A NEW FILM TELLS THE STORY OF HOW THE GREAT SCIENTIST TRANSFORMED THE FIELD OF COSMOLOGY WHILE FIGHTING A DEGENERATIVE DISEASE.
Stephen Hawking is one of the greatest scientists ever–comparable to Darwin, Einstein, and Newton. Yet few people know the story of his life. In a new biopic, The Theory of Everything, Oscar-winning director James Marsh examines the challenges Hawking endured as he transformed the field of cosmology while fighting a degenerative motor neuron disease. Ahead of the November 7 premiere, we looked back at Hawking’s greatest achievements and talked to Marsh about working with a true Popular Science hero.
Hawking’s Greatest Achievements
Defining and Redefining Black Holes
In 1974, Hawking presented a radical theory: Black holes actually emit energy, bleeding what would later be called “Hawking radiation.” This seemingly minor point reconciled key aspects of classical and quantum physics and changed the way in which scientists see the universe.
Analyzing The Beginning of Time and Space
In collaboration with James Hartle, Hawking proposed in 1983 that the universe has no physical boundaries. Traveling its length would be a wraparound trip, similar to circumnavigating the globe. This mathematical model of the early universe also suggested that time, too, could exhibit a wraparound effect despite its finite beginning.
With the 1988 release of his cosmology primer, A Brief History of Time, Hawking became a global publishing phenom, eventually selling 10 million copies in 40 languages. The book introduced readers to the physics of black holes and the Big Bang, as well as Hawking’s major theories.
Director James Marsh On…
“It’s like meeting the Queen, or meeting God,” says Marsh. “You don’t quite know what you should be saying, or how you should be saying it, or what kind of answer you need to wait for.”
The movie’s biggest eureka moment features Hawking stuck while putting on a sweater–a predicament that inspired Hawking radiation theory. “We modeled the scene exactly on that breakthrough, which [his ex-wife] acted out for me in the room where it happened,” Marsh says.
After seeing a rough cut of the movie, Hawking volunteered his unique voice software. “It made a big difference,” Marsh says. “The film was just better with the real voice. It has a music to it. It has more emotion, oddly enough, than the voice that we managed to create for ourselves.”
Warning: SPOILER ALERT! This infographic contains details about the new space film “Interstellar.”
The film “Interstellar” relies on real science for many of its stunning visuals. Physicist Kip Thorne, an expert on black holes and wormholes, provided the math that the special effects artists turned into movie magic.
The spaceship Endurance’s destination is Gargantua, a fictional supermassive black hole with a mass 100 million times that of the sun. It lies 10 billion light-years from Earth and is orbited by several planets. Gargantua rotates at an astounding 99.8 percent of the speed of light.
Gargantua’s accretion disc contains gas and dust with the temperature of the surface of the sun. The disc provides light and heat to Gargantua’s planets.
The black hole’s complex appearance in the film is due to the image of the accretion disc being warped by gravitational lensing into two images: one looping over the black hole and the other under it.
One feature of Einstein’s equations is that time passes slower in higher gravity fields. So on a planet orbiting close to a black hole, a clock ticks much more slowly than on a spaceship orbiting farther away.
Our three-dimensional universe can be thought of as a flat membrane (or “brane”) floating in a four-dimensional void called the “Bulk.” The presence of mass distorts the membrane as if it were a rubber sheet.
If enough mass is concentrated at a point, a singularity is formed. Objects approaching the singularity pass through an event horizon from which they can never return. If two singularities in far-apart locations could be merged, a wormhole tunnel through the Bulk could be formed. Such wormholes cannot form naturally, however.
Beings able to control gravity and travel through the Bulk could create wormholes and cross space much faster than light.
In two-dimensional diagrams, the wormhole mouth is shown as a circle. Seen in person, a wormhole would be a sphere. A gravitationally distorted view of space on the other side can be seen on the sphere’s surface.
The film’s wormhole is 1.25 miles (2 kilometers) in diameter and 10 billion light-years long.
As if having a heart attack isn’t bad enough, cardiologists know that the worst damage may actually occur after it’s over.
Blocked arteries are typically the trigger, stopping the flow of blood and starving the heart muscle of oxygen. But when the blockage is removed and the blood comes rushing back, it wreaks havoc of its own. The result is called reperfusion injury, a life-threatening flood of inflammation and cellular destruction that has stumped scientists for 40 years.
Now, however, a potentially groundbreaking study by Fred Hutchinson Cancer Research Center scientists, published online today in the journal PLOS ONE, suggests that the worst effects of reperfusion injury may be prevented with a safe, simple solution: a dose of iodide, a chemical form of the element added to ordinary table salt.
