Researchers at the University of Rochester Medical Center in New York gave teriparatide (Forteo) to 145 people who had bone fractures that had not healed, many for six months or more. They found that 93 percent of them showed significant healing and pain control after eight to 12 weeks.

Teriparatide speeds the healing of fractures by changing the behavior and number of cartilage and bone stem cells involved in the healing process, the researchers found.

"The decreased healing time is significant, especially when fractures are in hard-to-heal areas like the pelvis and the spine, where you can’t easily immobilize the bone — and stop the pain," Dr. Susan V. Bukata, medical director of the university’s Center for Bone Health, said in a news release from the center.

"Typically, a pelvic fracture will take months to heal, and people are in extreme pain for the first eight to 12 weeks," she said. "This time was more than cut in half. We saw complete pain relief, callus formation and stability of the fracture in people who had fractures that up to that point had not healed."

Based on the findings, the news release said, the U.S. National Institutes of Health has funded a clinical trial of the drug’s use on fractures. The study will include men and post-menopausal women older than 50 who have what’s called a low-energy pelvic fracture and who are admitted to the emergency department of Strong Memorial Hospital in Rochester.

Participants in the study will be given either teriparatide or a placebo and will be followed for 16 weeks to measure fracture healing in a number of ways, including pain levels, microscopic bone growth determined through CT scans and functional testing of bone strength.

Teriparatide was approved by the U.S. Food and Drug Administration in 2002 as a treatment for osteoporosis.

If clinical trials prove that the drug speeds bone healing, it could prove especially important for older adults, who suffer the majority of broken bones that heal slowly.

"In many people, as they get older, their skeleton loses the ability to heal fractures and repair itself," J. Edward Puzas, head of orthopedic bone research at the medical center and the lead investigator for the clinical trial, said in the news release. "With careful application of teriparatide, we believe we’ve found a way to turn back the clock on fracture healing through a simple, in-body stem cell therapy."

Bracing and immobilization cannot be used for the approximately 60,000 Americans who suffer a pelvic fracture each year.

"It takes three to four months for a typical pelvis fracture to heal," Bukata said. "But, during those three months, patients can be in excruciating pain, because there are no medical devices or other treatments that can provide relief to the patient."

"Imagine if we can give patients a way to cut the time of their pain and immobility in half?" she said.

Speeding the healing time for pelvic fractures could also reduce the risk of death and medical costs.

Pelvic fractures carry the same risk of death as hip fractures. About "one-quarter of all older women with pelvic fractures will die from complications," Bukata said. "And during that year of recovery, a patient typically puts a greater strain on our health-care system, not to mention their pain and suffering."

Slow-Healing Bones May Get Boost From Drug – Health Updates

An independent committee monitoring the study recommended halting it after concluding that patients on Sutent stayed free of disease progression for longer than those on placebo plus best supportive care.

The patients in the study had advanced pancreatic islet cell tumors, a rare cancer with limited treatment options, according to Pfizer.

Sutent is currently approved for treating both advanced renal cell carcinoma and gastrointestinal stromal tumors.

Pfizer Cancer Drug Shows Benefits, Shares Rise

The technique, which leaves healthy cells unaffected, could potentially offer hope to people with hard-to-treat cancers where surgery is not possible.

Although it has only been tested in mice so far, the researchers hope for human trials in two years.

The UK study is published online by the journal Cancer Research.

The genes were wrapped up in microscopic nano-particles which were taken up by cancer cells, but not their healthy neighbours.

Once inside, the genes stimulated production of a protein which destroys the cancer.

The researchers say the technology could potentially be particularly relevant for people with cancers that are inoperable because they are close to vital organs.

They hope it will eventually also be used to treat cancer that has spread.

‘Exciting step’

Lead researcher Dr Andreas Schatzlein, from the School of Pharmacy in London, said: “Gene therapy has a great potential to create safe and effective cancer treatments but getting the genes into cancer cells remains one of the big challenges in this area.

