Sunday, August 28, 2011

Sunday Aug 28, A Week in Science

Double Amputee qualifies for semi-finals in 400 m dash in World Athletics Championships

Oscar Pistorius was eleven months old when doctors amputated both of his legs between the knee and ankle. He had been born without a fibula in each leg, and health complications from his condition required that they be removed.

Oscar never let that slow him down. By the age of 11 he had been fitted with prosthesis and participated in rugby, water polo, and tennis. At 17 he suffered a serious knee injury while playing rugby and began physical therapy, where he discovered running. In the following years he set multiple world records in parathlete sprinting events and competed against able-bodied athletes in international events.

In 2007 the International Association of Athletics Federations (IAAF) banned "any technical device that incorporates springs, wheels or any other element that provides a user with an advantage over another athlete not using such a device" in running events, a move that it said was unrelated to Oscar's recent successes. Oscar successfully appealed the decision and won the right to compete in world sprinting and Olympic events, despite claims that his lightweight prosthesis gave him an unfair advantage.

In 2008 he competed for the South African track team for the Beijing Olympics but missed qualifying by .70 seconds. Still determined to achieve his dream of competing in the Olympics, he continued to train and on Sunday, August 28 he qualified for the 400m semi-finals at the IAAF World Athletics Championship in Daegu, South Korea. If he is able to run another 'A' qualification time he will have won the right to run with the best in London in 2012, and to be the first amputee in history to compete in the Olympic games.

Experiments at the LHC continue to find no evidence of supersymmetry.

Modern physics is an uneasy blend of two revolutionary ideas from the twentieth century: general relativity and quantum mechanics. Like two competing nations, their laws work well within their own specific realms (relativity at large scales, quantum mechanics at very small ones) but those laws break down and become meaningless or even incomprehensible in the opposite domain. Between the two is a nebulous border region where strange, inexplicable things seem to occur.

Supersymmetry is a theory that attempts to bridge that gap. Experimental physics has confirmed the existence of a great many particles which make up the matter and energy we interact with every day. Many, such as photons and electrons, you may have heard of. Several, like muons and top quarks, are more obscure. By positing the existence of a set of massive, hard to observe partner for each of these particles, theoretical physicists had hoped that they untangled the thorny mess of conflict between relativity and quantum mechanics. As an added plus, it was hoped that experimental data would reveal these massive partner particles to be the source of the mysterious dark matter which pervades our universe.

Enter the Large Hadron Collider (LHC), the most powerful and expensive science experiment ever conceived. At 27 km in circumference, it is more of a man-made geographic feature than an edifice, and it contains detectors sensitive enough to detect the flickering of a candle from the moon. One of its main missions has been to evaluate the different models of supersymmetry. The data so far is not encouraging.

At the Lepton Photon Symposium in Mumbai, India, physicists from CERN, which operates the LHC, presented data which fails to find any evidence of supersymmetry. Although the findings do not rule out every version of the theory, there is a sense among physicists that a new theory may be needed to explain this data.

"It could be that this whole framework has some fundamental flaws and we have to start over again and figure out a new direction," said Dr Joseph Lykken of Fermilab, a competing detector in the United States with much less sensitivity and power. Dr. Lykken is a leading proponent of supersymmtry and organizer of a yearly conference for its advocates. "It's a beautiful idea. It explains dark matter, it explains the Higgs boson, it explains some aspects of cosmology; but that doesn't mean it's right.

Interbreeding with Neanderthals was important for Human Immune System Evolution

While popular depictions of human evolution show a straight progression from ape to hominid to modern Homo sapiens, it has long been known that human evolution was actually a branching tree. Rival species of hominids coexisted and competed until modern humans outlived or exterminated their rivals by about 30,000 years ago. New data suggests that some of those branches of the human family tree live on in our DNA, specifically in certain genes in the immune system which may have been key to our success as a species.

The study was published in this week's Science magazine by a group of researchers from Stanford and other universities. In it they report that an important set of genes in the human immune system preserves evidence of ancient interbreeding between humans and two other species of hominids, Neanderthals and Denisovans.

Using gene sequencing, the researchers were able to identify an allele known as HLA-B*73 which is far more distantly removed from other typed of HLA genes than those genes are from each other. In essence, using a form of statistical analysis paired with comparisons to living human relatives (chimpanzees and gorillas), they could determine that the allele evolved in isolation from other human genes before being reintroduced by interbreeding sometime in our ancient past. Similar analyses of other alleles in the same region of the human genome reveals another likely cross-breeding event, with Neanderthals, at a different geographical location.

