October 2009 – artdiamondblog.com

Google Does Good

Source of cartoon: online version of the NYT commentary quoted and cited below.

(p. A25) . . . the vast majority of books ever written are not accessible to anyone except the most tenacious researchers at premier academic libraries. Books written after 1923 quickly disappear into a literary black hole. With rare exceptions, one can buy them only for the small number of years they are in print. After that, they are found only in a vanishing number of libraries and used book stores. As the years pass, contracts get lost and forgotten, authors and publishers disappear, the rights holders become impossible to track down.

Inevitably, the few remaining copies of the books are left to deteriorate slowly or are lost to fires, floods and other disasters. While I was at Stanford in 1998, floods damaged or destroyed tens of thousands of books. Unfortunately, such events are not uncommon — a similar flood happened at Stanford just 20 years prior. You could read about it in The Stanford-Lockheed Meyer Library Flood Report, published in 1980, but this book itself is no longer available.
Because books are such an important part of the world’s collective knowledge and cultural heritage, Larry Page, the co-founder of Google, first proposed that we digitize all books a decade ago, when we were a fledgling startup. At the time, it was viewed as so ambitious and challenging a project that we were unable to attract anyone to work on it. But five years later, in 2004, Google Books (then called Google Print) was born, allowing users to search hundreds of thousands of books. Today, they number over 10 million and counting.
. . .
In the Insurance Year Book 1880-1881, which I found on Google Books, Cornelius Walford chronicles the destruction of dozens of libraries and millions of books, in the hope that such a record will “impress the necessity of something being done” to preserve them. The famous library at Alexandria burned three times, in 48 B.C., A.D. 273 and A.D. 640, as did the Library of Congress, where a fire in 1851 destroyed two-thirds of the collection.
I hope such destruction never happens again, but history would suggest otherwise. More important, even if our cultural heritage stays intact in the world’s foremost libraries, it is effectively lost if no one can access it easily. Many companies, libraries and organizations will play a role in saving and making available the works of the 20th century. Together, authors, publishers and Google are taking just one step toward this goal, but it’s an important step. Let’s not miss this opportunity.

For the full commentary, see:
SERGEY BRIN. “A Library to Last Forever.” The New York Times (Fri., October 9, 2009): A25.
(Note: ellipses added.)
(Note: the online version is dated October 8th.)

Samuel Johnson Saw Benefits of Free Markets

(p. A19) In “A Journey to the Western Islands of Scotland,” an account of his travels with James Boswell through the Hebrides in 1773, Johnson vividly described the desolation of a feudal land, untouched by commercial exuberance. He was struck by the utter hopelessness in a country where money was largely unknown, and the lack of basic material improvements–the windows, he noticed, did not operate on hinges, but had to be held up by hand, making the houses unbearably stuffy.

He was even more struck by the contrast between places where markets thrived and those where they didn’t. In Old Aberdeen, where “commerce was yet unstudied,” Johnson found nothing but decay, whereas New Aberdeen, which “has all the bustle of prosperous trade,” was beautiful, opulent, and promised to be “very lasting.”
Johnson also understood that what Smith would later call the division of labor was instrumental for human happiness and progress. “The Adventurer 67,” which he wrote in 1753 at the height of a commercial boom (and 23 years before Smith published “The Wealth of Nations”), delights in the sheer number of occupations available in a commercial capital like London.

For the full commentary, see:
ELIZA GRAY. “Samuel Johnson and the Virtue of Capitalism; The great 18th century writer on commerce and human happiness.” The Wall Street Journal (Fri., Sept. 11, 2009): A19.

Federal “Stimulus” Money Delays Omaha Road Work

“Work has been put on hold for this stretch of 132nd Street between Blondo Street and West Maple Road. Omaha officials say the stimulus funds will be worth the wait, but some nearby residents are upset about the slowdown.” Source of caption and photo: online version of the Omaha World-Herald article quoted and cited below.

We live near the still-two-lane stretch of 132nd pictured above, and were happy to read in the Omaha World-Herald early last spring that the city would be finishing the widening of 132nd, by widening the above stretch during the summer of 2009. As the summer progressed and widening did not, we became more and more puzzled.
Well, after you read the passages quoted below, you will ‘know the rest of the story’ as Paul Harvey used to say:

(p. 1A) The federal stimulus program, which was designed to accelerate roads projects around the country, instead put the brakes on widening a major Omaha thoroughfare.

