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Paper-thin Batteries Made from Algae
Batteries made of paper may power electronics in the future, researchers say. Shown are images from an experimental paper-based battery. Credit: The American Chemical Society
Batteries made of paper may power electronics in the future, researchers say. Shown are images from an experimental paper-based battery. Credit: The American Chemical Society
Imagine wrapping paper that could be a gift in and of itself because it lights up with words like "Happy Birthday." That is one potential application of a new biodegradable battery made of cellulose, the stuff of paper.
Scientists worldwide are striving to develop thin, flexible, lightweight, inexpensive, environmentally friendly batteries made entirely from nonmetal parts. Among the most promising materials for these batteries are conducting polymers.
However, until now these have impractical for use in batteries — for instance, their ability to hold a charge often degrades over use.
Easy to make
The key to this new battery turned out to be an often bothersome green algae known as Cladophora. Rotting heaps of this hairlike freshwater plant throughout the world can lead to unsightly, foul-smelling beaches.
This algae makes an unusual kind of cellulose typified by a very large surface area, 100 times that of the cellulose found in paper. This allowed researchers to dramatically increase the amount of conducting polymer available for use in the new device, enabling it to better recharge, hold and discharge electricity.
"We have long hoped to find some sort of constructive use for the material from algae blooms and have now been shown this to be possible," said researcher Maria Strømme, a nanotechnologist at Uppsala University in Sweden. "This creates new possibilities for large-scale production of environmentally friendly, cost-effective, lightweight energy storage systems."
The new batteries consisted of extremely thin layers of conducting polymer just 40 to 50 nanometers or billionths of a meter wide coating algae cellulose fibers only 20 to 30 nanometers wide that were collected into paper sheets.
"They're very easy to make," Strømme said.
Quick to charge
They could hold 50 to 200 percent more charge than similar conducting polymer batteries, and once better optimized, they might even be competitive with commercial lithium batteries, the researchers noted. They also recharged much faster than conventional rechargeable batteries — while a regular battery takes at least an hour to recharge, the new batteries could recharge in anywhere from eight minutes to just 11 seconds.
The new battery also showed a dramatic boost in the ability to hold a charge over use. While a comparable polymer battery showed a 50 percent drop in the amount of charge it could hold after 60 cycles of discharging and recharging, the new battery showed just a 6 percent loss through 100 charging cycles.
"When you have thick polymer layers, it's hard to get all the material to recharge properly, and it turns into an insulator, so you lose capacity," said researcher Gustav Nyström, an electrochemist at Uppsala University. "When you have thin layers, you can get it fully discharged and recharged."
Flexible electronics
The researchers suggest their batteries appear well-suited for applications involving flexible electronics, such as clothing and packaging.
"We're not focused on replacing lithium ion batteries — we want to find new applications where batteries are not used today," Strømme told LiveScience. "What if you could put batteries inside wallpaper to charge sensors in your home? If you could put this into clothes, can you couple that with detectors to analyze sweat from your body to tell if there's anything wrong?"
Future directions of research include seeing how much charge these batteries lose over time, a problem with polymer batteries and all batteries in general. They also want to see how much they can scale up these batteries, "see if we can make them much, much larger," Strømme said.
The scientists detailed their last month in the journal Nano Letters.
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Scientists successfully reprogram blood cells
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Researchers have transplanted genetically modified hematopoietic stem cells into mice so that their developing red blood cells produce a critical lysosomal enzyme –preventing or reducing organ and central nervous system damage from the often-fatal genetic disorder Hurler's syndrome.
The research team from Cincinnati Children's Hospital Medical Center reports its preclinical laboratory results this week in the early edition of Proceedings of the National Academy of Sciences.
The study suggests a new approach to molecular gene therapy and a much-needed improved treatment option for children with Hurler's syndrome, said Dao Pan, Ph.D., a researcher in the Division of Experimental Hematology/Cancer Biology at Cincinnati Children's and the study's principal author. It also is the first study to demonstrate that developing red blood cells can be used to produce lysosomal enzymes.