“If this turns out to be positive, it could transform medicine and the leading cause of death in the Western world,” said Mark B. Roth, Ph.D., the Fred Hutch cell biologist whose lab came up with the new technique.
When mice with induced heart attacks were given intravenous infusions of sodium iodide five minutes before reperfusion, it reduced myocardial infarction, or MI, damage by as much as 75 percent. And when mice were given sodium iodide in their drinking water for two days before the procedure, they showed similar significant protection against the damage.
That’s the latest finding from Roth, the 2007 MacArthur Foundation “genius” grant recipient best known for his work using hydrogen sulfide to induce a state of reversible suspended animation in mice and other model organisms. The ultimate goal of Roth’s research in metabolic flexibility is to reduce the need for oxygen and potentially buy time for trauma patients before they can get definitive care.
The technique is still a long way from being used in the 720,000 Americans who suffer heart attacks annually, or in helping the 600,000 in the U.S. who die of heart disease – the top cause of death – each year. The extent of harm from reperfusion injury in humans is hard to estimate, but in animal models, it may account for up to a third of the damage from a heart attack.
But if the protective effect of the iodide infusions and oral iodide shown in mice is borne out in other animal models – and, eventually, in people – it could eventually change how doctors treat heart attacks and conduct cardiac-bypass procedures.
“If this works in other animals as effectively as it does in our own hands, I would guarantee you that it would be a big deal,” Roth said.
And that’s not just Roth talking.
Rakesh Kukreja, Ph.D., a member of the operations committee of CAESAR, the National Institutes of Health’s Cardioprotection Consortium, said he was “very impressed” with Roth’s findings.
“It’s truly incredible, in my opinion,” said Kukreja, who is also director of the molecular cardiology program at Virginia Commonwealth University.
The study by Roth and his laboratory associates, Akiko Iwata, Ph.D., and Mike Morrison, Ph.D., provided a thoroughly researched and documented potential solution to the longstanding paradox of reperfusion injury, Kukreja said.
“Even today, after 40 years of research and spending billions of dollars of NIH money, there’s no accepted method of reducing infarct size,” he said, referring to the area of cardiac muscle tissue damage caused by a heart attack.
“These mouse studies are very, very encouraging.”
In addition to confirming the effect of iodide on reperfusion in other preclinical models, scientists need to nail down exactly how the element works. In their paper, Roth and colleagues suggested that iodide might function via thyroid hormone.
” … The benefit of iodide may be conferred by depressing thyroid hormone production and as a result decreasing cardiac metabolism that is linked to reperfusion injury,” the authors wrote.
In contrast, they found that iodide didn’t have the same protective effect in mice with depleted thyroid function.
The U.S. government’s Defense Advanced Research Projects Agency, or DARPA, funded the study. Heart attacks are such a significant public health problem that federal officials have supported Roth’s research into the area, which started him thinking about using elemental reducing agents to prevent reperfusion injury.
Iwata and Morrison tested the procedure on dozens of mice during the past two and a half years. Iwata, an expert in animal models of human injuries, said even she was taken aback by the findings.
“It’s surprising,” she said.
Roth and Morrison said there are other elemental reducing agents such as iodide in what they call the “southeast corner of the Periodic Table” that can reduce reperfusion-injury damage. These include sulfide, bromide and selenide.
But only iodide boasts a superior safety profile. Even in large quantities, iodide is very safe, they noted. And it’s already approved for human ingestion – and widely available. “You can buy it on Amazon right now,” Roth noted.
No one can say at this point how soon the iodide could – or would – proceed to trials in humans. Roth cautioned that it’s far too early for people with heart problems to start popping iodide before surgery.
Roth said the Seattle biotech company he started, Faraday Pharmaceuticals, is moving the work forward. With further research, the promise of dramatically reducing reperfusion injury in people could become a reality, he added.
“I think this is well worth exploring further,” he said. “I am as encouraged as anyone could be.”
Your joints, including those in your knuckles, are surrounded by a membrane called the synovial membrane, which forms a capsule around the ends of your bones. Inside this membrane is synovial fluid, which acts as a lubricant and shock absorber so your bones don’t grind together when you move.
Cracking your knuckles is not linked to an increased risk of arthritis
Habitual knuckle cracking has been linked to hand swelling, lower grip strength, knuckle pads, and injuries, including dislocated fingers, and overstretched ligaments
Some experience a “therapeutic release” upon cracking their knuckles, but the potential for damage outweighs any perceived psychological benefit
When you “crack” your knuckles, or any other joint, it expands the space between your bones, creating negative pressure that draws synovial fluid into the new gap.
