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Scooped by Dr. Stefan Gruenwald!

Periodic Table of Mathematical Objects: The L-functions and Modular Forms Database

Periodic Table of Mathematical Objects: The L-functions and Modular Forms Database | Amazing Science |

A team of more than 80 mathematicians from 12 countries has begun charting the terrain of rich, new mathematical worlds, and sharing their discoveries on the Web. The mathematical universe is filled with both familiar and exotic items, many of which are being made available for the first time.


The "L-functions and Modular Forms Database," abbreviated LMFDB, is an intricate catalog of mathematical objects and the connections between them. Making those relationships visible has been made possible largely by the coordinated efforts of a group of researchers developing new algorithms and performing calculations on an extensive network of computers. The project provides a new tool for several branches of mathematics, physics, and computer science.


A "periodic table" of mathematical objects

Project member John Voight, from Dartmouth College, observed that "our project is akin to the first periodic table of the elements. We have found enough of the building blocks that we can see the overall structure and begin to glimpse the underlying relationships." Similar to the elements in the periodic table, the fundamental objects in mathematics fall into categories. Those categories have names like L-function, elliptic curve, and modular form. The L-functions play a special role, acting like 'DNA' which characterizes the other objects. More than 20 million objects have been catalogued, each with its L-function that serves as a link between related items. Just as the value of genome sequencing is greatly increased when many members of a population have been sequenced, the comprehensive material in the LMFDB will be an indispensible tool for new discoveries.


The LMFDB provides a sophisticated web interface that allows both experts and amateurs to easily navigate its contents. Each object has a "home page" and links to related objects, or "friends." Holly Swisher, a project member from Oregon State University, commented that the friends links are one of the most valuable aspects of the project: "The LMFDB is really the only place where these interconnections are given in such clear, explicit, and navigable terms. Before our project it was difficult to find more than a handful of examples, and now we have millions."

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Scientists reveal new super-fast form of computer that ‘grows as it computes’

Scientists reveal new super-fast form of computer that ‘grows as it computes’ | Amazing Science |

Researchers from The University of Manchester have shown that it is possible to build a new super-fast form of computer that “grows as it computes”.

Professor Ross D King and his team have demonstrated for the first time the feasibility of engineering a nondeterministic universal Turing machine (NUTM), and their research is to be published in the prestigious Journal of the Royal Society Interface.

The theoretical properties of such a computing machine, including its exponential boost in speed over electronic and quantum computers, have been well understood for many years – but the Manchester breakthrough demonstrates that it is actually possible to physically create a NUTM using DNA molecules.

“Imagine a computer is searching a maze and comes to a choice point, one path leading left, the other right,” explained Professor King, from Manchester’s School of Computer Science. “Electronic computers need to choose which path to follow first.

“But our new computer doesn’t need to choose, for it can replicate itself and follow both paths at the same time, thus finding the answer faster.

“This ‘magical’ property is possible because the computer’s processors are made of DNA rather than silicon chips. All electronic computers have a fixed number of chips.

Via Integrated DNA Technologies
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Visualising the genome: Researchers create first 3D structures of active DNA

Visualising the genome: Researchers create first 3D structures of active DNA | Amazing Science |

Scientists have determined the first 3D structures of intact mammalian genomes from individual cells, showing how the DNA from all the chromosomes intricately folds to fit together inside the cell nuclei.


Researchers from the University of Cambridge and the MRC Laboratory of Molecular Biology used a combination of imaging and up to 100,000 measurements of where different parts of the DNA are close to each other to examine the genome in a mouse embryonic stem cell. Stem cells are 'master cells', which can develop -- or 'differentiate' -- into almost any type of cell within the body.


Most people are familiar with the well-known 'X' shape of chromosomes, but in fact chromosomes only take on this shape when the cell divides. Using their new approach, the researchers have now been able to determine the structures of active chromosomes inside the cell, and how they interact with each other to form an intact genome. This is important because knowledge of the way DNA folds inside the cell allows scientists to study how specific genes, and the DNA regions that control them, interact with each other. The genome's structure controls when and how strongly genes -- particular regions of the DNA -- are switched 'on' or 'off'. This plays a critical role in the development of organisms and also, when it goes awry, in disease.