"The idea behind this is gene insertion so that after one treatment a person would be cured," said Dr. Pan. "In the mouse models receiving this treatment, the pathology of the peripheral organs tested was completely normalized. And although not as complete, we also saw significantly improved neurological function and brain pathology."
Hurler's syndrome is the severe form of MPS type1, or mucopolysaccharidoses. MPS type1 and similar genetic disorders are known as lysosomal storage disease, which are caused by the body's inability to produce specific lysosomal enzymes. Lysosomes, part of a cell's internal machinery, help the body's cells break down large molecules and recycle materials to fuel the healthy development and maintenance of vital organ and nerve tissues.
The lysosomes in the cells of children with Hurler syndrome do not have a vital enzyme called IDUA (/a-/L-idunronidase). This causes their cells to accumulate too much of a class of biochemical known as mucopolysaccharides, in this instance dermatan sulfate and heparin sulfate. This excess accumulation results in progressive tissue damage to organs and the central nervous system and typically results in early death.
Dr. Pan and her colleagues initially experimented on the cells of patients with Hurler syndrome that were cultured in the laboratory. They successfully used what is called a viral vector (in this case a lentivirus) to insert a healthy version of the IDUA gene into early stage red blood cell cultures, and a hybrid promoter gene, to prompt the cells to produce the IDUA enzyme. This could allow the enzyme to be absorbed by a patient's other cells to correct functional defects in the lysosomes.
Encouraged by the initial cell experiments, the research team next cultured hematopoietic stem cells taken from mouse models of MPS I. They did so using the same hybrid promoter gene from the earlier experiments to reprogram the stem cells to produce IDUA. They then performed bone marrow transplantation on the MPS I mice with the reprogrammed cells. The developing red blood cells in these mice produced large amounts of IDUA in the blood stream, which was absorbed by other cells that help make tissues for vital organs and the central nervous system.
Of particular interest to Dr. Pan and her colleagues was the ability of the IDUA in circulating blood to somehow bypass the blood brain barrier – normally a severe limitation in treating diseases that affect the central nervous system.
Besides Hurler syndrome, Dr. Pan said the study will have positive implications in the treatment of many other lysosomal storage diseases, which affect different parts of the body, depending on the specific enzyme deficiency. She also said this particular approach to gene therapy carries considerably less risk of stimulating cancer genes, which has been a concern with some forms of gene therapy. This is because the researchers used a promoter gene specific to red cells to stimulate IDUA production, and they did so in just one specific subset of blood cells (and not in any other offspring from genetically modified blood stem cells).
One current treatment method for Hurler syndrome includes bone marrow transplant from a healthy matched donor. These treatments have a mortality rate of 20 to 30 percent if patients can find a matched donor. Dr. Pan said reprogramming a patient's own developing red blood cells by gene therapy would provide a viable option for patients who cannot find a donor and avoid potential complications caused by an immune response to donor cells.
Another current treatment option is a pharmaceutical version of IDUA, although the therapy is limited because it cannot cross the blood brain barrier to address problems in the central nervous system. It also requires repeated life-long treatment.
Dr. Pan said additional research is needed to further verify the viral vectors used by the researchers, to evaluate the efficacy of this approach in larger animal models and to explain the molecular reasons for its success, especially the ability to cross the blood-brain barrier.
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How induced pluripotent stem cells differ from embryonic stem cells?
The same genes that are chemically altered during normal cell differentiation, as well as when normal cells become cancer cells, are also changed in stem cells that scientists derive from adult cells, according to new research from Johns Hopkins and Harvard.
Although genetically identical to the mature body cells from which they are derived, induced pluripotent stem cells (iPSCs) are notably special in their ability to self-renew and differentiate into all kinds of cells. And now scientists have detected a remarkable if subtle molecular disparity between the two: They have distinct "epigenetic" signatures; that is, they differ in what gets copied when the cell divides, even though these differences aren't part of the DNA sequence.
"Relatively little study has been done on the epigenetic nature of stem cells," says Andrew Feinberg, M.D., M.P.H., a professor of medicine at the Johns Hopkins University School of Medicine. "To date, the bulk of what is known about stem cells is focused on how you create them and grow them and so forth, but not on the essence of them, and what is fundamentally different about these cells."