This influx of synovial fluid is what causes the popping sound and feeling when you crack a knuckle.1 If you continually crack your knuckles, the synovial membrane and the surrounding ligaments will loosen, making it easier and easier for your joints to crack.
More than 20 years ago, I co-authored a paper titled “Cracking down on neck cracking,” which was published in the journal American Family Physician.2 In it, I argued that self-manipulation may lead to lax ligaments. Personally, I don’t think it’s wise to crack your joints on a regular basis, and research suggests it could have some significant repercussions.
Is Cracking Your Knuckles Associated with Arthritis?
The biggest concern most people have about cracking their knuckles is that it could lead to arthritis, specifically osteoarthritis. If you have osteoarthritis, the cartilage within your joints is progressively being damaged, and the synovial fluid is typically reduced as well.
The pain and joint stiffness that you feel is a result of your bones starting to come into contact with each other as cartilage and synovial fluid diminishes. To date, research has not shown a correlation between knuckle cracking and osteoarthritis in your hands.
In one study of more than 200 people, the prevalence of osteoarthritis in any joint was similar among those who cracked knuckles and those who did not.3The same held true when specific joint types were examined. The authors stated:
“Total past duration (in years) and volume (daily frequency x years) of knuckle-cracking (KC) of each joint type also was not significantly correlated with OA [osteoarthritis] at the respective joint. A history of habitual KC – including the total duration and total cumulative exposure ‘does not seem to be a risk factor for hand OA.'”
If you’re interested in lowering your risk of osteoarthritis, it is typically caused by wear-and-tear on your joints along with lifestyle and diet factors, and aging. Repetitive movements often play a role as well, but while it would seem plausible that cracking your joints is also a type of repetitive movement, so far no link has emerged.
Habitual Knuckle Cracking Might Impair Your Hand Function
While cracking your knuckles might not lead to arthritis, it does appear to have other consequences. In a study of 300 people aged 45 and older, habitual knuckle crackers were again not found to have an increased risk of arthritis in their hands. They were, however, more likely to have hand swelling and lower grip strength.4
They also found that knuckle cracking appears to be associated with manual labor, nail biting, smoking, and drinking alcohol… they concluded that habitual knuckle cracking results in functional hand impairment. The damage was likely the result of the repeated stretching and loosening of the ligaments during repeated knuckle cracking.
Interestingly, those researchers noted that cracking your knuckles has been shown to produce “rapid release of energy in the form of sudden vibratory energy, much like the forces responsible for the destruction of hydraulic blades and ship propellers.” This hardly sounds like a completely innocuous habit.
In fact, there are reports in the literature of various injuries that have occurred from knuckle cracking, including overstretching of ligaments in the fingers, dislocated fingers, and a partially torn ligament in the thumb.5
Knuckle Cracking Might Be Linked to Knuckle Pads
Knuckle pads are firm nodules that sometimes form over certain joints in your fingers. They’re often associated with repetitive trauma or movement, and they’ve been known to exist since ancient times (Michelangelo’s statue of David has knuckle pads).6
Knuckle pads are quite common and while they don’t cause physical symptoms, they can have psychological and cosmetic effects. It seems that knuckle cracking may play a role in at least certain cases of this condition.
There is at least one reported case of knuckle pads in a teenaged girl who reported frequently cracking her knuckles daily. In her case, the nodules slowly enlarged over the course of several years, and cracking of the knuckles was listed as the possible cause.7
Are There Benefits to Cracking Your Knuckles?
When you crack your knuckles, the joints become looser and have more mobility for a short period afterward. This perceived positive feeling may be why some people become habitual knuckle crackers.
Another explanation, as reported by one study, is that the movement offers a sort of “therapeutic release.” Chronic knuckle crackers may come to regard the habit as a form of stress relief, although it resembles more of a “nervous habit” like biting your nails (which it is associated with).
Ultimately, there are no significant benefits to cracking your knuckles, and a possibility that it could cause injury or damage to your joints and ligaments over time, so this is one habit that you’re better off without.
If you crack your knuckles and find it difficult to stop, I suggest you to try theEmotional Freedom Technique (EFT). EFT is a powerful self-help method that is very effective for regular stress management as well as for breaking all kinds of addictions, including knuckle cracking. Once the emotional distress is reduced or removed, your body can often rebalance itself and accelerate healing.
Specifically, EFT is a form of psychological acupressure, based on the same energy meridians used in traditional acupuncture to treat physical and emotional ailments for over five thousand years, but without the invasiveness of needles.
Instead, simple tapping with your fingertips is used to input kinetic energy into specific meridians on your head and chest while you think about your specific problem — whether it is a traumatic event, an addiction, pain, etc. – and voice positive affirmations.