The chance to grab $3.5 million in stimulus funds was worth delaying a widening project along 132nd Street between West Maple Road and Blondo Street, Omaha officials decided.
Work was supposed to begin last summer. Now the project between the Champions and Eagle Run golf courses won’t begin until next spring.
Preliminary work was begun in March, when utility lines were moved out of the way. Part of the street was closed for that work.
Area residents expected more crews to start work during the summer.
When nothing happened for months, a handful of residents in the nearby Sunridge neighborhood called the city. They com-(p. A2)plained that digging from the utility work was causing mud and rainwater to pool near the subdivision’s entrances off 132nd Street.
Resident Mary Ellen Pollard was surprised to find out that the widening work had been put on hold because of the stimulus program.
“I thought that stimulus package was for projects that were ready to go,” she said Monday. “If it was ready to go, why didn’t they proceed with it? . . . The barricades are up. Let’s go get it done.”
Plans change, public works officials said.
Meeting federal stimulus guidelines for environmental studies on the 132nd Street project, plus other planning and documentation requirements, took several months, City Engineer Charlie Krajicek said.
“We expected to have some work going this year, but it just didn’t work out,” he said.

For the full story, see:
Tom Shaw. “Stimulus slows 132nd St. work.” Omaha World-Herald (Tuesday October 6, 2009): 1A-2A.
(Note: the online version of the article is dated Weds., October 7 and has the slightly expanded title: “Stimulus Watch: Program slows 132nd St. work.”)
(Note: ellipsis in original.)

Source of map: online version of the Omaha World-Herald article quoted and cited above.

“A Man of Science Past Sixty Does More Harm than Good” (Unless His Name is “Avery”)

(p. 421) . . . , in 1928, Fred Griffith in Britain published a striking and puzzling finding. Earlier Griffith had discovered that all known types of pneumococci could exist with or without capsules. Virulent pneumococci had capsules; pneumococci without capsules could be easily destroyed by the immune system. Now he found something much stranger. He killed virulent pneumococci, ones surrounded by capsules, and injected them into mice. Since the bacteria were dead, all the mice survived. He also injected living pneumococci that had no capsules, that were not virulent. Again the mice lived. Their immune systems devoured the unencapsulated pneumococci. But then he injected dead pneumococci surrounded by capsules and living pneumococci without capsules.
The mice died. Somehow the living pneumococci had acquired cap-(p. 422)sules. Somehow they had changed. And, when isolated from the mice, they continued to grow with the capsule–as if they had inherited it.
Griffith’s report seemed to make meaningless years of Avery’s work– and life. The immune system was based on specificity. Avery believed that the capsule was key to that specificity. But if the pneumococcus could change, that seemed to undermine everything Avery believed and thought he had proved. For months he dismissed Griffith’s work as unsound. But Avery’s despair seemed overwhelming. He left the laboratory for six months, suffering from Graves’ disease, a disease likely related to stress. By the time he returned, Michael Dawson, a junior colleague he had asked to check Griffith’s results, had confirmed them. Avery had to accept them.
His work now turned in a different direction. He had to understand how one kind of pneumococcus was transformed into another. He was now almost sixty years old. Thomas Huxley said, “A man of science past sixty does more harm than good.” But now, more than ever, Avery focused on his task.

Source:
Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.
(Note: ellipsis added.)
(Note: italics in original.)

Fossil Found of Much Earlier Human Ancestor

Source of graphic: online version of the NYT article quoted and cited below.

(p. A1) Ardi, short for Ardipithecus ramidus, is the newest fossil skeleton out of Africa to take its place in the gallery of human origins. At an age of 4.4 million years, it lived well before and was much more primitive than the famous 3.2-million-year-old Lucy, of the species Australopithecus afarensis.