“This is the first time that nanoparticles have been shown to target tumours in such a selective way, and this is an exciting step forward in the field.

“Once inside the cell, the gene enclosed in the particle recognises the cancerous environment and switches on. The result is toxic, but only to the offending cells, leaving healthy tissue unaffected.

“We hope this therapy will be used to treat cancer patients in clinical trials in a couple of years.”

Traditional chemotherapy indiscriminately kills cells in the affected area of the body, which can cause side effects like fatigue, hair loss or nausea.

It is hoped that gene therapy will have fewer associated side effects by targeting cancer cells.

Dr Lesley Walker, of the charity Cancer Research UK, said: “These results are encouraging, and we look forward to seeing if this method can be used to treat cancer in people.

“Gene therapy is an exciting area of research, but targeting genetic changes to cancer cells has been a major challenge.

“This is the first time a solution has been proposed, so it’s exciting news.”

Nano-treatment to torpedo cancer

The hippocampus is widely known to be integral to memory, but researchers say they now see just how images are stored and recalled in this part of the brain.

Wellcome Trust scientists trained four participants to recognise several virtual reality environments.

Discernible patterns in brain activity then signalled where they were, they wrote in the journal Current Biology.

Neurons in the hippocampus, also known as “place cells”, activate when we move around to tell us where we are.

The team, based at University College London, then used specialised scanning equipment which measures changes in blood flow in the brain.

This allowed them to examine the activity of these cells as the participants – all young men with experience of playing videogames – moved around the virtual reality environment. The data was then passed through a computer.

“We asked whether we could see any interesting patterns in the neural activity that could tell us what the participants were thinking, or in this case where they were,” said Professor Eleanor Maguire.

Are you lying?

“Surprisingly, just by looking at the brain data we could predict exactly where they were in the virtual reality environment. In other words we could ‘read’ their spatial memories.”

“By looking at activity over tens of thousands of neurons, we can see that there must be a functional structure – a pattern – to how these memories are encoded.”

But they stressed that the prospect of genuinely reading someone’s most intimate thoughts – or working out if they were lying – was still a long way off.

Their participants were all willing subjects who allowed their brains to be trained and monitoring to take place.

“It would be very easy not to co-operate, and then it wouldn’t work,” said Demis Hassabis, who developed the computer programme to read the data. “These kind of scenarios would require a great technological leap.”

It is brain diseases such as Alzheimer’s which could stand to benefit from such research.

“Understanding how we learn and store memories could aid our understanding of conditions in which memory is compromised and potentially help patients in the rehabilitation process,” said Professor Maguire.

Professor Clive Ballard, director of research at the Alzheimer’s Society, said: “This exciting development will boost our understanding of the hippocampus, a key area affected in Alzheimer’s disease and the most important part of the brain for memory.

“Learning more about how the brain works could help us work out which types of nerve cells are lost in Alzheimer’s.”

Rebecca Wood, of the Alzheimer’s Research Trust, said the research was “fascinating”.

She said: “Understanding how memories are formed may help researchers discover how this process goes wrong in diseases like Alzheimer’s.”

A step closer to reading the mind

The $278 million Orbiting Carbon Observatory was designed to monitor how CO2 enters and exits the Earth’s atmosphere — hoping to yield a picture of a rhythm that is much like taking a breath. Forests and oceans absorb the greenhouse gas from the atmosphere, while burning fossil fuels and decaying plant and animal life send more back.

There is a delicate balance between the two processes that shifts with seasons and weather patterns — plants, for example, pull in more CO2 in spring than in winter, when many lose their leaves.

But while scientists have a basic understanding of the carbon cycle, they can’t account for all the CO2 humans produce, said Scott Denning, a professor at Colorado State University who worked on the NASA project’s science team. “The basic idea is that between the oceans and the land, about half of the fossil-fuel carbon dioxide is being taken up and not going into the air,” he said. “We need to understand that better to predict what’s going to happen in the future.”