This combination of tapping the energy meridians and voicing positive affirmation works to clear the “short-circuit” — the emotional block — from your body’s bioenergy system, thus restoring your mind and body’s balance, which is essential for optimal emotional health and the healing of physical disease.
A 30-year-old graduate student presented with fevers associated with shaking chills and severe headaches. He had been well until 1 week before presentation, when he began to have daily fevers, with temperatures as high as 39.4°C. Any fever in a patient who has had possible exposure to malaria should prompt consideration of this diagnosis.
•What is the annual incidence of malaria in the United States?
In the United States, the annual incidence of malaria is approximately 1500 cases. In 2010, a total of 1691 cases were reported to the Centers for Disease Control and Prevention (CDC), the largest number reported since 1980; P. falciparum, P. vivax, P. malariae, and P. ovale were identified in 58%, 19%, 2%, and 2% of cases, respectively.
•How do malaria and babesiosis differ in appearance on a peripheral blood smear?
Intraerythrocytic parasites are seen in both malaria and babesiosis. Plasmodia metabolize heme to form an intracellular crystallized pigment, hemozoin. Although hemozoin is not invariably identified in cases of malaria, its presence reliably distinguishes malaria infection from babesia infection. Malaria parasites can be distinguished from B. [Babesia] microti by the presence of recognizable gametocytes (characteristically banana-shaped in Plasmodium falciparum and round, with a granular appearance, in nonfalciparum species). In addition, intracellular vacuoles and extracellular merozoites are unusual in malaria but common in babesiosis, and the classic “Maltese cross” (a tetrad of parasites budding at right angles) is unique to babesia species. Morning Report Questions
Q: Which malaria species can remain dormant in the liver?
A: In the case of P. vivax and P. ovale, some sporozoites (immature malaria parasites) do not replicate immediately when they invade hepatocytes but remain dormant (as hypnozoites) for prolonged periods. The average time to relapse is approximately 9 months, but it can range from weeks to years. The interval to relapse depends on the strain (earlier with tropical strains and later with temperate strains), the initial inoculum, and host factors (e.g., febrile illnesses can trigger relapse associated with P. vivax). None of the commonly used prophylactic agents (chloroquine, mefloquine, doxycycline, or atovaquone-proguanil) eliminate hypnozoites. Primaquine, the only effective drug against dormant hypnozoites, has not been approved by the Food and Drug Administration for primary prophylaxis, but the CDC endorses its use for prophylaxis in Latin American countries where P. vivax predominates, because the drug can prevent both primary attacks and relapses caused by all species that are a source of malarial infection.
Q:How is acute or recurrent P. vivax infection treated?
A: In patients with acute or recurrent malaria infection, treatment depends on the species and the resistance status in the area where the infection was acquired. P. falciparum is resistant to chloroquine in most regions in which it is endemic and resistant to mefloquine in parts of Southeast Asia. In contrast, nonfalciparum malaria parasites do not have substantial resistance to mefloquine, and the distribution of chloroquine-resistant P. vivax malaria is limited, occurring primarily in Indonesia and Papua New Guinea. After treatment is initiated, peripheral-blood smears should be obtained daily for 4 days (parasitemia is typically eliminated by day 4), on days 7 and 28 to confirm eradication, and at any time symptoms recur, suggesting treatment failure. In areas other than those with known chloroquine resistance, chloroquine, followed by a 14-day course of primaquine to prevent subsequent relapses, remains the standard treatment for P. vivax parasitemia. Given the risk of hemolysis in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who receive treatment with primaquine, potential recipients should be tested for G6PD deficiency. Among patients with a contraindication to primaquine therapy, treatment with chloroquine alone carries a 20% risk of relapse; extended chloroquine prophylaxis can be offered to patients who have frequent relapses.
New research conducted at the University of Alabama at Birmingham has shown that the common blood pressure drug verapamil completely reverses diabetes in animal models. Now, thanks to a three-year, $2.1 million grant from the JDRF, UAB researchers will begin conducting a potentially groundbreaking clinical trial in 2015 to see if it can do the same in humans.
The trial, known as “the repurposing of verapamil as a beta cell survival therapy in type 1 diabetes,” is scheduled to begin early next year and has come to fruition after more than a decade of research efforts in UAB’s Comprehensive Diabetes Center.
The trial will test an approach different from any current diabetes treatment by focusing on promoting specialized cells in the pancreas called beta cells, which produce insulin the body needs to control blood sugar. UAB scientists have proved through years of research that high blood sugar causes the body to overproduce a protein called TXNIP, which is increased within the beta cells in response to diabetes, but had never previously been known to be important in beta cell biology. Too much TXNIP in the pancreatic beta cells leads to their deaths and thwarts the body’s efforts to produce insulin, thereby contributing to the progression of diabetes.