The researchers have illustrated the structure in accompanying videos, which show the intact genome from one particular mouse embryonic stem cell. In the film, above, each of the cell's 20 chromosomes is colored differently.


In a second video regions of the chromosomes where genes are active are colored blue, and the regions that interact with the nuclear lamina (a dense fibrillar network inside the nucleus) are colored yellow. The structure shows that the genome is arranged such that the most active genetic regions are on the interior and separated in space from the less active regions that associate with the nuclear lamina. The consistent segregation of these regions, in the same way in every cell, suggests that these processes could drive chromosome and genome folding and thus regulate important cellular events such as DNA replication and cell division.


Professor Ernest Laue, whose group at Cambridge's Department of Biochemistry developed the approach, commented: "Knowing where all the genes and control elements are at a given moment will help us understand the molecular mechanisms that control and maintain their expression.


"In the future, we'll be able to study how this changes as stem cells differentiate and how decisions are made in individual developing stem cells. Until now, we've only been able to look at groups, or 'populations', of these cells and so have been unable to see individual differences, at least from the outside. Currently, these mechanisms are poorly understood and understanding them may be key to realizing the potential of stem cells in medicine."

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Scientific First: Quantum microscope offers MRI for Molecules

Scientific First: Quantum microscope offers MRI for Molecules | Amazing Science |

A quantum microscope that uses a sensor built from diamonds could allow researchers to study such nanoscale mysteries as how DNA folds in a cell, why drugs work or how bacteria metabolize metals. Crucially, the microscope can image individual ions in a solution and reveal biochemical reactions as they occur — without interfering in the process. The team behind the system described the results in a 14 February preprint on the arXiv server1.


Researchers have long wanted an imaging system for molecular structures that works like hospital magnetic resonance imaging (MRI) machines, which reveal structures inside the human body without harming them. The idea behind a quantum MRI — which images at the quantum level using electron spins — is to do the same for chemical reactions including those involving metal ions. Current magnetic resonance techniques can only reveal structures measuring 10 micrometers or more, and the only way to detect metal ions inside a cell is to add reactive chemicals or freeze the cell so it can be imaged under powerful microscopes — procedures that kill the cell.


A hospital MRI machine works by placing a patient inside a magnetic field, such that protons in the body's atoms align with the machine's magnet. The machine then sends radio pulses through the body area being imaged, which knocks the protons out of alignment. When these pulses are switched off, the protons realign and emit electromagnetic waves at a particular frequency. If the frequency emitted by the body's tissues matches that of sensors in the machine, the two frequencies will resonate like guitar strings tuned to the same note. The machine uses this resonance to reconstruct an image of the body.

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Shape-shifting molecular robots respond to DNA signals

Shape-shifting molecular robots respond to DNA signals | Amazing Science |

A research group at Tohoku University and Japan Advanced Institute of Science and Technology has developed a molecular robot consisting of biomolecules, such as DNA and protein. The molecular robot was developed by integrating molecular machines into an artificial cell membrane. It can start and stop its shape-changing function in response to a specific DNA signal.


This is the first time that a molecular robotic system has been able to recognize signals and control its shape-changing function. What this means is that molecular robots could, in the near future, function in a way similar to living organisms.

Using sophisticated biomolecules such as DNA and proteins, living organisms perform important functions. For example, white blood cells can chase bacteria by sensing chemical signals and migrating toward the target. In the field of chemistry and synthetic biology, elemental technologies for making various molecular machines, such as sensors, processors and actuators, are created using biomolecules.


A molecular robot is an artificial molecular system that is built by integrating molecular machines. The researchers believe that realization of such a system could lead to a significant breakthrough -- a bio-inspired robot designed on a molecular basis.