The crash yesterday morning of NASA’s carbon observatory is going to make getting those answers more difficult, scientists said.

Airplanes, weather balloons and ground-monitoring stations can measure how much CO2 is in the air at certain points, but they can’t cover the whole globe like a satellite would. The Orbiting Carbon Observatory, for example, was designed to collect 8 million measurements every day for at least two years.

Using only measurements of CO2 levels taken from the Earth’s surface is like trying to map New York City by standing in the middle of Manhattan, said Paul Wennberg, a professor at the California Institute of Technology who operates a series of ground-based measuring stations. “You get an idea there are streets and buildings, but it’s very hard to imagine what the broader image looks like,” he said. “What [satellites] do is provide that context.”

Scientists look to Japan

Many scientists who worked with NASA are now hoping to use data from a carbon-monitoring satellite, GOSAT, that Japan’s space agency launched last month.

Take Steven Wofsy of Harvard University, a lead scientist with HIPPO, a recently launched five-year project that uses airplanes to fly pole to pole, gathering information about how much CO2 they encounter along their journeys.

“HIPPO provides a cross-section of the atmosphere,” Wofsy said. “The idea was to use that to help ensure [data from] the satellite was consistent with data being acquired at ground stations.”

With the crash of the NASA satellite yesterday, Wofsy’s team hopes to collaborate with the Japanese GOSAT scientists.

“It’s not as if we’re without anything to do,” he said. “But now it’s, ‘Uh-oh, we need to figure out what to do next.’ We didn’t make contingency plans for failure.”

Loss of the U.S. satellite comes at a time when many recent scientific studies have suggested that the world’s oceans and forests are losing their ability to absorb CO2, said Scott Doney, a senior scientist at the Woods Hole Oceanographic Institution. Doney called the crash yesterday “a substantial setback.”

“There have been some studies in the North Atlantic and the Southern Ocean that suggest the ocean is becoming a less effective ‘sink,’” he said.

It also comes as world leaders prepare to negotiate a successor to the Kyoto Protocol.

“In the long run, satellites will provide the information we need to evaluate how much fossil fuel CO2 we’re actually emitting,” Doney said. That information would form the basis for any international agreement. Satellite can also help monitor the effectiveness of policies to cut greenhouse gas emissions.

‘Something was terribly wrong’

Agency officials said yesterday that it appears the fairing, a nose cone that shields the satellite as it travels through Earth’s atmosphere, did not detach from the satellite the way it was supposed to.

That left the satellite carrying extra weight that prevented it from reaching orbit. It likely crashed into the ocean near Antarctica minutes later, said John Brunschwyler of Orbital Sciences, which manufactures the Taurus XL rocket used in yesterday’s aborted launch.

“Certainly, for the scientific community, it’s a huge disappointment,” he said. “It’s taken so long to get here.”

Ross Salawitch of the University of Maryland, a founding member of the carbon observatory’s science team, offered a sober firsthand account of the launch on his Web site. Many of the scientists who had traveled to Vandenberg Air Force Base to watch the launch did not realize it had failed until they returned to their hotel 45 minutes later, he wrote.

“When I walked into the hotel lobby, it was clear from the blank look on several hundred people’s faces that something was terribly wrong,” Salawitch said. “Those of us in the hotel had no contact with our friends and colleagues inside mission control … about 40 of us lingered in the hotel lobby for about 2.5 hrs, from 2:30 a.m. until 5:00 a.m., to watch the press conference on a few laptops.”

Michael Freilich, director of NASA’s Earth science programs, said it was too soon to tell whether the agency would seek to rebuild the carbon observatory.

“OCO was an important mission to measure critical elements of the carbon cycle,” he told reporters yesterday morning. “Over the next several days, weeks and months we are going to carefully evaluate how to move forward and advance the science.”

