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Observatory: Research at the Source of a Pennsylvania Flood
By HENRY FOUNTAIN, The New York Times, October 27, 2009
Like many people who come to Johnstown, Pa., Carrie Davis Todd, a hydrologist who was hired to teach at a local university a little over a year ago, was curious about the great Johnstown Flood of 1889, in which 2,209 people were killed when a dam failed 14 miles away. “One of the first things I did was go out and look at the dam site,” Dr. Davis Todd said.
The lake behind the dam held a huge volume of water that roared down the winding course of the Little Conemaugh River before slamming into Johnstown in one of the worst disasters in American history. While there were many witness accounts of the dam failure and the torrent of water that ensued, Dr. Davis Todd, an assistant professor of geology at the University of Pittsburgh at Johnstown, was surprised to find that the beginnings of the flood had never been rigorously assessed.
With three colleagues, Neil Coleman, Uldis Kaktins and Reed Myers, Dr. Davis Todd set out to rectify that situation. They surveyed the remains of the dam and the lake and stretches along the Little Conemaugh, examined historical photographs and modeled the flow of water through the breach and downstream.
Chief among their findings, which Dr. Davis Todd presented last week at a meeting of the Geological Society of America in Portland, Ore., was that the lake held about 23.5 million cubic yards of water, which at one point passed through the breach at nearly 11,800 cubic yards per second.
But the researchers found that the peak flow occurred about four miles downstream, where a stone railroad viaduct acted as a second dam, creating a huge temporary reservoir behind it. When the bridge collapsed, the water and debris headed toward Johnstown at a rate probably greater than 15,600 cubic yards per second - about equal, Dr. Davis Todd said, to the average flow of the Mississippi River.
Observatory: Two-Pound Dinosaur Holds North American Record
By HENRY FOUNTAIN, The New York Times, October 27, 2009
Small dinosaurs are big these days. Researchers recently announced the discovery of a tiny prototype of a Tyrannosaurus from China. Now paleontologists are reporting the smallest dinosaur ever found in North America.
The animal, Fruitadens haagarorum, had a body length of about 30 inches and weighed an estimated 2 pounds.
Fossils dating from the late Jurassic period were excavated in Colorado in the 1970s and kept at the Natural History Museum of Los Angeles County, where they have now been studied and described by Richard J. Butler, of the Bavarian State Collection for Paleontology in Germany, and colleagues.
Fruitadens is also the smallest ornithischian dinosaur ever found. Ornithischians, one of the two main groups of dinosaurs, generally ate plants, and “plant eaters require a fairly large gut,” said Luis M. Chiappe, director of the museum’s Dinosaur Institute and a co-author of a paper describing the finding in The Proceedings of the Royal Society B: Biological Sciences. The small size of Fruitadens and an absence of grinding wear on its teeth, Dr. Chiappe added, suggest it probably supplemented its diet with small animals and insects.
Fruitadens is one of a subgroup of ornithischians that survived for more than 100 million years. Dr. Chiappe said that dinosaur species became morphologically more specialized in evolution but that Fruitadens was “conventional and unspecialized.” That, he said, may be why the subgroup survived for so long: species like it were better able to adapt.
CT scan, left, of a female skull at a burial site at Ur. Women were buried with elaborate adornments, right, and warriors with their weapons.
At Ur, Ritual Deaths That Were Anything but Serene
By JOHN NOBLE WILFORD, The New York Times, October 27, 2009
A new examination of skulls from the royal cemetery at Ur, discovered in Iraq almost a century ago, appears to support a more grisly interpretation than before of human sacrifices associated with elite burials in ancient Mesopotamia, archaeologists say.
Palace attendants, as part of royal mortuary ritual, were not dosed with poison to meet a rather serene death. Instead, a sharp instrument, a pike perhaps, was driven into their heads.
Archaeologists at the University of Pennsylvania reached that conclusion after conducting the first CT scans of two skulls from the 4,500-year-old cemetery. The cemetery, with 16 tombs grand in construction and rich in gold and jewels, was discovered in the 1920s. A sensation in 20th century archaeology, it revealed the splendor at the height of the Mesopotamian civilization.
The recovery of about 2,000 burials attested to the practice of human sacrifice on a large scale. At or even before the demise of a king or queen, members of the court — handmaidens, warriors and others — were put to death. Their bodies were usually arranged neatly, the women in elaborate headdress, the warriors with weapons at their side.
C. Leonard Woolley, the English archaeologist who directed the excavations, a collaboration between Penn and the British Museum, eventually decided that the attendants had been marched down into burial chambers, where they drank poison and lay down to die. That became the conventional story.
Among the many human remains, only a few skulls were preserved, and those had been smashed into fragments — not in death but from the overburden of earth accumulating over the centuries to crush skulls flat as pancakes. That had frustrated earlier efforts to reconstruct the skulls.