West Asians are the most likely population to exhibit this gene, with a smaller prevalence in parts of Africa and token appearance in other populations around the world. This pattern suggests that the interbreeding event between humans and Denisovans took place in West Asia and spread to Africa and elsewhere over the following generations. Another interbreeding event between humans and Neanderthals happened somewhere in Eurasia, probably in Northern Europe where the Neanderthals were most established.

Previous work has suggested that Neanderthal genes make up between 1 and 6% of the human genome thanks to past interbreeding, but up to 50% of the genes examined by this study may have been inherited from those distant cousins. Such a high proportion suggests that these genes were important to the evolution of our immune systems and to our species' success in the face of constant threat from viral, bacterial, and parasitic infections.

Friday, August 26, 2011

UPenn Clinical Study Cures late stage Leukemia

A Hopeful Headline

In a new study published in the New England Journal of Medicine, researchers cured cancer using modified HIV viruses to turn the patient's own white blood cells into “cancer cell serial killers”. This gene therapy technique was tested in three patients afflicted with B-cell neoplasms, a form of leukemia. , (Perhaps start a new sentence and discuss one patient who one who had been continually diagnosed with the disease since 1996 and the other patients with advanced or chronic or …?. Over the course of six weeks, the disease disappeared from two of the patients entirely and was reduced by 70% in the third. The most serious side effects observed were similar to an intense fever, and one year later the disease remains in remission.

Researchers are hopeful that, based on these initial results, they have developed a powerful new treatment which may help those diagnosed with B-cell neoplasms and other forms of cancer.

The Science of Leukemia

Leukemia is a type of cancer which primarily afflicts the bone marrow and blood cells. Up to 250,000 people worldwide are diagnosed with it every year, and 210,000 die from it. It is the eleventh most common form of cancer, but the most common variety diagnosed in children. Depending on the type it causes tumors in the bone marrow and/or uncontrolled multiplication of certain blood cells.

Leukemia can treated by many avenues, but is notoriously difficult to eradicate completely. In later stages, cancerous cells may multiply so wildly that they crowd out healthy, functioning blood cells, or infiltrate internal organs and grow into tumors. Tumors can also develop in the bone marrow itself.

Treatments almost always include chemotherapy targeted at the type of leukemia the patient has, as well as radiation therapy if malignant tumors are present. Another common procedure is the bone marrow transplant, also called hematopoietic stem cell transplantation (HSCT). Hematopoietic stem cells exist in bone marrow and have the ability to divide and transform into any type of blood cell. In a healthy person the bone marrow continually replenishes blood cells that wear out with fresh-grown replacements. In advanced cases of leukemia, unhealthy cells can accumulate in the marrow, continually producing diseased cancer cells no matter how many times they are cleansed from the blood stream. An HSCT procedure removes healthy stem-cell containing bone marrow from a compatible donor and transfers it to the patient, replacing the cancerous marrow.

HSCT is a powerful tool, but is fraught with potential complications. Bone marrow produces blood cells of all types, including white blood cells whose job it is to attack anything they encounter that is foreign or unfamiliar. When white blood cells from a donor find themselves in a new body, they can sometimes confuse it with dangerous foreign material and attack. When this happens, it is called graft versus host disease, and it is extremely dangerous.

The graft versus host phenomenon and its underlying medical causes have been known since early immunology experiments with mice in the 1940's. In the 1980's, researchers began to observe a similar effect with positive ramifications for the patient, which was christened the graft versus tumor or graft versus leukemia effect. Like in graft versus host disease, donor white cells recognize parts of the host as foreign and attack. In this case, however, they specifically single out and attack leukemia cells, slowing the progress of the cancer. Unfortunately, the strength of the graft versus tumor effect is generally linked with the severity of the graft versus host disease, requiring a balancing act on the part of attending oncologists to keep the patient alive while combating the cancer as aggressively as possible.

There has been a lot of interest among researchers to develop treatments which take advantage of the graft versus tumor effect without the drawback of graft versus host disease. A number of projects have attempted to manufacture white blood cells, which would target only cancer cells while leaving healthy ones alone.

A new avenue

Reprogramming a cell requires the use of an advanced and controversial technique known as gene therapy. Gene therapy allows researchers to edit the DNA of target cells directly, rewriting the code of life in order to treat a disease. Since cancer is often the result of dangerous mutations in a cell's DNA, gene therapy is ale to rewrite the cancer cells' genes to turn of their malignancy, rendering them dormant or harmless.