Convening a ‘mishap board’ and looking for new sources of money

That will include looking at instruments already in orbit, which could be modified to collect more information about CO2 in the atmosphere, or seeking access to measurements collected by Japan’s CO2-measuring satellite, GOSAT. There may also be “flight spares” for the carbon observatory, Freilich said.

NASA is putting together a “mishap board” to investigate why the launch failed, said launch manager Charles Dovale.

But ultimately, the agency’s decision to rebuild or replace the observatory likely hinges on whether it can use money from the recent economic stimulus bill, which included $400 million for climate research at NASA, or whether Congress would be willing to include money for the project in upcoming spending legislation.

On Monday, House Democrats introduced an omnibus spending bill for fiscal year 2009 that includes $260 million in new funding for climate science programs, including satellite programs at NASA and the National Oceanic and Atmospheric Administration.

Meanwhile, the fiscal year 2010 spending cycle kicks off tomorrow, when President Obama is set to release his first budget request to Congress.

Scientists Mull Future After Carbon Satellite Crash – Science and Technology

Although the battery-powered derailleur by Shimano promises to bring ease and accuracy to changing gears by enabling riders to shift with a light touch to two electronic switches, traditionalists worry that it may erode the basic tenets of the sport.

“People choose bicycles precisely because a bicycle’s motion requires only human effort, and nothing could be more simple, independent and autonomous,” Raymond Henry, a cycling historian in St. Etienne, France, wrote in an e-mail message. “Any source of external energy, however weak, runs counter to this philosophy.”

Whether the gear system becomes the next iPod and redefines bicycle technology or ends up as the sport’s version of the eight-track tape will hinge on a number of factors, the most obvious being performance, reliability and cost.

Two earlier attempts at electronic gear changing by a French company, Mavic, often malfunctioned in rain. Another company, Campagnolo, has delayed bringing its version to market because of the economic downturn.

Shimano’s version, known as the Dura-Ace Di2 7970, is being used by three professional teams competing in California: Columbia High Road, Garmin Slipstream and Rabobank. About 10 riders will race with the system even though they have used it on only one or two training rides after receiving them late this week.

Bob Stapleton, the owner and general manager of Columbia, said many of his riders had doubts about using bicycles that could literally run out of power. The Di2 system has no manual override if its battery goes dead. That event can be an irritation or a disaster, depending on the terrain and what gear ratio the bike is stuck in. Shimano estimates the battery will last for about 1,000 miles per charge.

“Their careers can be made on the results from one race,” Stapleton said of his riders. “So they prize reliability over everything.”

Stapleton, an experienced amateur cyclist, has used the Di2 system extensively and is a convert.

“I think every high-end bike within three years will have this, maybe sooner,” he said, adding that the system also eliminates much of the maintenance required by mechanical systems.

A full set of components with electronic gears will cost about $1,250 more than the newest mechanical version, which sells for about $2,750. Upgrading an existing Shimano system is expected to cost about $2,200. The system will fit onto nearly all racing bicycles.

Later this year, Giant, the largest bicycle manufacturer in the world, will offer a bike designed to use only electronic parts for about $14,000, which includes the cost of Di2. If consumers fancy the device, it will likely follow the pattern of other new electronics and drop significantly in price over time.

Electronic gear-shifting technology has spent a long time in development. Prototypes of Mavic’s first system, the Zap, made a cameo appearance at the 1992 Tour de France and the company introduced its second attempt, the Mektronic, in 1999.

For much of this decade, both Shimano, which dominates bicycle parts the way Microsoft dominates computer software, and its venerable Italian competitor Campagnolo occasionally tested prototype systems on the bikes of pro riders. More often than not, the prototypes were devoid of trademarks, presumably to limit embarrassment if results proved as unfortunate as the Zap.

The Campagnolo and Shimano systems share the basic design of current mechanical derailleurs. That is, a parallelogram that moves the chain back and forth and, in the rear, two spring-loaded wheels to keep the chain taut.