Since finding fragments of the older hominid in 1992, an international team of scientists has been searching for more specimens and on Thursday presented a fairly complete skeleton and their first full analysis. By replacing Lucy as the earliest known skeleton from the human branch of the primate family tree, the scientists said, Ardi opened a window to “the early evolutionary steps that our ancestors took after we diverged from our common ancestor with chimpanzees.”
. . .
(p. A6) Scientists not involved in the new research hailed its importance, placing the Ardi skeleton on a pedestal alongside notable figures of hominid evolution like Lucy and the 1.6-million-year-old Turkana Boy from Kenya, an almost complete specimen of Homo erectus with anatomy remarkably similar to modern Homo sapiens.
David Pilbeam, a professor of human evolution at Harvard University who had no role in the discovery, said in an e-mail message that the Ardi skeleton represented “a genus plausibly ancestral to Australopithecus” and began “to fill in the temporal and structural ‘space’ between the apelike common ancestor and Australopithecus.”
Andrew Hill, a paleoanthropologist at Yale University who was also not involved in the research, noted that Dr. White had kept “this skeleton in his closet for the last 15 years or so, but I think it has been worth the wait.” In some ways the specimen’s features are surprising, Dr. Hill added, “but it makes a very satisfactory animal for understanding the changes that have taken place along the human lineage.”
The first comprehensive reports describing the skeleton and related findings, the result of 17 years of study, are being published Friday in the journal Science. Eleven papers by 47 authors from 10 countries describe the analysis of more than 110 Ardipithecus specimens from a minimum of 36 different individuals, including Ardi.
The paleoanthropologists wrote in one of the articles that Ardipithecus was “so rife with anatomical surprises that no one could have imagined it without direct fossil evidence.”
A bounty of animal and plant material — “every seed, every piece of fossil wood, every scrap of bone,” Dr. White said — was gathered to set the scene of the cooler, more humid woodland habitat in which these hominids had lived.
This was one of the first surprises, said Giday WoldeGabriel, a geologist at Los Alamos National Laboratory, because it upset the hypothesis that upright walking had evolved as an adaptation to life on grassy savanna.

For the full story, see:
JOHN NOBLE WILFORD. “Fossil Skeleton From Africa Predates Lucy.” The New York Times (Fri., October 1, 2009): A1 & A6.
(Note: ellipsis added.)

“A fairly complete skeleton of Ardipithecus ramidus, which replaced Lucy as the earliest known skeleton from the human branch of the primate family tree.” Source of caption and photo: online version of the NYT article quoted and cited above.

Health Care Incentives and Information Improve When Patients Are Payers

Nobel Prize winning economist Vernon Smith sees that the current health care system is an incentive and information “nightmare.” The third parties, who pay, have neither the incentive nor the information to reward the providers who do a good job. And patients, who have the information, do not have the power or incentives to reward those who do a good job. And since providers are not being rewarded for doing a good job, they will only avoid becoming cynical bureaucrats as long as they are mission-driven saints.
A better system, that goes a long way toward Smith’s “solution,” has been suggested by Susan Feigenbaum, who suggests that third parties provide payments directly to patients, who then may choose what services to buy from which providers.
Here is the core of Smith’s analysis:

(p. A11) The health-care provider, A, is in the position of recommending to the patient, B, what B should buy from A. A third party–the insurance company or the government–is paying A for it.

This structure defines an incentive nightmare.
. . .

I don’t know whether this problem has a solution. If it does, I think it requires us to find mechanisms whereby third-party payment is made to the patient, B, who in turn pays A, supplemented with any co-payment from B for services. Hence, from the moment B seeks services from A both know who is going to be paying A for what is delivered. A and B each has need for what the other brings to the table, and this structure carries the potential for nurturing the relationship between A and B. B is empowered to become better informed about the services recommended by various A’s that he might choose among, and the A’s might find it particularly important to build good reputations with B’s.

For the full commentary, see:
VERNON L. SMITH. “The ABC Dilemma of Health Reform; Third-party payment creates a big incentive problem.” The Wall Street Journal (Sat., OCTOBER 16, 2009): A11.
(Note: ellipsis added.)

Feigenbaum’s prescient suggestion for reform can be found in:
Feigenbaum, Susan. “Body Shop’ Economics: What’s Good for Our Cars May Be Good for Our Health.” Regulation 15, no. 4 (Fall 1992): 26-27.

Harvard Medical School Conference on the Quest for Eternal Life

“AGE WELL. David Sinclair, left, and Christoph Westphal, co-founders of Sitris Pharmaceuticals, in Dr. Sinclair’s laboratory in Cambrdge, Mass. The company develops drugs that mimic resveratrol, a chemical found in some red wines.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. D4) BOSTON — Who would have thought it? The quest for eternal life, or at least prolonged youthfulness, has now migrated from the outer fringes of alternative medicine to the halls of Harvard Medical School.