To compare and contrast mature connective tissue cells called fibroblasts with the pluripotent stem cells into which they were reprogrammed, the investigators focused on a chemical change known as methylation. This chemical change which, associated with silencing genes, is classified as epigenetic because, although not part of the DNA sequence, is copied when a cell divides. They identified and then measured so-called differentially methylated regions (DMRs) of genes whose expression was changed in the process of being reprogrammed from a parent cell to a stem cell.
Building on previous research that looked at where differently methylated sites were located in cancer cells, as well as on research that had shown these same sites matching up with many of the methylated areas that had been implicated in the differentiation of normal brain, liver and spleen tissues, the team discovered that the reprogramming of a cell to become a stem cell apparently involves many of the very same DMRs and genes.
"The surprise," says Feinberg, "is that there is such a degree of overlap between the differently methylated regions and genes that are involved in turning a fibroblast into a stem cell and turning a normal cell into a cancer cell."
The study, done jointly with George Q. Daley, M.D., Ph.D., and colleagues from Harvard University, was published Nov. 1 in the advanced online edition of Nature Genetics. The researchers suggest in the study that certain sites throughout the genome appear to be generally involved in distinguishing DNA methylation among different cell types and cancers, and these same sites are involved in reprogramming fibroblasts back into stem cells.
The scientists used the CHARM method (comprehensive high-throughput arrays for relative methylation) to survey where, across the genomes of nine human iPS cell lines, genes had been silenced, or turned off, and then compared these DNA methylation sites with those of the fibroblasts the iPS cells were derived from.
"This type of research gets to the fabric of the fundamental differences between stem cells and their parental cells," says Akiko Doi, a doctoral candidate in the graduate program in Cellular and Molecular Medicine at Johns Hopkins. "Clearly, that fabric involves these DMRs, which are essential to our understanding the nature of these potentially therapeutic iPS cells."
As scientists learn more about the epigenetics of reprogrammed cells, they may find new ways of creating them or using them. "If we discover that certain genes or regions are altered in iPS cells," says Feinberg, "then we might be able to target these and come up with new ways of approaching stem cell therapy.
"We can try to correlate these differences with the ways these iPS cells behave, and answer questions such as which ones are more stable and which ones form tumors. If we can use the epigenetic information to characterize these cells, this could inform how we might use them therapeutically."
Adds Daley, director of the Stem Cell Transplantation Program at HHMI/Children's Hospital in Boston, "Our data also point to differences between iPS cells and embryonic stem (ES) cells, which everyone has felt were similar if not identical. Such differences may prove important in the behavior of iPS cells in studies on tissue formation and may complicate therapies based on iPS cells. We need to develop ways of generating iPS cells that are a closer match to ES cells in their methylation patterns. Only then will we be confident that iPS cells are a safe replacement for ES cells in research and therapy."
Source : Johns Hopkins Medical Institutions
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To make memories, new neurons must erase older ones
Short-term memory may depend in a surprising way on the ability of newly formed neurons to erase older connections. That's the conclusion of a report in the November 13th issue of the journal Cell, a Cell Press publication, that provides some of the first evidence in mice and rats that new neurons sprouted in the hippocampus cause the decay of short-term fear memories in that brain region, without an overall memory loss.
The researchers led by Kaoru Inokuchi of The University of Toyama in Japan say the discovery shows a more important role than many would have anticipated for the erasure of memories. They propose that the birth of new neurons promotes the gradual loss of memory traces from the hippocampus as those memories are transferred elsewhere in the brain for permanent storage. Although they examined this process only in the context of fear memory, Inokuchi says he "thinks all memories that are initially stored in the hippocampus are influenced by this process."
In effect, the new results suggest that failure of neurogenesis will lead to problems because the brain's short-term memory is literally full. In Inokuchi's words, we may perhaps experience difficulties in acquiring new information because the storage capacity of the hippocampus is "occupied by un-erased old memories."
Of course, Inokuchi added, "our finding does not necessary deny the important role of neurogenesis in memory acquisition." Hippocampal neurogenesis could have a dual role, he says, in both erasing old memories and acquiring new ones.