Two paddle-shaped electronic switches that sit behind the brake lever allow riders to shift gears. Tapping either paddle lightly in Di2 sends an electronic signal through a wire to a small motor inside the derailleur, moving the body and thus the chain by turning a worm gear. Even Devin Walton, a spokesman for Shimano, acknowledges that when it comes to the rear derailleur, there is little or no difference in shifting between the electronic and comparable mechanical offerings from the company.

The gains are move obvious, however, with the front derailleur, which moves the chain between the two large, toothed rings on the bicycle’s crank.

Cycling Enters Electronic Age With Gear-Shifting System

He couldn’t avoid it forever, of course. He eventually wrote another tome nearly as famous, “The Descent of Man.” But he knew in 1859, when “Species” was published, that to jump right into a description of how human beings had tussled with the environment and one another over eons, changing their appearance, capabilities and behavior in the process, would be hard for people to accept.

Better to stick with birds and barnacles.

Darwin was born 200 years ago this week. “On the Origin of Species” will be 150 years old in a few months. There’s no such reluctance now.

The search for signs of natural selection in human beings has just begun. It will ultimately be as revelatory as Newton’s description of the mathematics of motion 322 years ago, or the unlocking of the atom’s secrets that began in the late 1800s.

The inundation of data since the completion of the Human Genome Project in 2003, and the capacity to analyze it at the finest level of detail — the individual DNA nucleotides that make up the molecule of heredity — are giving us a look at humanity’s autobiography in a way that was once unimaginable.

In small, discrete changes in our genes that have accumulated over time, we are seeing evolution’s tracery, as durable as it is delicate. It is slowly revealing how climate, geography, disease, culture and chance sculpted Homo sapiens into the unique and diverse species it is today.

Biologists are discovering that the size of our limbs and brains, the enzymes in our spit and stomachs, the color of our skin, the contour of our hair, and the armament of our immune systems are each to some degree the products of evolutionary adaptation. They are the hard-earned, but unintended, bequests of our ancestors’ struggle to survive.

This, of course, is no surprise. Darwin knew it was so — and he’d never heard of a gene.

The surprise is our capacity to see the mechanical changes — for genes are nothing more than little machines operating in water — that are evolution’s working material. Natural selection has moved beyond metaphor. We can see the thing itself.

“Why are we the way we are? That has always been a sort of fundamental question, hasn’t it? But it is only now that we can really begin to address it,” said Carlos Bustamante, a professor of computational biology at Cornell University. “Over the ages we catalogued the anatomical differences between people and eventually biochemical differences, too. Now we can get down to the molecular differences. We really mean it this time.”

Understanding which of our 25,000 genes have changed since we climbed out of the trees may have practical results as well. Many of mankind’s most common health problems — hypertension, diabetes and obesity are examples — may partly be consequences of natural selection that occurred long ago, in a world far different from today’s. Identifying which genes have undergone the most rapid evolution, and then figuring out what they do, may shed important light on these ailments.

Out of this research may come one other tantalizing insight: How, if at all, are we still evolving?

Promising Leads, Few Complete Answers

At the moment, though, there are a lot more promising leads than mysteries solved.

More than 300 human genes show strong evidence of recent mutations that favored survival in the face of new threats or novel environments, and consequently spread quickly through populations. For only a few, however, have researchers nailed down the full story of what the mutations did and how they helped our ancestors.

“We are really just beginning to see the landscape of human evolution. We’re working toward a coherent picture of how we evolved over time,” said Pardis Christine Sabeti, an evolutionary biologist at Harvard University.

Some of that landscape is visible on a map of the world. Many of the differences in appearance and physiology between ethnic groups are products of natural selection that occurred eons ago in the geographic regions those groups still inhabit.

Natural selection, of course, didn’t begin just when human ancestors and chimpanzees diverged 6 million years ago and we became our own, distinct lineage. Much of what makes us special (at least in our own eyes) was already underway.