In planning for a new exhibition of Ur artifacts, which opened Sunday at Penn’s Museum of Archaeology and Anthropology, Richard L. Zettler, the co-curator and a specialist in Mesopotamian archaeology, said researchers had taken CT scans of skull bones of a woman and a man. From those they obtained three-dimensional images of each fragment and so determined where the pieces fit.
The researchers, led by Janet M. Monge, a physical anthropologist at Penn, applied forensic skills to arrive at the probable cause of death in both cases.
There were two round holes in the soldier’s cranium and one in the woman’s, each about an inch in diameter. But the most convincing evidence, Dr. Monge said in an interview, were cracks radiating from the holes. Only if the holes were made in a living person would they have produced such a pattern of fractures along stress lines. The more brittle bones of a person long dead would shatter like glass, she explained.
Dr. Monge surmised that the holes were made by a sharp instrument and that death “by blunt-force trauma was almost immediate.”
Ritual killing associated with a royal death was practiced by other ancient cultures, archaeologists say, and raises a question: Why would anyone, knowing their probable fate, choose a life as a court attendant?
“It’s almost like mass murder and hard for us to understand,” Dr. Monge said. “But in the culture these were positions of great honor, and you lived well in the court, so it was a trade-off. Besides, the movement into the next world was not for them necessarily something to fear.”
Dr. Zettler said the new research also turned up evidence that the bodies of some victims had been heated, baked not burned, and treated with a compound of mercury. It was a primitive mummification process, not as advanced as techniques in contemporary Egypt.
“This was just to keep the bodies from decomposing during extensive funerary ceremonies,” he said.
On a brighter note, Dr. Zettler said the site of the ancient city-state Ur, near present-day Nasiriyah in Iraq, has been spared in the recent warfare that brought damage and looting to other ancient digs. Ur is protected within the perimeter of an air base, which was recently handed back to the Iraqis.
Basics: A Molecule of Motivation, Dopamine Excels at Its Task
By NATALIE ANGIER, The New York Times, October 27, 2009
If you’ve ever had a problem with rodents and woken up to find that mice had chewed their way through the Cheerios, the Famous Amos, three packages of Ramen noodles, and even that carton of baker’s yeast you had bought in a fit of “Ladies of the Canyon” wistfulness, you will appreciate just how freakish is the strain of laboratory mouse that lacks all motivation to eat.
The mouse is physically capable of eating. It still likes the taste of food. Put a kibble in its mouth, and it will chew and swallow, all the while wriggling its nose in apparent rodent satisfaction.
Yet left on its own, the mouse will not rouse itself for dinner. The mere thought of walking across the cage and lifting food pellets from the bowl fills it with overwhelming apathy. What is the point, really, of all this ingesting and excreting? Why bother? Days pass, the mouse doesn’t eat, it hardly moves, and within a couple of weeks, it has starved itself to death.
Behind the rodent’s fatal case of ennui is a severe deficit of dopamine, one of the essential signaling molecules in the brain. Dopamine has lately become quite fashionable, today’s “it” neurotransmitter, just as serotonin was “it” in the Prozac-laced ’90s.
People talk of getting their “dopamine rush” from chocolate, music, the stock market, the BlackBerry buzz on the thigh — anything that imparts a small, pleasurable thrill. Familiar agents of vice like cocaine, methamphetamine, alcohol and nicotine are known to stimulate the brain’s dopamine circuits, as do increasingly popular stimulants like Adderall and Ritalin.
In the communal imagination, dopamine is about rewards, and feeling good, and wanting to feel good again, and if you don’t watch out, you’ll be hooked, a slave to the pleasure lines cruising through your brain. Hey, why do you think they call it dopamine?
Yet as new research on dopamine-deficient mice and other studies reveal, the image of dopamine as our little Bacchus in the brain is misleading, just as was the previous caricature of serotonin as a neural happy face.
In the emerging view, discussed in part at the Society for Neuroscience meeting last week in Chicago, dopamine is less about pleasure and reward than about drive and motivation, about figuring out what you have to do to survive and then doing it. “When you can’t breathe, and you’re gasping for air, would you call that pleasurable?” said Nora D. Volkow, a dopamine researcher and director of the National Institute on Drug Abuse. “Or when you’re so hungry that you eat something disgusting, is that pleasurable?”
In both responses, Dr. Volkow said, the gasping for oxygen and the wolfing down of something you would ordinarily spurn, the dopamine pathways of the brain are at full throttle. “The whole brain is of one mindset,” she said. “The intense drive to get you out of a state of deprivation and keep you alive.”