Earlier studies had shown a crucial role for the hippocampus in memorizing new facts. Studies in people with impaired and normal memories and in animals also showed that information recall initially depends on the hippocampus. That dependence progressively decays over time as memories are transferred to other regions, such as the neocortex. Scientists have also observed a similar decay in the strength of connections between neurons of the hippocampus, a phenomenon known as long-term potentiation (LTP) that is considered the cellular basis for learning and memory.
Scientists also knew that new neurons continue to form in the hippocampuses of adults, even into old age. But it wasn't really clear what those newborn brain cells actually do. Inokuchi's team suspected that the integration of new neurons was required to maintain neural connections, but they realized it might also go the other way. The incorporation of new neurons into pre-existing neural circuits might also disturb the structure of pre-existing information, and indeed that is what their new findings now show.
The researchers found that irradiation of rat's brains, which drastically reduces the formation of new neurons, maintains the strength of neural connections in the hippocampus. Likewise, studies of mice in which hippocampal neurogenesis was suppressed by either physical or genetic means showed a prolonged dependence of fear memories on that brain region.
On the other hand, voluntary exercise, which causes a rise in the birth of new neurons, sped up the decay rate of hippocampus-dependency of memory, without any memory loss.
"Enhanced neurogenesis caused by exercise may accelerate memory decay from the hippocampus and at the same time it may facilitate memory transfer to neocortex," Inokuchi said. "Hippocampal capacity of memory storage is limited, but in this way exercise could increase the [brain's overall] capacity."
The study sets the stage for further examination of the connections between neurogenesis and learning capacity, the researchers say. They also plan to examine how the gradual decay of memory dependence on the hippocampus relates to the transformation of memory over time from a detailed and contextually-rich form to a more generic one.
Source : Cell Press
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Why can't chimps speak?
Scientists suspect that part of the answer to the mystery lies in a gene called FOXP2. When mutated, FOXP2 can disrupt speech and language in humans. Now, a UCLA/Emory study reveals major differences between how the human and chimp versions of FOXP2 work, perhaps explaining why language is unique to humans.
Published Nov. 11 in the online edition of the journal Nature, the findings provide insight into the evolution of the human brain and may point to possible drug targets for human disorders characterized by speech disruption, such as autism and schizophrenia.
"Earlier research suggests that the amino-acid composition of human FOXP2 changed rapidly around the same time that language emerged in modern humans," said Dr. Daniel Geschwind, Gordon and Virginia MacDonald Distinguished Chair in Human Genetics at the David Geffen School of Medicine at UCLA. "Ours is the first study to examine the effect of these amino-acid substitutions in FOXP2 in human cells.
"We showed that the human and chimp versions of FOXP2 not only look different but function differently too," said Geschwind, who is currently a visiting professor at the Institute of Psychiatry at King's College London. "Our findings may shed light on why human brains are born with the circuitry for speech and language and chimp brains are not."
FOXP2 switches other genes on and off. Geschwind's lab scoured the genome to determine which genes are targeted by human FOXP2. The team used a combination of human cells, human tissue and post-mortem brain tissue from chimps that died of natural causes.
The chimp brain dissections were performed in the laboratory of coauthor Todd Preuss, associate research professor of neuroscience at Emory University's Yerkes National Primate Research Center.
The scientists focused on gene expression — the process by which a gene's DNA sequence is converted into cellular proteins.
To their surprise, the researchers discovered that the human and chimp forms of FOXP2 produce different effects on gene targets in the human cell lines.
"We found that a significant number of the newly identified targets are expressed differently in human and chimpanzee brains," Geschwind said. "This suggests that FOXP2 drives these genes to behave differently in the two species."
The research demonstrates that mutations believed to be important to FOXP2's evolution in humans change how the gene functions, resulting in different gene targets being switched on or off in human and chimp brains.
"Genetic changes between the human and chimp species hold the clues for how our brains developed their capacity for language," said first author Genevieve Konopka, a postdoctoral fellow in neurology at the David Geffen School of Medicine at UCLA. "By pinpointing the genes influenced by FOXP2, we have identified a new set of tools for studying how human speech could be regulated at the molecular level."