But UAB scientists have also uncovered that the drug verapamil, which is widely used to treat high blood pressure, irregular heartbeat and migraine headaches, can lower TXNIP levels in these beta cells—to the point that, when mouse models with established diabetes and blood sugars above 300 milligrams per deciliter were treated with verapamil, the disease was eradicated.
“We have previously shown that verapamil can prevent diabetes and even reverse the disease in mouse models and reduce TXNIP in human islet beta cells, suggesting that it may have beneficial effects in humans as well,” said Anath Shalev, M.D., director of UAB’s Comprehensive Diabetes Center and principal investigator of the verapamil clinical trial. “That is a proof-of-concept that, by lowering TXNIP, even in the context of the worst diabetes, we have beneficial effects. And all of this addresses the main underlying cause of the disease—beta cell loss. Our current approach attempts to target this loss by promoting the patient’s own beta cell mass and insulin production. There is currently no treatment available that targets diabetes in this way.”
The trial will enroll 52 people between the ages of 19 and 45 within three months of receiving a diagnosis of type 1 diabetes. Patients enrolled will be randomized to receive verapamil or a placebo for one year while continuing with their insulin pump therapy. In addition, they will receive a continuous glucose monitoring system that will enable them to measure their blood sugar 24 hours a day, seven days a week.
Fernando Ovalle, M.D., director of UAB’s Comprehensive Diabetes Clinic and co-principal investigator of the study, helped develop the clinical trial and will oversee all clinical aspects of the trial, including subject recruitment, treatment, testing, and data acquisition and analysis. Recruitment for the trial will begin in early 2015.
“Currently, we can prescribe external insulin and other medications to lower blood sugar; but we have no way to stop the destruction of beta cells, and the disease continues to get worse,” Ovalle said. “If verapamil works in humans, it would be a truly revolutionary development in a disease affecting more people each year to the tune of billions of dollars annually.”
Diabetes, which is the nation’s seventh-leading cause of death, raises risks for heart attacks, blindness, kidney disease and limb amputation. Recent federal government statistics show that 12.3 percent of Americans 20 and older have diabetes, either diagnosed or undiagnosed. Another 37 percent have pre-diabetes, a condition marked by higher-than-normal blood sugar. That is up from 27 percent a decade ago.
While a new report in the Journal of the American Medical Association showed rates at which new cases are accumulating have slowed in recent years, the numbers remain high and are still increasing overall, with 8.3 percent of adults diagnosed with the disease as of 2012. And no slowing of the disease has been seen in new cases among blacks and Hispanics or in overall rates among people with high school educations or less.
Plus, the annual cost to treat the disease is exorbitant—and rising. The American Diabetes Association reports that the disease cost the nation $245 billion in 2013.
Shalev says replacing this beta cell mass by transplantation has proved more difficult and problematic than initially thought, but creating an environment that would enable beta cells to survive and possibly regenerate or become functional again does provide an attractive alternative by increasing the body’s own beta cell mass. UAB lab studies have shown verapamil to be extremely effective in this area, which has helped to make this clinical trial—funded by the JDRF, the largest charitable supporter of type 1 diabetes research—a possibility now.
JDRF is funding this study as part of its beta cell restoration research program whose goal is to restore a person’s ability to produce their own insulin—in essence, a biological cure for type 1 diabetes.
“A first step towards that goal may be the ability to improve the survival and functioning of a person’s beta cells shortly after diagnosis,” said JDRF director of Discovery Research, Andrew Rakeman, Ph.D. “This study represents the result of years of investment in basic research at JDRF. We are now at the stage of translating basic laboratory research into potential significant new therapies for type 1 diabetes and we’re excited to support Dr. Shalev’s team to test this concept in a study of people with type 1 diabetes. Finding a therapy to improve beta cell survival and functioning would put JDRF’s efforts to find a cure on a new trajectory.”
Ovalle will manage all patients with the use of insulin pumps and continuous glucose sensors and co-manage patients who are already seeing another endocrinologist remotely. UAB’s clinic team will analyze patients’ blood sugar control and their ability to produce insulin. They will also use a more complex test known as c-peptide response as a way to measure beta cell insulin production and functional beta cell mass.
One of the truly unique and different aspects of this clinical trial is that, unlike most type 1 diabetes trials, the verapamil trial does not include the use of any immunosuppressive or immune modulatory medications, which often have very severe side effects.
“This trial is based on a well-known blood pressure medication that has been used for more than 30 years and is unlikely to have any severe side effects,” Shalev said. “This study is also backed by a lot of strong mechanistic data in different mouse models and human islets, and we already know the mechanisms by which verapamil acts. Finally, unlike any currently available diabetes treatment, the trial targets the patient’s own natural beta cell mass and insulin production.”