Unfortunately it can be difficult to find all the malignant cells and edit their DNA, and a single surviving cancer cell may eventually multiply and reestablish the disease. In addition, the genetics of cancer are vastly complex and poorly understood, making it hard to know how exactly what changes to make to cure the patient. Even if a particular sequence could be singled out as the culprit, cancer is an individual disease that manifests in varying, often unique ways in different patients. A gene therapy regimen may have to be individualized in order to maximize its effectiveness, a slow and very expensive prospect.

Dr. June and his collaborators chose a different approach. Instead of finding and rewriting the cancer cells, they chose to use gene therapy principles to reprogram the host's own white blood cells, which are already specialized at hunting down contaminants and attacking them. These modified cells would be told how to recognize dangerous cancer cells, which normally hide from white blood cells because they look so similar to the rest of the body.

The result would hopefully be what the study's authors call “cancer cell serial killers”. If it worked, it would be the most advanced form of immunotherapy ever administered, skirting many of the dangers of chemotherapy and HSCT by using the patient's own reprogrammed immune cells to fight off the cancer.

How to build a cure for cancer

The researchers chose a kind of white blood cell called T-cells to be their tool. T-cells are the body's assassins, pillars in its defense against infection and contamination that specialize in binding and killing enemy cells. They are the rank and file, seeking out foreign bodies and going where they are directed by the rest of the immune system, but for this project the researchers taught them a few new tricks.

Before the reprogrammed cells can get to work, researchers need a way to deliver their instructions to the interior of the cell and edit the DNA. This is a complex task requiring precision at the molecular level, a technique far beyond the capability of researchers to accomplish directly. To do it they again co-opted machinery that evolved in nature for a very different purpose. In this case they took a virus, usually known for causing disease, and re-purposed it to deliver their package to target white blood cells.

Many scientists do not consider viruses to be living things, in part because they are unable to reproduce alone. Instead they invade a host and hijack its reproductive capabilities to produce copies of themselves. A particular group of viruses, called retroviruses, actually do this by editing the host cell's DNA. If a virus could be altered to edit DNA in a particular, useful way, it would allow researchers to reprogram a target cell indirectly.

HIV, the virus responsible for AIDS, is perhaps the most famous and feared of the retroviruses. It specializes in infecting immune cells, particularly T-cells, killing them off as its first wave of attack while tricking them into producing millions of copies of the virus. In an ironic twist, the same qualities that make it so devastating to an infected immune system also make it the perfect tool to deliver the package of genetic material which turns a normal T-cell into a cancer killer.

Researchers of course removed the parts of the genome that lead to AIDS, leaving only the instructions needed for slipping into the cell and changing the host DNA. With AIDS this process tricks the host cell into producing copies of HIV, but the researchers edited those instructions as well. By piggybacking HIV's normally deadly lifecycle, the researchers now had a way to tell a white blood cell to do whatever they wanted.

Anti-cancer vigilantes

Being able to order someone around, of course, tends to be the easy part. Researchers still had to tell the T-cell what to do. They could tell it to ignore its usual restraints and attack the leukemia, but an indiscriminate killer could prove as dangerous to the patient as to the cancer. Researchers had to teach these T-cells to tell the difference between healthy cells and dangerous ones.

B-cell neoplasms involve the aggressive and out-of-control multiplication of B-cells, a type of white blood cell. B-cells produce antibodies, tiny pieces of protein which find and identify foreign contaminants. Antibodies and the B-cells that produce them are scouts for the rest of the immune system's army.

In another example of adapting natural tools for medicinal purposes, researchers used the ability of antibodies to recognize very specific targets as part of the treatment. Every type of cell in nature has different surface markers, they “look” different on a chemical level. Because those differences are microscopic it's hard to recognize them, though many white blood cells have evolved for that very purpose. Antibodies in particular are extremely good at noticing the subtle differences between a liver cell, a bacterial cell, and a B-cell because of their function as the immune system's scout.

Normally the body does not produce antibodies which could attack its own cells. When it does, the patient experiences what is known as an autoimmune disorder. Arthritis and Lupus are common autoimmune disorders, as is graft versus host disease. In the latter case donated white blood cells don't recognize the host's unfamiliar cell markers as “friendly”, and attack. This is why most cases of graft versus tumor treatment involve an associated graft versus host disease; antibodies that target canerous tumors also tend to target other, healthy parts of the patient's body.