The discovery will provide insight into the evolution of humans' ability to learn through the use of higher cognitive skills, such as perception, intuition and reasoning.
"This study demonstrates how critical chimps and macaques are for studying humans," noted Preuss. "They open a window into understanding how we evolved into who we are today."
Because speech problems are common to both autism and schizophrenia, the new molecular pathways will also shed light on how these disorders disturb the brain's ability to process language.
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Why do snakes have forked tongue ?
Snakes are deaf and unable to hear air-borne sounds. Instead, they detect vibrations on the ground through their bodies. A two-tip tongue enables snakes to track other animals far more accurately by sweeping across trails left by their quarry and gauging very accurately where they lead.
Snakes flick their tongues in and out incredibly quickly to taste the chemical environment in front of them. The tongue tips sample the environmental chemicals mostly from air, but also from the ground. Each individual tip picks up odor molecules and, when the tongue reacts, it delivers them to two chemosensors called eronasal organ through separate holes in the top of the palate. As long as both tips are on the odor trail, the snake keeps going straight. But when the tongue diverts from the trail, the snake veers in the opposite direction in order to put itself back on track. If neither of them is on the trail, the snake stops and waves its head back and forth to pick up the odor again.
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What Makes a Scientist?
The scientist's job is to figure out how the world works, to "torture" Nature to reveal her secrets, as the 17th century philosopher Francis Bacon described it. But who are these people in the lab coats (or sports jackets, or suits, or T-shirts and jeans) and how do they work?
It turns out that there is a good deal of mystery surrounding the mystery-solvers.
"One of the greatest mysteries is the question of what it is about human beings—brains, education, culture etc.—that makes them capable of doing science at all," said Colin Allen, a cognitive scientist at Indiana University.
Few scientists have turned the microscope (or brain scanner) back on themselves. So even though the scientific method—with its hypotheses, data collection and statistical analysis—is well documented, the method by which scientists come to conclusions remains largely hidden.
"If we could understand scientifically what makes a scientist, this would potentially feed back on science itself and accelerate scientific progress," Allen said.
A curious development
Two vital ingredients seem to be necessary to make a scientist: the curiosity to seek out mysteries and the creativity to solve them.
"Scientists exhibit a heightened level of curiosity," reads a 2007 report on scientific creativity for the European Research Council. "They go further and deeper into basic questions showing a passion for knowledge for its own sake."
According to one definition, curiosity is a sensitivity to small discrepancies in an otherwise ordered world. Studies have shown that curious people have a mixture of seemingly conflicting desires: they seek novelty and strangeness and yet they also want everything in its proper place.
The curious scientist believes there is an order to the universe but is always looking for unexpected data points that will test the accepted theory.
Creative tool kit
To resolve the conflict between data and theory, a scientist often has to think outside the box and approach the problem from different angles.
Max Planck, one of the fathers of quantum physics, once said, the scientist “must have a vivid and intuitive imagination, for new ideas are not generated by deduction, but by an artistically creative imagination.”
To understand this scientific creativity, some philosophers of science have made an analogy with child development. The idea is that a scientist uses the same strategies for investigating the world as an infant does discovering his/her surroundings for the first time.
"This makes scientific abilities seem like part of a very basic 'tool kit' that is not specific to science itself," Allen said.
It harkens to something the astronomer Carl Sagan once said, "Everybody starts out as a scientist. Every child has the scientist's sense of wonder and awe."
Unwilling subjects
But others disagree with this universal scientific mind. They believe that scientists have special abilities that set them apart.
Discovering these abilities may be hard, Allen thinks, as many scientists will be reluctant to reveal them and would prefer to preserve the mystery of creativity, fearing that if it became an object of study it would lose its magic.
But for Allen, this is all part of a bigger question of what lies behind anyone's behavior.
"We are only just beginning to understand how the traits of organisms, including ourselves, aren't the fixed products of either genes or of environment/culture, but each of us is the product of a continual interactive process in which we help build the environments that in turn shape us," he said.