A first step
Shalev says the trial is a first step in the direction of such a novel diabetes treatment approach.
“While in a best-case scenario, the patients would have an increase in beta cells to the point that they produce enough insulin and no longer require any insulin injections—thereby representing a total cure—this is extremely unlikely to happen in the current trial, especially given its short duration of only one year,” Shalev said.
Shalev expects verapamil to have a much more subtle yet extremely important effect.
“We know from previous large clinical studies that even a small amount of the patient’s own remaining beta cell mass has major beneficial outcomes and reduces complications,” Shalev said. “That’s probably because even a little bit of our body’s own beta cells can respond much more adequately to very fine fluctuations in our blood sugar—much more than we can ever do with injections or even sophisticated insulin pumps.”
Because verapamil’s mode of action is different from current drugs or interventions, this opens up an entirely new field for diabetes drug discovery—one that UAB’s Comprehensive Diabetes Center is already engaged in with the Alabama Drug Discovery Alliance, a partnership between UAB’s School of Medicine and Southern Research Institute. The group is actively looking for small therapeutic molecules that inhibit TXNIP to protect the beta cells and treat diabetes.
“We want to find new drugs—different from any current diabetes treatments—that can help halt the growing, worldwide epidemic of diabetes and improve the lives of those affected by this disease,” Shalev said. “Finally, we have reason to believe that we are on the right track.”
One of the biggest gambles in space history comes to a climax on Wednesday when Europe attempts to make the first-ever landing on a comet.
Speeding towards the Sun at 65,000 kilometres (40,600 miles) per hour, a lab called Philae will detach from its mothership Rosetta, heading for a deep-space rendezvous laden with risk.
The 100-kilogram (220-pound) probe will seek out a minuscule landing site on the treacherous surface of an object darker than coal, half a billion kilometres (300 million miles) from home.
“It’s not going to be an easy business,” was the understated prediction of Philippe Gaudon of France’s National Centre for Space (CNES) as the mission prepared to enter countdown mode.
But when Rosetta finally caught up with it in August, it witnessed a sight that caused despondency back on Earth.
Far from being a simple potato shape, “67P” turned out be two gnarled lobes about four km across joined by a narrow neck.
It looked like an super-dark rubber duck, ravaged by aeons in orbit, turning slowly in space.
Its surface was a nightmare of crests and gullies, studded with hundreds of rocks as high as 50 metres (165 feet) and wicked slopes with an incline greater than 30 degrees.
This was a huge, unexpected problem, said Francis Rocard, a French astrophysicist.
“It took a billion calculations to find a decent landing site”—one offering a fair chance that Philae could survive and meet scientific goals, he said.
If final “go/no-go” assessments give the green light, Philae will separate from Rosetta about 20 kilometres (12 miles) from the comet at 0835 GMT on Wednesday.
“Then it’s a very gentle freefall for the next seven hours,” said Sylvain Lodiot, in charge of flight operations.
After that comes the hard bit.
No one knows what a comet’s surface is like.
Is it hard and crusty, like a shell? Crumbly? Slippery? Is it brittle—will it crack, causing Philae to sink into some fudgy or spongey substance below?
Seeking to cover all the possibilities, Philae’s designers have equipped the lander with three outstretched legs designed to dampen the impact.
When the lab touches down, it will fire two harpoons to secure it to what—hopefully—will be a robust surface, while a thruster on top of the lander will fire to cancel out bounce. Ice screws in the lander feet will deploy for extra grip.
The chances of success? “Seventy percent,” said Gaudon, admitting to days of doubt that the chances were much better than one in two.
“We need to be lucky,” added Andrea Accomazzo, flight director.
And only then can Philae start its real mission of analysing the makeup of the comet.
Batteries will be enough to keep the probe going for 60 hours, but recharging from sunlight “could keep us going until March,” said Rocard.
Stage set for comet drama
The stage is set for the most dramatic scene yet in the epic voyage of Europe’s space probe Rosetta, whose payload, Philae, will make the first landing on a comet next Wednesday:
The historic attempt to land on a comet will take place more than 500 million kilometres (310 million miles) from Earth.
Approved in 1993, the production cost about 1.3 billion euro ($1.61 billion), involving around 200 backstage staff and 50 companies from 14 European countries and the United States.
ROSETTA, a three-tonne aluminium box of 2.8 x 2.1 x 2.0 metres (9.2 x 6.9 x 6.5 feet) with two 14m solar arrays.
The orbiter carries 11 instruments to map the comet’s surface and analyse its atmosphere, gases in its tail, the dust it emits and its subsurface temperature, mass, density and gravity.