Antibodies can be specific enough to attack the cancer and not the rest of the patient, if you know how to get them to tell the difference. In B-cell neoplasms, the researcher's approach was simply to teach antibodies to recognize B-cells. In yet another ironic twist, the very weapons employed by B-cells to defend the body are adapted as weapons used to attack them when they go rogue. Thanks to the modified HIV virus, they can then implant those antibodies in a T-cell's DNA, creating a dedicated killing machine whose sole target is cancerous B-cells.

Persistence is key

While the science that creates these cancer hunting T-cells is exciting, other groups have attempted to make them before. The problem so far has been that the T-cells work for a little while, but soon die off, allowing the cancer to quickly reassert itself. In healthy individuals those cells would be soon replaced by the bone marrow, but the diseased marrow of leukemia patients is unable to do this, and the modified T-cells are introduced from the outside in the first place. A method was needed to ensure that modified T-cells are around for the many months needed to clear the cancer completely.

The researchers working in this study tried out a particular gene known as CD137, which had been observed in other studies to enhance the lifespan and replication of T-cells. By including it with the DNA package delivered by the HIV derived viral vector, they hoped to increase the longevity of the treatment.

The clinical results were striking. In previous trials, modified T-cells without the enhanced longevity were administered to patients, but steadily declined in number and effectiveness over the following days. When the patients were examined three weeks after the initial infusion of T-cells in this study, the cells had multiplied a thousand fold.

Soon patients experienced a condition known as tumor lysis syndrome. Symptoms include muscle weakness, seizures, blood toxicity, and others. While the condition is serious and can be fatal, there was a bright side: tumor lysis syndrome occurs when the body is overloaded by debris from dying cancer cells. Patients lost as much as five pounds of cancerous tissue in those weeks as the T-cells purged them from their bodies.

It was like the worse flu of their life,” said Dr. June. “But after that, it's over. They're well.”

Three months later, the cancer was in remission and levels of the synthetic T-cell remained high. Tumors could no longer be detected in two of the patients at all, and had shrunk by 70% in the third. No symptoms of the cancer or tumor lysis syndrome were apparent, though a few side effects of the treatment necessitated further medication. In hunting down the cancer cells, the T-cells indiscriminately wiped out all B-cells present in the body. While this side effect was expected, it does severely compromise the immune systems of the patients, exposing them to infections. In cases of terminal cancer, a patient surviving to worry about this complication is a step in the right direction.

As the patients were monitored following their dramatic recoveries, another benefit of the treatment became apparent. Some of the synthetic T-cells had made the transition to “memory” T-cells. Once a disease has been fought off, some T-cells become dormant as an insurance policy for future attacks. If the disease were to reappear, these memory T-cells would reactivate and multiply in order to fight it off. Researchers are hopeful that their presence will grant a lasting ability to fight off any reemergence of the patients' leukemia.

One year after treatment, the patients' physicians haven't detected any resurgence of the disease. Following the publication of their findings in the New England Journal of Medicine, the study's authors are sure to expand the trial to include more patients, and other groups are looking to adapt the technique to other types of cancer. The reaction by experts in the field has been very optimistic and positive, with certain reservations with regards to the treatment's long term effects.

What's next

Physicians and researchers are not the only people likely to show great interest in the treatment. Patients suffering from B-cell neoplasms, as well as any form of cancer that might benefit from this experimental treatment, will be asking their doctors about it in the months to come. Since it is still in phase I clinical trial, the total number of patients that can benefit from it is limited and patients will be carefully screened to see if they meet the criteria for the trial. The treatment is also very complex and expensive, and it will take a great deal of time for clinics around the country to gain the expertise and equipment required to administer it.

There is also the question of long-term effectiveness and side effects, which won't be answered until the patients can be observed over a longer time period. The lack of B-cells in treated patients is sure to expose them to further health complications, and the T-cells themselves may exhibit unpredictable behaviors over longer time frames.

All of these observations, as well as an expansion of the number of test patients benefiting from the treatment, will form the rest of its phase I clinical trials. It is impossible to know how long this phase will last, though several years of continued testing and observation is a certainty. Upon entering phase II, the scope and availability of the treatment will expand, but its a long and expensive road to get there.

Whatever the results of this long process, at least three patients have received the treatment and are thankful for the extra time it affords them. Before Bill Ludwig was inducted into the study one year ago, he was told that the leukemia would kill him within weeks. "I'm more closer to the people I love and I appreciate them more... I'm getting emotional... the grass is greener and flowers smell wonderful," he said of his recovery.

