Humans have been deceiving themselves for thousands of years that they’re smarter than the rest of the animal kingdom, despite growing evidence to the contrary, according to University of Adelaide experts in evolutionary biology.
by Nancy Ambrosiano | December 6, 2013
Corals have long been popular as souvenirs, for home decor, and in jewelry, but many consumers are unaware that these beautiful structures are made by living creatures. Fewer still realize that corals are dying off at alarming rates around the world.
Coral reefs are some of the most biologically rich and economically valuable ecosystems on Earth, but they are increasingly threatened by pollution, invasive species, fishing, disease, bleaching, and global climate change.
Strong consumer demand for coral, heightened over the holiday season, is another factor that is contributing to the decline of coral reefs.
Each year, the U.S. imports tons of dead coral for home decorations and curios. Most of these corals are shallow-water species.
The U.S. is also the world’s largest documented consumer of Corallium, red and pink corals often used to create jewelry. Finished pieces of jewelry and art crafted from this type of coral can fetch anywhere between $20 and $20,000 in the marketplace.
Continued consumer demand is contributing to the decline of these delicate corals around the world. Commercial harvesting to satisfy the demand for coral jewelry has reduced colony size, density, and age structure of Corallium over time. Harvesting is also lowering the reproduction capability of this species and is decreasing its genetic diversity.
Research indicates that removal of red and pink corals for the global jewelry and art trade is also leading to smaller and smaller Corallium in the wild. The average base diameter of Corallium is now about two centimeters (0.8 inches), down from an average of 10 centimeters (3.9 inches) just a few decades ago.
Since corals grow at rates of 0.24 to 1.5 millimeters (0.01 to 0.06 inches) per year, they are extremely long-lived and do not reach maturity until they are seven to 12 years old. Once this coral is harvested—especially when it’s extracted at a young age—surrounding coral beds often do not recover.
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DECEMBER 6, 2013 by Paige Brown Original online publication LSU Research News PDF Time Warp_ LSU Researcher Shows Possibility of Cloning Quantum Information from the Past_LSU
Popular television shows such as “Doctor Who” have brought the idea of time travel into the vernacular of popular culture. But problem of time travel is even more complicated than one might think. LSU’s Mark Wilde has shown that it would theoretically be possible for time travelers to copy quantum data from the past.
It all started when David Deutsch, a pioneer of quantum computing and a physicist at Oxford, came up with a simplified model of time travel to deal with the paradoxes that would occur if one could travel back in time. For example, would it be possible to travel back in time to kill one’s grandfather? In the Grandfather paradox, a time traveler faces the problem that if he kills his grandfather back in time, then he himself is never born, and consequently is unable to travel through time to kill his grandfather, and so on. Some theorists have used this paradox to argue that it is actually impossible to change the past.
“The question is, how would you have existed in the first place to go back in time and kill your grandfather?” said Mark Wilde, an LSU assistant professor with a joint appointment in the Department of Physics and Astronomy and with the Center for Computation and Technology, or CCT.
Deutsch solved the Grandfather paradox originally using a slight change to quantum theory, proposing that you could change the past as long as you did so in a self-consistent manner.
“Meaning that, if you kill your grandfather, you do it with only probability one-half,” Wilde said. “Then, he’s dead with probability one-half, and you are not born with probability one-half, but the opposite is a fair chance. You could have existed with probability one-half to go back and kill your grandfather.”
But the Grandfather paradox is not the only complication with time travel. Another problem is the no-cloning theorem, or the no “subatomic Xerox-machine” theorem, known since 1982. This theorem, which is related to the fact that one cannot copy quantum data at will, is a consequence of Heisenberg’s famous Uncertainty Principle, by which one can measure either the position of a particle or its momentum, but not both with unlimited accuracy. According to the Uncertainty Principle, it is thus impossible to have a subatomic Xerox-machine that would take one particle and spit out two particles with the same position and momentum – because then you would know too much about both particles at once.
“We can always look at a paper, and then copy the words on it. That’s what we call copying classical data,” Wilde said. “But you can’t arbitrarily copy quantum data, unless it takes the special form of classical data. This no-cloning theorem is a fundamental part of quantum mechanics – it helps us reason how to process quantum data. If you can’t copy data, then you have to think of everything in a very different way.”
But what if a Deutschian closed timelike curve did allow for copying of quantum data to many different points in space? According to Wilde, Deutsch suggested in his late 20th century paper that it should be possible to violate the fundamental no-cloning theorem of quantum mechanics. Now, Wilde and collaborators at the University of Southern California and the Autonomous University of Barcelona have advanced Deutsch’s 1991 work with a recent paper in Physical Review Letters (DOI: 10.1103/PhysRevLett.111.190401). The new approach allows for a particle, or a time traveler, to make multiple loops back in time – something like Bruce Willis’ travels in the Hollywood film “Looper.”