Dopamine is also part of the brain’s salience filter, its get-a-load-of-this device. “You can’t pay attention to everything, but you want to be adept as an organism at recognizing things that are novel,” Dr. Volkow said. “You might not notice a fly in the room, but if that fly was fluorescent, your dopamine cells would fire.”
In addition, our dopamine-driven salience detector will focus on familiar objects that we have imbued with high value, both positive and negative: objects we want and objects we fear. If we love chocolate, our dopamine neurons will most likely start to fire at the sight of a pert little chocolate bean lying on the counter. But if we fear cockroaches, those same neurons may fire even harder when we notice that the “bean” has six legs. The pleasurable taste of chocolate per se, however, or the anxiety of cockroach phobia, may well be the handiwork of other signaling molecules, like opiates or stress hormones. Dopamine simply makes a relevant object almost impossible to ignore.
Should the brain want to ignore what it might otherwise notice, dopamine must be muzzled. Reporting recently in Nature Neuroscience, Regina M. Sullivan of New York University Medical Center, Gordon A. Barr of Children’s Hospital of Philadelphia and their colleagues found that, whereas rats older than 12 days would quickly develop an aversion to any odors that were paired with a mild electric shock, young rats would perversely show a preference for such odors if their mothers were nearby when the tutorial jolt was delivered. The researchers traced that infantile Candide spirit to a suppression of dopamine activity in the amygdala, where fear memories are born. Infant rats know their mother by smell, Dr. Sullivan explained, and they must not learn to avoid her, for even an abusive caretaker is better than none.
Large as its impact may be, dopamine is a compact molecule, built of 22 atoms, with the characteristic nitrogenous amine knob at one end. (Dopamine, by the way, takes its name from its chemical composition, and has nothing to do with the word dope — as in heroin or other recreational drugs — which is thought to derive from the Dutch term for stew.)
The dopamine production corps is tiny as well. Fewer than 1 percent of all neurons generate the neurotransmitter, most of them in midbrain structures like the substantia nigra, which helps control movement; it is the degradation of this population of dopamine cells that results in the tremors and other symptoms of Parkinson’s disease.
There is also dopamine activity higher up, in the prefrontal cortex parked right behind the forehead, that great executive brain where storylines are written, impulses controlled and excuses contrived. An impoverishment of prefrontal dopamine is thought to contribute to schizophrenia.
Wherever their station, brain cells respond to the release of dopamine through one or more of five distinct dopamine receptors poking up from their surface, proteins designed to lock onto dopamine and respond accordingly. Another key player is the dopamine transporter, a kind of janitor that picks up used dopamine molecules and sweeps them back into the cells where they were born. Recreational drugs like cocaine tend to block that transporter, allowing dopamine to linger in the neuronal vestibule and keep punching its signal along.
People differ from one another at every juncture of the dopamine matrix, in the tonal background pace at which their dopamine neurons rhythmically fire, the avidity with which the cells spike in response to need or news, and the ease with which hyperstimulated cells revert to baseline.
Some researchers have looked at genetic variations in receptor types for clues to personality differences. According to Dan T. A. Eisenberg of Northwestern University, scientists have detected a modest connection between a relatively elongated version of dopamine receptor No. 4 and a tendency toward impulsivity and risk-taking behavior, particularly financial risk-taking.
One can’t make too much of these preliminary correlations in behavioral genetics, but maybe before the next bailout, we should demand that bankers be tested for the presence of risky, long-form receptors. It’s the economy, dopamine.
Cancers Can Vanish Without Treatment, but How?
By GINA KOLATA, The New York Times, October 27, 2009
Call it the arrow of cancer. Like the arrow of time, it was supposed to point in one direction. Cancers grew and worsened.
But as a paper in The Journal of the American Medical Association noted last week, data from more than two decades of screening for breast and prostate cancer call that view into question. Besides finding tumors that would be lethal if left untreated, screening appears to be finding many small tumors that would not be a problem if they were left alone, undiscovered by screening. They were destined to stop growing on their own or shrink, or even, at least in the case of some breast cancers, disappear.
“The old view is that cancer is a linear process,” said Dr. Barnett Kramer, associate director for disease prevention at the National Institutes of Health. “A cell acquired a mutation, and little by little it acquired more and more mutations. Mutations are not supposed to revert spontaneously.”
So, Dr. Kramer said, the image was “an arrow that moved in one direction.” But now, he added, it is becoming increasingly clear that cancers require more than mutations to progress. They need the cooperation of surrounding cells and even, he said, “the whole organism, the person,” whose immune system or hormone levels, for example, can squelch or fuel a tumor.
Cancer, Dr. Kramer said, is a dynamic process.
It was a view that was hard for some cancer doctors and researchers to accept. But some of the skeptics have changed their minds and decided that, contrary as it seems to everything they had thought, cancers can disappear on their own.