Another patient , himself a former scientist, released an anonymous statement. “I am still trying to grasp the enormity of what I am a part of – and of what the results will mean to countless others with CLL or other forms of cancer. When I was a young scientist, like many I’m sure, I dreamed that I might make a discovery that would make a difference to mankind – I never imagined I would be part of the experiment.”

The Bottom Line

The study done by Dr. Carl June and his collaborators at the University of Pennsylvania took patients' own immune systems and programmed it with a modified HIV virus to recognize and destroy cancer cells. It avoids the destructive side effects of marrow transplantation while harnessing their strengths. The side effects of the treatment are manageable but potentially serious over the long term, though not nearly so serious as the cancer if left untreated. By programming the cells to multiply and persist in the patients' bodies, the study has advanced the fledgling science of immunotherapy, raising hopes that it may someday replace the toxic chemotherapy that currently dominates cancer treatment.

Much progress been made over the decades in combating cancer, yet many seeming miracle treatments have turned out to have serious negative ramifications, or limitations not anticipated during their development. With that in mind, this study will still give great hope to patients fighting cancer, their families who suffer with them, and to the doctors who deal with the tragedy of cancer every day.

Thursday, August 11, 2011

NASA orbiter discovers evidence of liquid water on Mars

The Headline

NASA scientists have released photographs from the Mars Reconnaissance Orbiter (MRO) which they claim show evidence of liquid water on the surface of Mars. This is the first clear evidence that water can exist in its liquid state on Mars, though ice has been observed near the planet's poles and under the soil. Reservoirs of water might prove to be an invaluable resource to any future missions to Mars, and raise hopes among many scientists that life might have been able to develop and evolve in the extreme Martian environment.

The Science

The MRO is a probe that entered orbit around Mars in 2006. Since then it has observed the planet and sent thousands of photos back to Earth over the course of three Martian years (one Martian year is 1.88 Earth years).

During this time scientists have made many interesting discoveries, but one set of photos stood out (pictured below). It shows a region of bluffs and valleys which slowly develop dark finger-like features which extend down the slope during the spring and summer, fade in the winter, and return as the atmosphere heats up again. Puzzlingly the soil does not appear to darken because it is wet, but rather because grains of dust are disturbed and rearranged due to something flowing or moving downhill.

image credit: NASA/JPL-Caltech/Univ. of Arizona

The best explanation for these observations so far is the flow of briny water,” said Alfred McEwen of the University of Arizona, Tucson. McEwen is the principal investigator for the orbiter’s High Resolution Imaging Science Experiment (HiRISE) and lead author of the paper about the flows, published in the journal Science.

Briny water is water that contains very high concentrations of dissolved salts, which are known to be prevalent on Mars' surface thanks to geological studies by the Spirit and Opportunity rovers. Briny water has a much lower freezing point than pure water, and is more viscous as well. This helps to explain how liquid water could exist on Mars, which features temperatures far below the freezing point of pure water.

Other qualities of the flows remain unexplained, for instance why no water or other volatile substances have been detected by the MRO's spectroscopy sensors. Scientists hypothesize that the water may evaporate into the atmosphere too quickly for the orbiter to detect, or that the flows may occur just under the surface of the soil. Another question is why the features disappear as the weather chills during the Martian winter.

It’s a mystery now, but I think it’s a solvable mystery with further observations and laboratory experiments,” McEwen said.

The possibility of water on any interstellar body is an exciting one for scientists, but especially on Mars, our most accessible planetary neighbor. Life as we know it cannot exist without water, meaning both that it will be an important resource for any possible manned mission, but also that its presence vastly increases the hopes that indigenous life might be discovered on a planet other than our own.

The Bottom Line

The announcement by NASA expresses confidence that liquid water is responsible for the features observed on the Martian surface, but doesn't rule out the possibility of other geological mechanisms. In terms of its impact on a future manned mission, ice has already been discovered on Mars, so the existence of liquid water wouldn't make or break such an expedition. It does increase the interest in organizing such a venture for many scientists, as life is presumed to be much more likely in the presence of liquid water. At the very least the announcement highlights the vast amount that remains to be discovered in even the most familiar regions (relatively speaking) of our interstellar neighborhood.

http://www.nasa.gov/mission_pages/MRO/news/mro20110804.html - NASA mission news

Tuesday, August 9, 2011

New Study Challenges Global Warming Theories

The Headline

A new analysis of data collected by NASA's Terra satellite suggests that current models of global climate change are flawed. The study, released in the July 25 issue of the journal Remote Sensing, claims that temperature variations in Earth's climate may be attributable to cyclical oceanic phenomen such as el nino and la nina, and provides evidence that the atmosphere is more efficient at radiating excess heat than current warming models predict. If the study withstands further peer review and testing, it may fundamentally shift the predictions made by climate scientists with regard to the hypothesized anthropogenic warming of the planet.