Rosetta got its name from the stone that led to the deciphering in the 19th century of Egyptian hieroglyphics.
PHILAE, a 100-kg (220-pound) lab named after an obelisk on the Nile whose inscriptions were a key to the Rosetta stone.
It carries 10 instruments, including X-ray detectors to scan the comet’s composition, micro-cameras for panoramic shots and radiowave probes of the comet’s internal structure.
Philae has a drill to take subsurface comet samples from a depth of about 20 centimetres (eight inches) for onboard chemical analysis.
It will relay the results of its experiments to Rosetta, to be passed to Earth.
Its battery is charged to give it around 60 hours’ operating time, but the probe could continue its work until March if the sunlight and temperature are right for its solar panels.
67P/CHURYUMOV-GERASIMENKO, a pitch-black 4-km comet named after two Ukrainian astronomers who first spotted it in 1969.
The first part of its moniker refers to the fact that it was the 67th “periodic comet” discovered—these orbit the Sun in less than 200 years.
The comet comprises two lobes joined by a narrow “neck”, giving it the silhouette of a toy bath duck.
If it could be brought back to Earth, it would smell like a bad mix of rotten eggs and horse urine, among other things, tests of its escaping gases suggest.
The prime landing site, dubbed Agilkia after an island on the Nile, is on the smaller lobe roughly where the duck’s forehead would be.
Launched on March 2, 2004, Rosetta was placed in a two-and-a-half-year hibernation in June 2011 to limit power and fuel consumption on its six-billion-kilometre (3.7-billion-mile) journey.
Because there was no rocket powerful enough to place it directly into orbit, the craft was designed to be catapulted around the Solar System with gravity boosts from Mars and Earth on four flybys between 2005 and 2009.
Awoken from slumber in January this year, Rosetta arrived at the comet on August 6.
AND NOW, SHOWTIME
Once Rosetta is aligned correctly, Philae is meant to self-eject at 0835 GMT from a distance of some 20 km and unfold its three legs for what will hopefully be a gentle touchdown.
The self-adjusting landing gear is meant to ensure Philae stays upright, even if it lands on a slope. It will avoid escaping the comet’s weak gravity by shooting two harpoons into its surface and using screws in its feet to secure itself to the surface.
If all goes well, signals giving confirmation of the landing will arrive on Earth at 1602 GMT.
Highlights of unmanned space exploration
In 1942, the Nazis’ V-2 rocket became the first man-made object to touch the fringes of space.
Since then, humankind has sent scouts around the Solar System to explore its central star, planets and other bodies.
If all goes well, another milestone will be reached next Wednesday when Europe lands a robot lab on a comet.
Here are other firsts in unmanned space exploration:
The first artificial satellite was launched by the Soviet Union on October 4, 1957, ushering in the space age and the Cold War tussle for the cosmos.
The beachball-sized, aluminium sphere took 98 minutes to orbit the Earth, and sent the first-ever message received from space.
Another pioneering satellite is NASA’s Hubble Space Telescope, placed in near-Earth orbit in 1990, which has provided dazzling pictures of objects in deep space.
Another Soviet record, this probe was the first man-made craft to reach another celestial body, crashing into the Moon in 1959 and scattering Soviet pennants on its surface.
Its successor Luna 3 sent back the first-ever picture of the far side of the Moon later that same year, and Luna 9 made the first soft landing on the Moon in 1966.
This Soviet lander was the first to touch the surface of another planet—Venus, in 1966. A landing capsule was released successfully, but contact with it was lost and no scientific data was returned.
The first soft landing on a planet, also Venus, was achieved by Venera 7, four years later.
Venera 7 transmitted the first signals from another planet, and revealed that Venus, far from being a home from home, would be lethal for humans.
In 1973, the NASA spacecraft carried out the first flyby of Jupiter, swinging past the biggest planet of the Solar System at a distance of 130,000 km (80,000 miles).
In 1983, it became the first spacecraft to travel past the orbit of Neptune, the outermost of the acknowledged planets.
Pioneer 10 and its sister, Pioneer 11, carry aluminium plaques with the drawing of a man and a woman along with information indicating where the probes came from.
VOYAGER 1 AND 2
Launched in 1977 to explore further afield than ever before, Voyager 1 returned detailed photographs of Jupiter and Saturn before becoming, in 1998, the most distant human-made object.
In 2012, it entered interstellar space, the region between the stars.
Like its companion Voyager 2, which in 1986 became the first spacecraft to fly past Uranus, the vessel carries a 30-cm gold-plated copper disc.
The record includes a “greeting to the universe” in 60 languages, music and 115 images of Earth—complete with a stylus with which to play it.