“That is, at certain locations in spacetime, there are wormholes such that, if you jump in, you’ll emerge at some point in the past,” Wilde said. “To the best of our knowledge, these time loops are not ruled out by the laws of physics. But there are strange consequences for quantum information processing if their behavior is dictated by Deutsch’s model.”
A single looping path back in time, a time spiral of sorts, behaving according to Deutsch’s model, for example, would have to allow for a particle entering the loop to remain the same each time it passed through a particular point in time. In other words, the particle would need to maintain self-consistency as it looped back in time.
“In some sense, this already allows for copying of the particle’s data at many different points in space,” Wilde said, “because you are sending the particle back many times. It’s like you have multiple versions of the particle available at the same time. You can then attempt to read out more copies of the particle, but the thing is, if you try to do so as the particle loops back in time, then you change the past.”
To be consistent with Deutsch’s model, which holds that you can only change the past as long as you can do it in a self-consistent manner, Wilde and colleagues had to come up with a solution that would allow for a looping curve back in time, and copying of quantum data based on a time traveling particle, without disturbing the past.
“That was the major breakthrough, to figure out what could happen at the beginning of this time loop to enable us to effectively read out many copies of the data without disturbing the past,” Wilde said. “It just worked.”
However, there is still some controversy over interpretations of the new approach, Wilde said. In one instance, the new approach may actually point to problems in Deutsch’s original closed timelike curve model.
“If quantum mechanics gets modified in such a way that we’ve never observed should happen, it may be evidence that we should question Deutsch’s model,” Wilde said. “We really believe that quantum mechanics is true, at this point. And most people believe in a principle called Unitarity in quantum mechanics. But with our new model, we’ve shown that you can essentially violate something that is a direct consequence of Unitarity. To me, this is an indication that something weird is going on with Deutsch’s model. However, there might be some way of modifying the model in such a way that we don’t violate the no-cloning theorem.”
Other researchers argue that Wilde’s approach wouldn’t actually allow for copying quantum data from an unknown particle state entering the time loop because nature would already “know” what the particle looked like, as it had traveled back in time many times before.
But whether or not the no-cloning theorem can truly be violated as Wilde’s new approach suggests, the consequences of being able to copy quantum data from the past are significant. Systems for secure Internet communications, for example, will likely soon rely on quantum security protocols that could be broken or “hacked” if Wilde’s looping time travel methods were correct.
“If an adversary, if a malicious person, were to have access to these time loops, then they could break the security of quantum key distribution,” Wilde said. “That’s one way of interpreting it. But it’s a very strong practical implication because the big push of quantum communication is this secure way of communicating. We believe that this is the strongest form of encryption that is out there because it’s based on physical principles.”
Today, when you log into your Gmail or Facebook, your password and information encryption is not based on physical principles of quantum mechanical security, but rather on the computational assumption that it is very difficult for “hackers” to factor mathematical products of prime numbers, for example. But physicists and computer scientists are working on securing critical and sensitive communications using the principles of quantum mechanics. Such encryption is believed to be unbreakable – that is, as long as hackers don’t have access to Wilde’s looping closed timelike curves.
“This ability to copy quantum information freely would turn quantum theory into an effectively classical theory in which, for example, classical data thought to be secured by quantum cryptography would no longer be safe,” Wilde said. “It seems like there should be a revision to Deutsch’s model which would simultaneously resolve the various time travel paradoxes but not lead to such striking consequences for quantum information processing. However, no one yet has offered a model that meets these two requirements. This is the subject of open research.”
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© 2013 American Physical Society
We show that it is possible to clone quantum states to arbitrary accuracy in the presence of a Deutschian closed timelike curve (D-CTC), with a fidelity converging to one in the limit as the dimension of the CTC system becomes large—thus resolving an open conjecture [Brun et al., Phys. Rev. Lett. 102, 210402 (2009)]. This result follows from a D-CTC-assisted scheme for producing perfect clones of a quantum state prepared in a known eigenbasis, and the fact that one can reconstruct an approximation of a quantum state from empirical estimates of the probabilities of an informationally complete measurement. Our results imply more generally that every continuous, but otherwise arbitrarily nonlinear map from states to states, can be implemented to arbitrary accuracy with D-CTCs. Furthermore, our results show that Deutsch’s model for closed timelike curves is in fact a classical model, in the sense that two arbitrary, distinct density operators are perfectly distinguishable (in the limit of a large closed timelike curve system); hence, in this model quantum mechanics becomes a classical theory in which each density operator is a distinct point in a classical phase space.
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Todd A. Brun, Mark M. Wilde, & Andreas Winter (2013).
