He showed me a lengthy computer plot of California earthquake “record-breakers,” quakes that happened when they weren’t expected.  “There may be trends in these data; quakes tend to follow trends, much like the stock market.”  Research associates are poring over data that include temperature and air pressure as well as readings from fault-creep strain meters.  “It seems we’re coming into a period of increased seismic activity in California, especially along the major faults in Central and Southern California,” Rundle said, “but we can’t just yet make the kind of forecasts that would be useful.”  He is, he says, working very hard on just that.

When visiting Lake Tahoe, keep a wary eye on that sparkling blue water.

New Eye In The Sky

May 15, 2009

Despite a stuck bolt and an hour longer spacewalking than planned, Atlantis astronauts successfully installed the half-ton piano-sized Wide Field and Planetary Camera 3 on the Hubble Space Telescope.  They also installed some other equipment.  For UC Berkeley astrophysicist and astronomy professor Alex Filippenko, a new scientific era is about to begin.

“I’ve been waiting two years,” said Filippenko in his corner office that sports a terrific view of Cal’s campanile.  He has a jar of pickles on his desk for “electrocution,” he says, a class demonstration on sodium absorption.  He sports a wide, boyish grin and remarkable enthusiasm for an astonishingly complicated problem in modern physics, what’s called “dark energy.”

“This is one of the most fundamental questions in all of science right now.  What is the physical nature of the dark energy?”  Filippenko patiently explained a tug-of-war that now shapes our universe.  It involves stuff no one really knows much about: dark matter and dark energy.

“Only about four percent of the mass in the universe is what we can see.  The rest we can’t see, and really haven’t yet identified,” Filippenko said carefully.  In the first five billion years or so after the Big Bang, dark matter (some kind of gravity-inducing stuff) as well as regular matter seemed to rule:  the universe spread out in a slightly slowing expansion.  It looked like what you’d expect from the normal laws of physics, in the grip of gravity as we know it.  But after about five billion years, something else seemed to take control, and without any other way to describe it, astrophysicists called it “dark energy.”  It seems to defy all logic.  It’s pushing galaxies farther apart, faster and faster.

To get a handle on the unexplained expansion, Filippenko says you need some way to measure distance reliably.  Relatively close by, where stars are easier to see, Cepheid variable stars serve as mileposts:  they have a known instrisic brightness, and so like a headlight on a car, you can tell how far away they are.  Filippenko showed me a Hubble photo of the stunning M101 spiral galaxy.  It is about 25 million light years distant, and Cepheids allow that to be measured with remarkable accuracy.  But Cepheids are too faint be seen from several billion light years away, so Filippenko and others use supernovae: exploding stars of a certain type, that also have a determinable brightness.  Even though they release an astonishing amount of energy, they are so faint at these distances, ordinary telescopes cannot see them.

That’s where the Hubble Space Telescope comes in.  To see and analyze these “mile markers” you need a powerful camera, above the ultraviolet-blocking atmosphere.  The new WFPC3 is more than 35 times more sensitive in ultraviolet than its predecessor.

“We’ll be albe to see these stars exploding within 650 million years of the Big Bang,” says Filippenko, “revealing the rate of expansion of the early universe, and hopefully allowing us to figure out what this mysterious dark energy really is.”

Filippenko was part of a team that recently published the most accurate estimate yet of the cosmic expansion (74 kilometers per second per megaparsec) but says new instruments on Hubble will greatly increase what are called “constraints” on the value, known as the “Hubble Constant” making experimental verification much more revealing.

Why is any of this important to anyone outside of the astrophysics community?  “We are all star stuff,” said Filippenko with a nod to Carl Sagan, “and knowing about the history and future of the cosmos helps us understand our place in the universe.”

Thanks to the Shuttle Atlantis astronauts we may put a smaller pin in the map.

Grab and Go

May 14, 2009

In the end, it seemed so easy. Astronaut Megan McArthur controlled the manipulator arm aboard Shuttle Atlantis, and snagged the Hubble Space Telescope as the two spacecraft sped along 350 miles over Australia.

This sets the stage for five spacewalks over five days, to repair and update the 17 year old Space Telescope.  It now may continue working for at least five, perhaps eight more years.

“I’m excited,” said NASA Astrophysicist Robert Rubin in his research-paper cluttered office at Ames Research Center in Mountain View, California.  “Assusming it gets fixed, we have another chance.”  A chance at solving a fundamental mystery about the origin of elements in the universe, that he says was cut short when the STIS (Space Telescope Imaging Spectrometer) aboard Hubble failed four years ago.

Rubin has been researching the M1-42 Nebula, an unusual planetary nebula 25,000 light years from Earth, in the constellation Saggitarius.  M1-42 is often called the “Bird’s Nest” nebula because of its oval shape.  It looks rather more like a lizard’s eye.

Rubin says this cluster of stars holds a key clue to a discrepancy about the abundance of elements found in the cosmos.  He’s been using Hubble images exclusively, especially ultraviolet images that could not be made by earth-based telescopes.   Those wavelengths penetrate the atmosphere poorly.

With a new Wide Field Camera, and a repaired STIS, Rubin says his team may finally discover the dense, relatively cool and hydrogen-deficient clumps of matter that, he says, will help confirm current theories.  He’s been unable to find them so far.  Without these clumps, astrophysicists may have to re-write the textbooks on how everything we see got here.

C’mon Astronauts, we’re rooting for you!  Re-writing the history of the Universe could get very messy.

Fingers Crossed

May 13, 2009

Shuttle Atlantis astronauts discovered some ‘dings’ to heat shield ceramic tiles on the right wing chine (near the fuselage) of the orbiter. NASA says the damage appears ‘minor’ and likely occurred 103 seconds after launch, when impact sensors registered an anomaly.

Engineers will go over detailed images from the robotic arm camera and telemetry from the external fuel tank camera before making a decision on the flight.

It was left wing Reinforced Carbon Carbon damage that brought down shuttle Columbia six years ago, killing all seven astronauts.  For now the Atlantis mission continues as scheduled.

“I’ve got my fingers crossed,” said UC Berkeley research astrophysicist Barry Welsh, who is an investigator with the the Cosmic Origins Spectrograph program. The COS camera is aboard Atlantis, heading for installation on the Hubble Space Telescope.

The camera was built partly at UC Berkeley Space Sciences Laboratory, where I had an opportunity to see an earlier version of the device in the lab’s clean room.

About the size of an astronomy textbook, the camera is a super-sensitive detector of ultraviolet photons.  It will be aimed at distant quasars, and their light will pass through the so called ‘cosmic web’ of matter scattered through the universe.

“Analyzing the spectra of that light, we can determine, mass, composition and other characteristics,” says Welsh, and that can help his team map the distribution of matter in the universe.

Welsh is an animated, quickly smiling 56-year old Brit, who wears shorts, running shoes and a Cal rugby shirt as he darts around the lab.

“Why is it laid out this way? Is it the gravitational effect of dark matter or dark energy or something else? No one knows.”

Welsh gained some fame a few years ago using similar technology to discover that our solar system lies near the center of a ‘gas free bubble’ in the Milky Way.  Something blew the ordinary cosmic dust and gas away about 5 million years ago, making a sort-of chimney through the disk of stars in which we reside.

“I’d really like to get a great discovery before I retire,” he said gesturing at the COS.  “It’d be wonderful if they named it the ‘Welsh Chimney’ or something,” he laughed.

It’s more than mock ego that drives him; he said he’s been fascinated by the stars since he was a child.  Now Barry Welsh’s camera may reveal the very fabric of space, and shine a light on the deepest of mysteries: What is the Universe all about?