At a conference on aging held here last week, the medical school’s dean, Jeffrey Flier, was to be seen greeting participants who ranged from members of the 120 club (they intend to live at least that long) to devotees of very low calorie diets.
. . .

Dr. Gallagher said that unpublished tests in mice showed that another chemical mimic, SRT-1720, increased both health and lifespan; after two years, twice as many mice taking the drug were alive compared with the undosed animals. Resveratrol itself has not been shown to increase lifespan in normal mice, although it does so in obese mice, laboratory roundworms and flies.
Sirtris has so far been doubly fortunate. No severe side effects have yet emerged from the clinical trials. The company has also been lucky in having apparently picked the right horse, or at least a good one, in a fast-developing field.
Besides the sirtuins, several other proteins are now known to influence longevity, energy use and the response to caloric restriction. These include the receptors for insulin and for another hormone called IGF-1, and a protein of increasing interest called TOR (“target of rapamycin”). Rapamycin is an antimicrobial that was recently found to extend lifespan significantly, even when given to mice at an advanced age. Since TOR is involved in the response to caloric restriction, rapamycin may extend life through this pathway.
. . .

“In five or six or seven years,” said Christoph Westphal, Sirtris’s other co-founder, “there will be drugs that prolong longevity.”
But neither Dr. Sinclair nor Dr. Westphal was the most optimistic person at the conference. That status belonged to the English gerontologist Aubrey de Grey, who sports a beard so luxuriant that it is hard to see if he is wearing a tie. His goal is “negligible senescence.”
. . .

Sirtris’s quest for longevity drugs is founded on solid and promising research. But most drugs fail at some stage during trials. So there is no guarantee that any of Sirtris’s candidate compounds will work in people. The first result from a Phase 2 clinical trial is not expected until the end of next year at the earliest.
Meanwhile, it is a pleasant and not wholly unfounded thought that, just possibly, a single drug might combat every degenerative disease of Western civilization.

For the full story, see:
NICHOLAS WADE. “Quest for a Long Life Gains Scientific Respect.” The New York Times (Tues., September 28, 2009): D4.
(Note: ellipses added.)

Rapid Mutation of RNA-Based Flu Virus Allows Rapid Adaptation to Immune System Response

I found the passage quoted below to be especially illuminating on how rapid mutation helps explain why the flu virus is so successful and dangerous. (An additional important factor is that the virus can survive in birds, without killing them.)
It occurs to me that something akin to rapid mutation (e.g., rapid experimentation) has also been advocated as a way to quickly advance science (Karl Popper), or enterprise (George Gilder).

(p. 105) Whenever an organism reproduces, its genes try to make exact copies of themselves. But sometimes mistakes–mutations–occur in this process.

This is true whether the genes belong to people, plants, or viruses. The more advanced the organism, however, the more mechanisms exist to prevent mutations. A person mutates at a much slower rate than bacteria, bacteria mutates at a much slower rate than a virus–and a DNA virus mutates at a much slower rate than an RNA virus.
DNA has a kind of built-in proofreading mechanism to cut down on copying mistakes. RNA has no proofreading mechanism whatsoever, no way to protect against mutation. So viruses that use RNA to carry their genetic information mutate much faster–from 10,000 to 1 million times faster–than any DNA virus.
Different RNA viruses mutate at different rates as well. A few mutate so rapidly that virologists consider them not so much a population of copies of the same virus as what they call a “quasi species” or a “mutant swarm.”
These mutant swarms contain trillions and trillions of closely related but different viruses. Even the viruses produced from a single cell will include many different versions of themselves, and the swarm as a whole will routinely contain almost every possible permutation of its genetic code.
Most of these mutations interfere with the functioning of the virus and will either destroy the virus outright or destroy its ability to infect. But other mutations, sometimes in a single base, a single letter, in its genetic code will allow the virus to adapt rapidly to a new situation. It is this adaptability that explains why these quasi species, these mutant swarms, can move rapidly back and forth between different environments and also develop extraordinarily rapid drug resistance. As one investigator has observed, the rapid mutation “confers a certain randomness to the disease processes that accompany RNA [viral] infections.”
Influenza is an RNA virus. So is HIV and the coronavirus. And of all RNA viruses, influenza and HIV are among those that mutate the fastest. The influenza virus mutates so fast that 99 percent of the 100,000 to 1 million new viruses that burst out of a cell in the reproduction process (p. 106) are too defective to infect another cell and reproduce again. But that still leaves between 1,000 and 10,000 viruses that can infect another cell.
Both influenza and HIV fit the concept of a quasi species, of a mutant swarm. In both, a drug-resistant mutation can emerge within days. And the influenza virus reproduces rapidly–far faster than HIV. Therefore it adapts rapidly as well, often too rapidly for the immune system to respond.