The molecular robot developed by the research group is extremely small -- about one millionth of a meter -- similar in size to human cells. It consists of a molecular actuator, composed of protein, and a molecular clutch, composed of DNA. The shape of the robot's body (artificial cell membrane) can be changed by the actuator, while the transmission of the force generated by the actuator can be controlled by the molecular clutch.


The research group demonstrated through experiments that the molecular robot could start and stop the shape-changing behavior in response to a specific DNA signal. "With more than 20 chemicals at varying concentrations, it took us a year and a half to establish good conditions for working our molecular robots," says Associate Professor Shin-ichiro Nomura at Tohoku University's Graduate School of Engineering, who led the study. "It was exciting to see the robot shape-changing motion through the microscope. It meant our designed DNA clutch worked perfectly, despite the complex conditions inside the robot."

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What Can You Do With the World's Largest Family Tree of 13 Million People?

What Can You Do With the World's Largest Family Tree of 13 Million People? | Amazing Science |

Your family tree might contain a few curious revelations. It might alert you to the existence of long-lost third cousins. It might tell you your 10-times-great-grandfather once bought a chunk of Brooklyn. It might reveal that you have royal blood. But when family trees includes millions of people—maybe even tens of millions of people—then we’re beyond the realm of individual stories.


When genealogies get so big, they’re not just the story of a family anymore; they contain the stories of whole countries and, at the risk of sounding grandiose, even all of humanity.


Last week, scientists using data from and each unveiled papers analyzing the genealogies for patterns like migrations, lifespan, and when people stopped marrying family members. sells both subscriptions to its genealogy research site and a popular genetic test through its subsidiary AncestryDNA. Its geneticists— along with a historian—used the genetic data of 770,000 AncestryDNA customers along with the genealogy records of their ancestors to map migrations in North America.


The team first analyzed the DNA tests to find clusters of closely related people in the present. Then, they matched up the people in those clusters with genealogy records containing 20 million people, which included the birthplaces of several generations of ancestors. With that, they could march backwards in time to see how those ancestors migrated across the U.S.

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Scientists Announce HGP-Write, Project to Synthesize the Full Human Genome

Scientists Announce HGP-Write, Project to Synthesize the Full Human Genome | Amazing Science |

Proposals for a large public–private initiative to synthesize an entire human genome from scratch — an effort that could take a decade and require billions of dollars in technological development — were formally unveiled on 2 June 2016, almost a month after they were first aired at a secretive meeting.


Proponents of the effort, named ‘Human Genome Project—Write’ (HGP-write), write in Science that US$100 million from a range of funding sources would help to get their vision off the ground1. The team is led by synthetic biologist Jef Boeke at New York University; genome scientist George Church at Harvard Medical School in Boston, Massachusetts; and Andrew Hessel, a futurist at the commercial design studio Autodesk Research in San Rafael, California. But the idea — which essentially aims to develop technologies that reduce the cost of DNA synthesis — has not met with universal excitement among researchers.


To some, the proposal to create a human genome is praiseworthy for its ambition and sheer chutzpah: at present, only tiny bacterial genomes and a portion of a yeast genome have been made from scratch. But other researchers feel that HGP-write represents a needless centralization of work that is already taking place in companies trying to lower the price of synthesizing strings of DNA. Some of HGP-write’s proponents have financial stakes in those firms, which include Gen9 in Cambridge, Massachusetts. “My first thought was ‘so what’,” says Martin Fussenegger, a synthetic biologist at the Swiss Federal Institute of Technology in Zurich. “I personally think this will happen naturally. It’s just a matter of price at the end.”


Others think that the project should be delayed until its leaders can win broader support for the idea. In an e-mail sent to reporters, synthetic biologist Drew Endy, at Stanford University in California, and religion scholar Laurie Zoloth, at Northwestern University in Evanston, Illinois, say that the HGP-write team has not properly justified its aims, and that the project should be abandoned. “We are still waiting for a serious public debate with participation from a broad range of people,” they say.