Take our brains.

The marvelous things they can do — and the use of language is right at the top of the list — didn’t leap fully formed from a profoundly inferior predecessor. Instead, our brains are the result of small structural changes, some more important than others, accumulating since deep in evolutionary time. That appears to be the case of a gene called FOXP2.

When a mutation occurs in that gene in people (a rare event), they lose the ability to make sense of language and to produce coherent speech. When the gene is knocked out in birds, their songs are incomplete and inaccurate. In bats, it seems to be involved in echolocation.

Across many species, the gene appears to play a role in processing sound and using the information to perform an action — making an intelligible grunt, singing the right song or avoiding a collision with a cave wall. And it turns out that human beings have two mutations in the FOXP2 gene that chimpanzees don’t. What do they mean for the functioning of our brain cells? Nobody knows, but the betting is: something that may be key to humans’ unique capacity for language.

Curiously, sometimes evolution lurches forward when a gene stops working. Making room in our skulls for our outsize brains may have been helped by such an occurrence.

Humans have completely lost the function of a gene called MYH16. It’s still there, but scientists can tell from the DNA sequence that it underwent a “frameshift mutation” and no longer works.

MYH16 codes for a protein that is a component of some muscles. In chimpanzees and other primates, it is active only in muscles of the head, especially ones used for chewing. Some scientists speculate that the mutation that disabled the gene freed our skulls of the physical constraints required to anchor large, powerful jaw muscles. That, in turn, may have helped make room for the brain’s rapid enlargement.

Brain size itself appears to be controlled by at least four other genes; mutations in them cause microcephaly, a birth defect characterized by a small head and mental retardation. These genes have been changing more rapidly in primates than in rodents, and the pace of that evolution has been especially fast in humans and chimps. That’s no surprise; they’re smart and we’re smarter.

Beneficial Traits Spread

It takes time for a mutation that produces an advantageous genetic trait to sweep through a population. How quickly that occurs depends, in part, on how big an advantage the change provides.

With many traits — big brains, upright posture, scant body hair, color vision — the advantage is so great that the DNA sequence for them reaches what geneticists call fixation. Everyone has it.

But fixation isn’t always the endpoint. A gene-altering mutation can sweep through one population but remain virtually absent in another. That’s because all that’s required for a mutation to spread is for it to improve its carriers’ chance of surviving and reproducing under their current circumstances. And circumstances are not the same for all people and can change over time.

That was certainly the case 2,000 generations ago, when groups of modern humans began to leave Africa and settle nearly every corner of a geographically, climatically and botanically diverse planet. Their genes changed as a result of their journeys, and the genes of people who stayed in Africa continued to evolve, too, as life there changed.

All of this occurred by chance, and the result is the world of human diversity we see today.

“Evolution in a pure Darwinian world has no goal or purpose,” biologist Edward O. Wilson wrote in the introduction to a collection of Darwin’s writings a few years ago.

In other words, evolution is not like an arrow shot at a target, but like a blind dog stumbling across an obstacle-strewn landscape. This is what caused Darwin to shy away from talking about evolution and mankind in the same breath, at least at the beginning. It is still the heresy that quickens the creationist’s pulse.

The current conservative estimate is that 10 percent of our genome has undergone “positive selection” since modern humans emerged about 200,000 years ago. Not surprisingly, the changes that tell the clearest stories involve basic needs — food, protection from the elements, resistance to disease.

The adaptation to malaria is the best and oldest example.

Children and pregnant women are at highest risk of dying from malaria (and about 900,000 still do each year). Any mutation that protects victims from early deaths and lets them reproduce will spread widely, because the survivors are more likely to carry it — and therefore pass it on to their descendants.

Over the past 10,000 years, such protective mutations have arisen and been “naturally selected” not once, but several times. They emerged in places where malaria was endemic — West Africa, Southern Africa, the Middle East — and took hold independently of one another.