Quantum state cloning using Deutschian closed timelike curves
Phys. Rev. Lett. 111, 190401 (2013)
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Dec. 5, 2013 Original online publication UC Irvine PDF How our vision dims: Chemists crack the code of cataract creation UCIrvine News
Groundbreaking new findings by UC Irvine and German chemists about how cataracts form could be used to help prevent the world’s leading cause of blindness, which currently affects nearly 20 million people worldwide. (PDF)
“That’s the dream, and this is a big step,” said Rachel Martin, UC Irvine associate professor of chemistry and co-author of a paper featured on the December cover of the journal Structure. “Understanding the molecular mechanism of what goes wrong in the eye that leads to a cataract could lead to the development of better treatment options, including more sophisticated artificial lenses and drugs.”
It has long been known that human eyes have a powerful ability to focus because of three kinds of crystallin proteins in their lenses, maintaining transparency via a delicate balance of both repelling and attracting light. Two types of crystallin are structural, but the third – dubbed a “chaperone” – keeps the others from clumping into cataracts if they’re modified by genetic mutation, ultraviolet light or chemical damage.
The UC Irvine team painstakingly explored and identified the structures of the normal proteins and a genetic mutation known to cause cataracts in young children. They found that the chaperone proteins bind far more strongly to the mutated proteins in an effort to keep the lens clear. One major problem: Every human eye contains a finite number of the helpful proteins. Once they’re used up, the researchers learned, weakened ones quickly begin to aggregate and form blinding cataracts.
Now that this mechanism has been mapped at the molecular level, the team is hopeful that organic chemists can create sight-saving treatments to prevent such aggregation.
While people with adequate medical care can have corrective surgery for cataracts, the World Health Organization has found that millions suffer major vision loss because they do not have access to laser surgery or other options. By 2019, the number of people older than 50 with impaired sight is expected to grow even higher, particularly in China, India, Southeast Asia and Eastern Mediterranean nations.
Martin’s co-authors are Carolyn Kingsley, William Brubaker and Amanda Brindley of UC Irvine and Stefan Markovic, Anne Diehl and Hartmut Oschkinat of Berlin’s Leibniz-Institut für Molekulare Pharmakologie. Funding was provided by National Institutes of Health grant 1R01EY021514 and a Deutsche Forschungsgemeinschaft grant.
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Structure, Volume 21, Issue 12, 2221-2227, 31 October 2013
Copyright © 2013 Elsevier Ltd All rights reserved.
Transparency in the eye lens is maintained via specific, functional interactions among the structural βγ- and chaperone α-crystallins. Here, we report the structure and α-crystallin binding interface of the G18V variant of human γS-crystallin (γS-G18V), which is linked to hereditary childhood-onset cortical cataract. Comparison of the solution nuclear magnetic resonance structures of wild-type and G18V γS-crystallin, both presented here, reveal that the increased aggregation propensity of γS-G18V results from neither global misfolding nor the solvent exposure of a hydrophobic residue but instead involves backbone rearrangement within the N-terminal domain. αB-crystallin binds more strongly to the variant, via a well-defined interaction surface observed via chemical shift differences. In the context of the αB-crystallin structure and the finding that it forms heterogeneous multimers, our structural studies suggest a potential mechanism for cataract formation via the depletion of the finite αB-crystallin population of the lens.
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This information was developed by the National Eye Institute to help patients and their families search for general information about cataracts. An eye care professional who has examined the patient’s eyes and is familiar with his or her medical history is the best person to answer specific questions.
Table of Contents
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Kingsley CN, Brubaker WD, Markovic S, Diehl A, Brindley AJ, Oschkinat H, & Martin RW (2013).
Preferential and Specific Binding of Human αB-Crystallin to a Cataract-Related Variant of γS-Crystallin.
Structure (London, England : 1993)
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December 5, 2013 Original online publication Tel Aviv University PDF American Friends of Tel Aviv University_ Coffee or Beer_ The Choice Could Affect Your Genome
TAU says caffeine and alcohol can change a part of DNA linked to aging and cancer
Coffee and beer are polar opposites in the beverage world. Coffee picks you up, and beer winds you down.
Now Prof. Martin Kupiec and his team at Tel Aviv University’s Department of Molecular Microbiology and Biotechnology have discovered that the beverages may also have opposite effects on your genome. Working with a kind of yeast that shares many important genetic similarities with humans, the researchers found that caffeine shortens and alcohol lengthens telomeres — the end points of chromosomal DNA, implicated in aging and cancer.
“For the first time we’ve identified a few environmental factors that alter telomere length, and we’ve shown how they do it,” said Prof. Kupiec. “What we learned may one day contribute to the prevention and treatment of human diseases.”