Launched in 1989, this NASA mission became the first to go into orbit around a gas giant planet, Jupiter, in 1995. It carried a range of science instruments and an atmospheric probe.
It found evidence for liquid water oceans under the icy surface of Jupiter’s moon Europa.
An innovative airbag cocoon cushioned the landing of this spacecraft on the Red Planet in 1997, from which emerged the first-ever wheeled rover, dubbed Sojourner, to explore another planet.
The first landing on an asteroid happened about 355 million km from Earth in 2001, touching down at a gentle 1.5 metres per second.
Four years later, Japan’s Hayabusa spacecraft was the first to land on, take a sample, and take off from an asteroid, Itokawa, and send the dust it collected back to Earth.
A joint project of NASA, the European Space Agency (ESA) and the Italian ASI, this explorer in 2004 became the first to enter the orbit of Saturn, from where it has closely studied the giant planet’s magnificent rings.
In 2005, Cassini sent down a probe, Huygens, to Saturn’s largest moon Titan—a strange world with lakes of liquid methane.
In 2004, this NASA mission was the first to collect samples from the wake of a comet, dubbed 81P/Wild, as it shaved by at a distance 236 km. The particles were returned to Earth in a capsule in January 2006 for analysis.
The stakes facing Rosetta managers in Darmstadt, Germany are daunting as the 1.3-billion-euro ($1.61-billion) project reaches a peak.
Two decades of work have been poured into what could be a crowning moment in space exploration.
The goal: the first laboratory research into the primeval matter of the Solar System—ancient ice and dust that, some experts believe, may have helped to sow life on Earth itself.
According to this theory, comets pounded the fledgling Earth 4.6 billion years ago, providing it with complex organic carbon molecules and precious water.
Rosetta has already sent home fascinating data on the comet, but Philae will provide the first boots-on-the-ground assessment, using 10 instruments to study the comet’s physical and chemical composition.
Like Rosetta, it will wield a mass spectrometer, a high-tech tool to analyse a sample’s chemical signature, aimed at drawing up a complete carbon inventory.
The showstopper find would be molecules known as left-handed amino acids, the European Space Agency (ESA) says.
“These are the ‘bricks’ with which all proteins on Earth are built,” it says.
But getting Philae into position will be a white-knuckle ride.
After its launch in 2004, Rosetta spent 10 years zig-zagging around Earth and Mars, using the planets’ gravitational pull as a slingshot to build up speed to reach its prey, Comet 67P/Churyumov-Gerasimenko.
Although the majority of patients with breast cancer have clinically negative axillary nodes at preoperative assessment, around 15–20% of these women will have metastatic disease within the lymph nodes at operative sentinel node biopsy, and additional selective treatment to the axilla might be required. Local treatment to the axilla can include axillary node clearance or axillary radiotherapy. The recent results of the American College of Surgeons Oncology Group Z0011 trial suggested that some women would be safe from recurrence without further axillary treatment if they have less than three involved sentinel nodes, with no extracapsular spread. We review the evidence base for management of the axilla after detection of a positive sentinel node, discuss the evidence for why micrometastatic disease requires systemic but not axillary therapy, and present data suggesting that axillary irradiation for macrometastases gives equivalent control to axillary node clearance, but causes less morbidity such as lymphoedema. Ongoing trials will confirm whether any further therapy can be omitted for all patients with low volume, sentinel-node macrometastases.
When a tumor is near critical speech areas of the brain, it may be important to determine the exact location of these speech-related areas.
Although functional MRI (fMRI) can show the various areas of activation during speech functions, it does not pinpoint the most important areas. These critical areas must be located using special speech mapping techniques while the patient is awake in the operating room.
Awake speech mapping involves applying mild electrical current to the surface of the exposed brain while the patient performs various tasks, such as reading. If the stimulation hinders the task, then that area of the brain is marked and preserved.
How it works
UCLA has pioneered the technique of sleep-awake-sleep craniotomy.
The operation is begun while the patient is deeply asleep under general anesthesia (on a breathing machine). This is for the comfort of the patient and is safer.
When the brain is exposed and the neurosurgeon is ready to begin mapping the speech areas, UCLA neuroanesthesiologists carefully lighten the sedation, and then remove the breathing tube and allow the patient to talk and interact with the neuropsychologist.
Typically, the patients feel minimal or no discomfort while awake.
Once the speech mapping is complete, often the tumor is removed while the speech testing continues. The procedure lessens the risk of undercutting the white matter fibers connecting speech areas.
When appropriate, the anesthesiologist skillfully places the patient back under general (deep) anesthesia, allowing the neurosurgeon to complete the operation safely with no discomfort to the patient.