Endy and Zoloth had already questioned the scientific rationale for synthesizing a human genome in May, when HGP-write was first aired at an invitation-only meeting at Harvard University that was attended by more than 100 scientists, entrepreneurs, lawyers and ethicists. The closed nature of the meeting also attracted criticism: Church told the health and medicine news service Stat that this was because the paper describing the effort was under embargo.


“There was a lot of confusion on the day about what was going on,” says Tom Ellis, a synthetic biologist at Imperial College London, who attended the meeting. “Some people were in the know on the [paper’s] review process and others were trying to find out.”


The three-page announcement of HGP-write fills in some detail. It notes that current technologies are both too expensive and too primitive to synthesize the 3-billion-base-pair human genome. The team calls for a series of pilot projects, including synthesizing much shorter segments of the genome and making slimmed-down chromosomes to do specific tasks, to make its eventual goal doable. The whole project should require less than $3 billion (the price of the publicly funded Human Genome Project), the researchers say.


“I think it’s a brilliant project,” says Paul Freemont, a structural biologist at Imperial College London, who attended the meeting. “If you want to do this, it’s going to be on the same scale as the Human Genome Project, it’s going to need some big funding agencies and hundreds and hundreds of researchers around the world.”


Read more in Nature



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How Life (and Death) Spring From Disorder

How Life (and Death) Spring From Disorder | Amazing Science |

Life was long thought to obey its own set of rules. But as simple systems show signs of lifelike behavior, scientists are arguing about whether this apparent complexity is all a consequence of thermodynamics.


Living organisms seem rather like Maxwell’s demon. Whereas a beaker full of reacting chemicals will eventually expend its energy and fall into boring stasis and equilibrium, living systems have collectively been avoiding the lifeless equilibrium state since the origin of life about three and a half billion years ago. They harvest energy from their surroundings to sustain this nonequilibrium state, and they do it with “intention.” Even simple bacteria move with “purpose” toward sources of heat and nutrition. In his 1944 bookWhat is Life?, the physicist Erwin Schrödinger expressed this by saying that living organisms feed on “negative entropy.”


They achieve it, Schrödinger said, by capturing and storing information. Some of that information is encoded in their genes and passed on from one generation to the next: a set of instructions for reaping negative entropy. Schrödinger didn’t know where the information is kept or how it is encoded, but his intuition that it is written into what he called an “aperiodic crystal”inspired Francis Crick, himself trained as a physicist, and James Watson when in 1953 they figured out how genetic information can be encoded in the molecular structure of the DNA molecule.


A genome, then, is at least in part a record of the useful knowledge that has enabled an organism’s ancestors — right back to the distant past — to survive on our planet. According to David Wolpert, a mathematician and physicist at the Santa Fe Institute who convened the recent workshop, and his colleagueArtemy Kolchinsky, the key point is that well-adapted organisms are correlated with that environment. If a bacterium swims dependably toward the left or the right when there is a food source in that direction, it is better adapted, and will flourish more, than one  that swims in random directions and so only finds the food by chance. A correlation between the state of the organism and that of its environment implies that they share information in common. Wolpert and Kolchinsky say that it’s this information that helps the organism stay out of equilibrium — because, like Maxwell’s demon, it can then tailor its behavior to extract work from fluctuations in its surroundings. If it did not acquire this information, the organism would gradually revert to equilibrium: It would die.


Looked at this way, life can be considered as a computation that aims to optimize the storage and use of meaningful information. And life turns out to be extremely good at it. Landauer’s resolution of the conundrum of Maxwell’s demon set an absolute lower limit on the amount of energy a finite-memory computation requires: namely, the energetic cost of forgetting. The best computers today are far, far more wasteful of energy than that, typically consuming and dissipating more than a million times more. But according to Wolpert, “a very conservative estimate of the thermodynamic efficiency of the total computation done by a cell is that it is only 10 or so times more than the Landauer limit.”