“At the end of the day, I’m not sure how certain I am about this, but I do believe it,” said Dr. Robert M. Kaplan, the chairman of the department of health services at the School of Public Health at the University of California, Los Angeles, adding, “The weight of the evidence suggests that there is reason to believe.”
Disappearing tumors are well known in testicular cancer. Dr. Jonathan Epstein at Johns Hopkins says it does not happen often, but it happens.
A young man may have a lump in his testicle, but when doctors remove the organ all they find is a big scar. The tumor that was there is gone. Or, they see a large scar and a tiny tumor because more than 95 percent of the tumor had disappeared on its own by the time the testicle was removed.
Or a young man will show up with a big tumor near his kidney. Doctors realize that it started somewhere else, so they look for its origin. Then they discover a scar in the man’s testicle, the only remnant of the original cancer because no tumor is left.
Testicular cancer is unusual; most others do not disappear. But there is growing evidence that cancers can go backward or stop, and researchers are being forced to reassess their notions of what cancer is and how it develops.
Of course, cancers do not routinely go away, and no one is suggesting that patients avoid treatment because of such occasional occurrences.
“Biologically, it is a rare phenomenon to have an advanced cancer go into remission,” said Dr. Martin Gleave, a professor of urology at the University of British Columbia.
But knowing more about how tumors develop and sometimes reverse course might help doctors decide which tumors can be left alone and which need to be treated, something that is now not known in most cases.
Cancer cells and precancerous cells are so common that nearly everyone by middle age or old age is riddled with them, said Thea Tlsty, a professor of pathology at the University of California, San Francisco. That was discovered in autopsy studies of people who died of other causes, with no idea that they had cancer cells or precancerous cells. They did not have large tumors or symptoms of cancer. “The really interesting question,” Dr. Tlsty said, “is not so much why do we get cancer as why don’t we get cancer?”
The earlier a cell is in its path toward an aggressive cancer, researchers say, the more likely it is to reverse course. So, for example, cells that are early precursors of cervical cancer are likely to revert. One study found that 60 percent of precancerous cervical cells, found with Pap tests, revert to normal within a year; 90 percent revert within three years.
And the dynamic process of cancer development appears to be the reason that screening for breast cancer or prostate cancer finds huge numbers of early cancers without a corresponding decline in late stage cancers.
If every one of those early cancers were destined to turn into an advanced cancer, then the total number of cancers should be the same after screening is introduced, but the increase in early cancers should be balanced by a decrease in advanced cancers.
That has not happened with screening for breast and prostate cancer. So the hypothesis is that many early cancers go nowhere. And, with breast cancer, there is indirect evidence that some actually disappear.
It is harder to document disappearing prostate cancers; researchers say they doubt it happens. Instead, they say, it seems as if many cancers start to grow then stop or grow very slowly, as has been shown in studies like one now being done at Johns Hopkins. When men have small tumors with cells that do not look terribly deranged, doctors at Johns Hopkins offer them an option of “active surveillance.” They can forgo having their prostates removed or destroyed and be followed with biopsies. If their cancer progresses, they can then have their prostates removed.
Almost no one agrees to such a plan. “Most men want it out,” Dr. Epstein said. But, still, the researchers have found about 450 men in the past four or five years who chose active surveillance. By contrast, 1,000 a year have their prostates removed at Johns Hopkins. From following those men who chose not to be treated, the investigators discovered that only about 20 percent to 30 percent of those small tumors progressed. And many that did progress still did not look particularly dangerous, although once the cancers started to grow the men had their prostates removed.
In Canada, researchers are doing a similar study with small kidney cancers, among the few cancers that are reported to regress occasionally, even when far advanced.
That was documented in a study, led by Dr. Gleave that compared an experimental treatment with a placebo in people with kidney cancer that had spread throughout their bodies.
As many as 6 percent who received a placebo had tumors that shrank or remained stable. The same thing happened in those who received the therapy, leading the researchers to conclude that the treatment did not improve outcomes.
The big unknown is the natural history of many small kidney tumors, many of which are early kidney cancers. How often do small tumors progress? Do they ever disappear? Do they all need surgical excision? At what stage do most kidney cancers reach a point of no return?
These days, Dr. Gleave said, more patients are having ultrasound or CT scans for other reasons and learning that there is a small lump on one of their kidneys. In the United States, the accepted practice is to take those tumors out. But, he asks, “Is that always necessary?”
His university is participating in a countrywide study of people with small kidney tumors, asking what happens when those tumors are routinely examined, with scans, to see if they grow. About 80 percent do not change or actually regress over the next three years.
With early detection, he said, “our net has become so fine that we are pulling in small fish as well as big fish.” Now, he said, “we have to identify which small fish we can let go.”