So great was their value that they became widespread, even though they can cause problems of their own — sickle cell anemia, thalassemia and G6PD deficiency, diseases most prevalent in places where malaria was a scourge.

Matching Skin Tone to Sunlight

Non-living threats have also exerted heavy pressure on our genes over the eons. Sunlight is the most obvious one.

Several mutations that lighten skin swept through the out-of-Africa migrants, though different populations have different “suites” of altered pigment genes. That probably explains why fairness in Europeans often extends to hair color, while in Asians it almost never does.

Curiously, the reason sunlight is such a driving force isn’t entirely clear.

Too much sun can burn the skin and damage folate, a vitamin essential to fertility and embryo growth. Too little blocks formation of Vitamin D, which is crucial for absorbing the calcium necessary for bones and muscle. Whatever the reason, having the right skin color for one’s home latitude has clearly been a huge evolutionary task.

Of course, it’s possible it could have happened by chance.

The random death of individuals carrying some genes and the chance survival of people bearing others — called genetic drift — has also shaped our genomes, most biologists believe. But the fact that so many mutations affecting skin color occurred in non-African populations and went to fixation (or close) makes chance an unlikely explanation.

“A big thing that makes you think this is natural selection is when you see ‘convergent evolution’ — different mutations with the exact same biological function,” said Sabeti, the Harvard geneticist. “Lightning strikes once, but it doesn’t often strike twice.”

Researchers are now showing that culture — what humans have created — also can drive natural selection with as much force as disease and the environment.

The ability to digest milk in adulthood, called lactase persistence, exists in more than 90 percent of Scandinavians but only 1 percent of Chinese. It is much more common in places where cattle, goat and camel herding are common — and milk is a big part of the diet — than in populations (such as hunter-gatherers) where herding is more rare.

Most Europeans have a mutation in the lactase gene that allows them to digest milk as adults. But it is virtually absent in Africans, many of whom can also drink milk.

In 2006, scientists found three previously unknown lactase mutations that swept through East African herding cultures in the past 5,000 years, long after the European one emerged.

“The reason for the advantage is not entirely clear,” said Sarah Tishkoff, a geneticist at the University of Pennsylvania who made the discovery. “It could be the protein in the milk; it could be the fat; it could be that it’s a source of water in an arid region — or none of the above.”

Are Humans Still Evolving?

Which brings us to the question: In a world of intensive-care units, vitamin pills, sunscreen, down jackets and (for many) too much food, has evolution ground to a halt? Or will global warming, urban crowding, HIV infection, the obesity and diabetes epidemics, and the galloping changes in technology crank it up again?

The answer seems to be: Nobody knows. But something is probably still happening.

“I definitely think people will come under new pressures,” said Eugene Harris, a biological anthropologist at Queensborough Community College in New York. “There are going to be micro-evolutionary adjustments that occur over time. Culture is imperfect and is not going to buffer all of us.”

But Bustamante, the computational biologist from Cornell, cautions that it takes 200 generations for natural selection to show its hand — and that’s when it’s working full tilt.

“What is going to happen in 200 generations? I don’t think we have any mathematical models to answer that,” he said.

Darwin, like evolution, took his time. He is the patron saint of dawdlers.

He got off the HMS Beagle, the ship that took him on the trip that taught him almost everything, on Oct. 2, 1836. He then spent 22 years in study, experiment and cogitation — capped with the equivalent of an all-nighter — to come up with his theory. He crashed it into print in a dead heat with Alfred Russel Wallace, a young man in a hurry, presenting it on the night of July 1, 1858, before the Linnean Society of London.

The truth is that even 200 years from today, on Darwin’s 400th birthday, when we’re all dead, our descendants still won’t have a clue as to what the traits just now starting to evolve may be.

Evolution moves slowly, and it grinds exceeding small. Darwin knew this, and wouldn’t be surprised.

Scientists begin to decode the history of human evolution