Researchers from TAU’s Blavatnik School of Computer Science and Columbia University’s Department of Biological Sciences collaborated on the research, published inPLOS Genetics.
Between death and immortality
Telomeres, made of DNA and proteins, mark the ends of the strands of DNA in our chromosomes. They are essential to ensuring that the DNA strands are repaired and copied correctly. Every time a cell duplicates, the chromosomes are copied into the new cell with slightly shorter telomeres. Eventually, the telomeres become too short, and the cell dies. Only fetal and cancer cells have mechanisms to avoid this fate; they go on reproducing forever.
The researchers set out to expand on a 2004 study by Nobel Prize-winning molecular biologist Prof. Elizabeth Blackburn, which suggested that emotional stress causes the shortening of the telomeres characteristic of aging, presumably by generating free radicals in the cells. The researchers grew yeast cells in conditions that generate free radicals to test the effect on telomere length. They were surprised to find that the length did not change.
They went on to expose the yeast cells to 12 other environmental stressors. Most of the stressors — from temperature and pH changes to various drugs and chemicals — had no effect on telomere length. But a low concentration of caffeine, similar to the amount found in a shot of espresso, shortened telomeres, and exposure to a 5-to-7 percent ethanol solution lengthened telomeres.
From yeasts to you
To understand these changes, the TAU researchers scanned 6,000 strains of the yeast, each with a different gene deactivated. They then conducted genetic tests on the strains with the longest and shortest telomeres, revealing that two genes, Rap1 and Rif1, are the main players mediating environmental stressors and telomere length. In total, some 400 genes interact to maintain telomere length, the TAU researchers note, underscoring the importance of this gene network in maintaining the stability of the genome. Strikingly, most of these yeast genes are also present in the human genome.
“This is the first time anyone has analyzed a complex system in which all of the genes affecting it are known,” said Prof. Kupiec. “It turns out that telomere length is something that’s very exact, which suggests that precision is critical and should be protected from environmental effects.”
More laboratory work is needed to prove a causal relationship, not a mere correlation, between telomere length and aging or cancer, the researchers say. Only then will they know whether human telomeres respond to the same signals as yeast, potentially leading to medical treatments and dietary guidelines. For now, Prof. Kupiec suggests, “Try to relax and drink a little coffee and a little beer.”
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Citation: Romano GH, Harari Y, Yehuda T, Podhorzer A, Rubinstein L, et al. (2013) Environmental Stresses Disrupt Telomere Length Homeostasis. PLoS Genet 9(9): e1003721. doi:10.1371/journal.pgen.1003721
Telomeres protect the chromosome ends from degradation and play crucial roles in cellular aging and disease. Recent studies have additionally found a correlation between psychological stress, telomere length, and health outcome in humans. However, studies have not yet explored the causal relationship between stress and telomere length, or the molecular mechanisms underlying that relationship. Using yeast as a model organism, we show that stresses may have very different outcomes: alcohol and acetic acid elongate telomeres, whereas caffeine and high temperatures shorten telomeres. Additional treatments, such as oxidative stress, show no effect. By combining genome-wide expression measurements with a systematic genetic screen, we identify the Rap1/Rif1 pathway as the central mediator of the telomeric response to environmental signals. These results demonstrate that telomere length can be manipulated, and that a carefully regulated homeostasis may become markedly deregulated in opposing directions in response to different environmental cues.
Over 70 years ago, Barbara McClintock described telomeres and hypothesized about their role in protecting the integrity of chromosomes. Since then, scientists have shown that telomere length is highly regulated and associated with cell senescence and longevity, as well as with age-related disorders and cancer. Here, we show that despite their importance, the tight, highly complex regulation of telomeres may be disrupted by environmental cues, leading to changes in telomere length. We have introduced yeast cells to 13 different environmental stresses to show that some stresses directly alter telomere length. Our results indicate that alcohol and acetic acid elongate telomeres, while caffeine and high temperatures shorten telomeres. Using expression data, bioinformatics tools, and a large genetic screen, we explored the mechanisms responsible for the alterations of telomere length under several stress conditions. We identify Rap1 and Rif1, central players in telomere length maintenance, as the central proteins directly affected by external cues that respond by altering telomere length. Because many human diseases are related to alterations in telomere length that fuel the disease’s pathology, controlling telomere length by manipulating simple stressing agents may point the way to effective treatment, and will supply scientists with an additional tool to study the machinery responsible for telomere length homeostasis.
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Romano GH, Harari Y, Yehuda T, Podhorzer A, Rubinstein L, Shamir R, Gottlieb A, Silberberg Y, Pe'er D, Ruppin E, Sharan R, & Kupiec M (2013). Environmental stresses disrupt telomere length homeostasis. PLoS genetics, 9 (9) PMID: 24039592
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