A brain doesn't work in a vacuum. It makes decisions that alter its surroundings, which in turn affects later decisions. Unraveling how this constant feedback loop works in a scientist will not be easy to do with current brain imaging techniques such as fMRI.
"As long as our best technology for seeing inside the brain requires subjects to lie nearly motionless while surrounded by a giant magnet, we're only going to make limited progress on these questions," Allen said.
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Does Alien Life Exist?
Life can be found in almost every nook and cranny of our planet Earth. Leaping, swimming, flying, sprinting, slithering, crawling or rooted firmly in place, organisms appear, die, and are replaced by new generations and new species.
Whether a similar bounty of life exists elsewhere in the universe is one of the oldest and most tantalizing questions of science. Considering the wide breadth of the universe and the countless stars it contains, the odds would seem in favor of the answer being "yes."
"We are here, made of stardust. Therefore, it is at least possible that there are others," said Jill Tarter, director of the Center for SETI Research in California.
Hardy critters
But today's scientists hope to get beyond mere statistics to find something more substantial, and more edifying. Perhaps more than at any other time in history, scientists are optimistic that extraterrestrial life does exist, and that a firm confirmation can be had.
Their hope is buoyed by recent discoveries of worlds beyond our solar system and new revelations recently learned about the hardiness of life here on our own planet.
"As we learn more about the diversity of life, particularly microbial life, we expand our definition of what life is and how life can exist in some very hostile (to humans) environments," said biologist Diana Northup of the University of New Mexico.
Scientists have discovered microbes that are resilient to levels of heat, cold, salt, acidity, and radiation that would kill humans. Some of these so-called "extremophiles" have been found thriving in complete darkness, in parched deserts and even miles below ground.
All of this is good news for astrobiologists who dream of finding life beyond Earth's confines, as many of the extreme environments on our planet are thought to be the norm for other worlds. Earth's deserts, for example, have analogues on dry, dusty Mars. Saturn's moon Titan is a world of meandering rivers and lakes, and beneath the icy crust of another Saturn moon, Enceladus, might lie environments resembling the frigid ocean depths of Earth.
Brave new worlds
Astrobiologists are also heartened by the recent explosion of new planets discovered outside our solar system. Since 1995, when astronomers spotted the first planet in orbit around another normal star, the number of extrasolar planets, or "exoplanets," has swelled to over 200. Scientists now know of more than 20 times more planets outside our solar system than in it.
The majority of exoplanets discovered so far are bloated, fast-spinning gas giants, known as "hot Jupiters," that orbit extremely close to their stars and are thus probably unsuitable for life.
But some exoplanets are wondrously Earth-like. Scientists recently spotted one world only 20.5 light-years away that lies within the habitable zone of its star—the region around a star where liquid water, and thus life, might exist. (It was later discovered the planet might be too hot for life, but another potentially habitable world in the same system was quickly found to take its place.)
With the ongoing refinement of current planet-finding techniques and the launch of new satellites, scientists expect not only to find a truly Earth-like world, but to also be able to probe it for life's spectral fingerprints carried by a planet's reflected light.
"Depending on what level of seeking and finding we are prepared to do, we could make discoveries in the next two decades that entirely change the way we understand the universe and life," said Margaret Turnbull, an astrobiologist at the Space Telescope Science Institute in Baltimore, Maryland.
SETI
Of course, there is always the chance that extraterrestrial life will find us first. Perhaps not in the form of a visiting UFO, but a radio transmission from an advanced alien civilization is still considered within the realm of possibility.
"Mankind has achieved scientific-technological civilization only in the last 200 years or so, out of about 4.5 billion years of life on Earth," said Frank Wilczek, a Nobel-Prize winning physicist at MIT. "So it seems we ought to expect there to be many scientific-technological civilizations that have had many millions, or even billions, of years to develop."
But even the discovery of one single-celled microbe on a distant world would be enough—enough to finally answer that age old question of "Are we alone in the universe?" and enough to change how humanity views itself.
"The discovery of life forms inhabiting the unexplored extremities of our own planet, and eventually, the discovery of life on other planets, will bring into greater awareness the magnificence of a living universe," Turnball told LiveScience, "and, hopefully, a better understanding of ourselves."