Source:
Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.
(Note: italics in original.)

Measuring High Level Entrepreneurship

The Measurement Center of the Fraser Institute held a contest on the theme of what most needed to be better measured. I entered the contest, arguing that high level entrepreneurs are crucial to economic growth and human progress, and yet are not often the subject of systematic (as contrasted with anecdotal) study.
It turns out that my one minute video submission was picked as one of four “runners-up” in the contest.

Details of the contest and the winners, can be found at:
http://www.fraserinstitute.org/programsandinitiatives/measurement_center.htm
My minute video can be viewed at:
http://www.fraserinstitute.org/files/videos/Motivation-characteristics-of-high-level-entrepreneurs.wmv

George Shultz Sceptical of War on Drugs

George Shultz has a distinguished résumé. He was Dean of the University of Chicago business school, Secretary of the Treasury under President Nixon, and Secretary of State under President Reagan. Along with the late Milton Friedman, he is sceptical about the War on Drugs, and is willing to express his scepticism:

(p. A17) He has long harbored skepticism about interdiction as a solution to drug abuse in the U.S. Those doubts were prescient.
. . .
Mr. Shultz recalls what happened shortly after he left government, when his view that interdiction is not the solution came up after a speech to a Stanford alumni group.
Then, as now, he believed that we need to look at the problem from an economic perspective and understand what happens when there is high demand for a prohibited substance. When his comment hit the press, he says he “was inundated with letters. Ninety-eight percent of them agreed with me and over half of those people said I’m glad you said it, but I wouldn’t dare say it. The most poignant comment was from [a former member of the House of Representatives] who wrote and said I was glad to see your statement. I said that a few years ago and that’s why I’m no longer a congressman!”

For the full commentary, see:
MARY ANASTASIA O’GRADY. “George Shultz on the Drug War; The former secretary of state has long doubted the wisdom of interdiction.” The Wall Street Journal (Mon., OCTOBER 12, 2009): A17.
(Note: the online version of the article is dated Oct. 11, 2009.)
(Note: ellipsis added.)

Small Evidence Kills Big Theory

Big Tyrannosaurus rex and much smaller Raptorex kriegsteini. Source of image: http://scienceblogs.com/notrocketscience/upload/2009/09/raptorex_tiny_king_of_thieves_shows_how_tyrannosaurus_body_p/Raptorex_Trex.jpg

(p. A5) Paleontologists said Thursday that they had discovered what amounted to a miniature prototype of Tyrannosaurus rex, complete with the oversize head, powerful jaws, long legs — and, as every schoolchild knows, puny arms — that were hallmarks of the king of the dinosaurs.

But this scaled-down version, which was about nine feet long and weighed only 150 pounds, lived 125 million years ago, about 35 million years before giant Tyrannosaurs roamed the earth. So the discovery calls into question theories about the evolution of T. rex, which was about five times longer and almost 100 times heavier.
“The thought was these signature Tyrannosaur features evolved as a consequence of large body size,” Stephen L. Brusatte of the American Museum of National History, an author of a paper describing the dinosaur published online by the journal Science, said at a news conference. “They needed to modify their entire skeleton so they could function as a predator at such colossal size.”
The new dinosaur, named Raptorex kriegsteini, “really throws a wrench into this observed pattern,” Mr. Brusatte said.

For the full story, see:
HENRY FOUNTAIN. “Fossil Discovery Challenges Theories on T. Rex Evolution.” The New York Times (Fri., September 18, 2009): A5.
(Note: the online version is dated Sept. 17th and has the slightly different title: “Fossil Find Challenges Theories on T. Rex” but the body of the article seems the same as the print version.)