The Science

The article's author's, Roy W. Spencer and William D. Braswell, analyzed 10 years worth of data collected by CERES (Clouds and Earth's Radiant Energy System), a sensor system in earth orbit on the Terra satellite, to address the simple but vital question of how much energy is absorbed by the atmosphere.

The major source of energy entering the atmosphere is sunlight (also called solar radiation). In fact the Earth receives about 2x1017 joules of sunlight every second, equivalent in energy to a 48 megaton explosion (two thousand times the power of the bomb dropped on Hiroshima). All of this energy has to go somewhere, and in simple terms it does one of three things. It could simply be reflected back into space, a process carried out quite efficiently by clouds and polar ice. Some incoming solar radiation will be absorbed and then re-emitted at a lower wavelength, typically infrared (IR), which can likewise travel back into space. The third and final possibility is that energy from incoming sunlight is retained by the atmosphere as heat, increasing global temperatures.

The main argument made by proponents of anthropogenic climate change (or the global warming hypothesis) is that the release of greenhouse gases by humanity will block the Earth's ability to radiate heat back into space, forcing it to be retained in the atmosphere. This then kicks off what is called a positive feedback loop whereby higher temperatures increase the amount of water vapor and methane in the air (both greenhouse gases), which traps more heat and raise the temperature and so on.

The typical approach to building climate models has been to take temperature measurements around the globe, then use this data to make determinations of how much solar radiation is being retained by the atmosphere as heat. Drs. Spencer and Braswell chose to use the inverse approach by measuring the amount of energy the earth received as sunlight and the amount reflected or radiated back into space with the delicate sensors of the Terra satellite. Armed with these two numbers they could make an accurate determination of how much heat is being retained in the atmosphere, as well as searching for correlations between decreased radiation of IR wavelengths and spikes in atmospheric temperature.The study examined data gathered between 2000 and 2010.

The results of this analysis will likely be contentious among climate scientists. According to the paper's analysis, the atmosphere is far better at radiating heat than most models predicted, and it begins doing so earlier in a warming event than scientists anticipated. In a graph from the paper (shown to the right) the authors plot predictions from IPCC (Intergovernmental Panel on Climate Change) models which represent the general consensus on how the atmosphere radiates energy in comparison to the observations of the Terra climate satellite.

Experimental observations are shown in green, while blue and red represent the IPCC conventional theories. A large mismatch between the two is clearly visible. In area 1, the graph shows a large increase in the amount of energy absorbed by the atmosphere (as measured by the total energy received from the sun minus energy reflected or re-emitted back into space) before a warming event, which is intuitive and agrees with existing models. In area 2, however, we see a rapid increase in the observed heat radiated from the atmosphere into space, even before the temperature maximum is achieved, while traditional models predict heat to be retained in the atmosphere for much longer.

The paper speculates briefly on what mechanisms might be responsible for this discrepancy, but admits that more work needs to be done. Still, if their analysis of the CERES data holds up, the atmosphere is somehow much better at radiating heat into space than is currently assumed, especially given elevated levels of carbon dioxide in the atmosphere due to human activity. Specifically the data suggests a negative feedback mechanism whereby increased temperatures are counteracted by developments which deflect and disperse the extra heat into space, preventing the kind of runaway warming which the most alarming models predict. Should this theory turn out to be correct, then the worst predictions of climate change will almost certainly turn out to be untrue. But there remains a great deal of work to be done before any such claims can be credibly made.

The Bottom Line

Even if all this paper's findings withstand the intense scrutiny that is certainly about to fall upon it, all the study does is reveal unexplained trends in the data which disagree with wide held assumptions about the way the atmosphere interacts with solar energy. It does not provide an explanation for this data beyond suggesting a few possibilities, as the authors themselves state. It certainly does not disprove or invalidate concerns about humanity's impact on the climate.

Instead it provides information that climate scientists will have to explain and incorporate into their models. Whether these enhanced models will turn out be more or less sanguine about the future of our planet remains to be determined.


http://www.uah.edu/news/newspages/campusnews.php?id=564press release

http://www.mdpi.com/2072-4292/3/8/1603/pdf - article