The implication, he said, is that “natural selection has been hugely concerned with minimizing the thermodynamic cost of computation. It will do all it can to reduce the total amount of computation a cell must perform.” In other words, biology (possibly excepting ourselves) seems to take great care not to overthink the problem of survival. This issue of the costs and benefits of computing one’s way through life, he said, has been largely overlooked in biology so far.

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Genome surgery with CRISPR-Cas9 to prevent blindness

Genome surgery with CRISPR-Cas9  to prevent blindness | Amazing Science |
IBS study proves that CRISPR-Cas9 can be delivered directly into the eye of living animals to treat age-related macular degeneration efficiently and safely.


It is estimated that almost one in every ten people over 65 has some signs of age-related macular degeneration (AMD), and its prevalence is likely to increase as a consequence of the aging population. AMD is a form of blindness, common in Caucasians, which causes distorted vision and blind spots. Scientists at the Center for Genome Engineering, within the Institute for Basic Science (IBS) report the use of CRISPR-Cas9 in performing "gene surgery" in the layer of tissue that supports the retina of living mice. Published in Genome Research, this study combines basic research and mouse model applications.


The most common retinopathies causing blindness are 'retinopathy of prematurity' in children, 'diabetic retinopathy' and 'AMD' in older adults. In these diseases, abnormally high levels of the Vascular Endothelial Growth Factor (VEGF) are secreted. In AMD, VEGF causes the formation of new blood vessels in the eyes but also leads to leakages of blood and fluid into the eye, damaging an area at the center of the retina called macula.


Injections of anti-VEGF drugs are the most common treatment against AMD, but at least seven injections per year are required, because VEGF is continuously overexpressed by the cells of the diseased retinal pigment epithelium. Instead of such invasive treatments, IBS scientists believe that gene therapy with the third generation gene editing tool CRISPR-Cas9 could improve the situation. "The injections tackle the effects, but not the main cause of the problem. By editing the VEGF gene, we can achieve a longer-term cure," explains KIM Jin-Soo, Director of the Center for Genome Engineering.


CRISPR-Cas9 can precisely cut and correct DNA at the desired site in the genome. The CRISPR-Cas9 system works by cutting DNA at a target site, in this case, inside the VEGF gene. Two year ago, IBS scientists proved that a pre-assembled version of CRISPR-Cas9, a.k.a, Cas9 ribonucleoprotein (RNP), can be delivered to cells and stem cells to modify target genes. The pre-assembled complex works rapidly and degrades before the body has time to build up an immune response against it. Despite these advantages and previous successes, the difficulty in delivering pre-assembled CRISPR-Cas9 has limited its use in therapeutic applications.


In this study, the research team successfully injected CRISPR-Cas9 into the eyes of a mice model with wet AMD and locally modified the VEGF gene. Initially they found that the delivery of the pre-assembled CRISPR-Cas9 complex is more efficient that the delivery of the same components in a plasmid form. Secondly, the complex disappeared after just 72 hours.


Scientists assessed the whole genome of the animals and found the CRISPR-Cas9 complex modified only the VEGF gene and did not affect other genes. The progression of the eye disease was monitored by looking at choroidal neovascularization (CNV), the creation of new blood vessels between the retina and the sclera - a common problem of 'wet' macular degeneration - and researchers found the CNV area reduced by 58%. Moreover, a likely side effect, namely cone dysfunction, that takes only 3 days to show in these mice, did not occur a week after the treatment.

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Extinct tortoise species with mostly intact DNA from a water-filled limestone sinkhole

Extinct tortoise species with mostly intact DNA from a water-filled limestone sinkhole | Amazing Science |

An extinct tortoise species that accidentally tumbled into a water-filled limestone sinkhole in the Bahamas about 1,000 years ago has finally made its way out, with much of its DNA intact.

As the first sample of ancient DNA retrieved from an extinct tropical species, this genetic material could help provide insights into the history of the Caribbean tropics and the reptiles that dominated them, said University of Florida ornithologist David Steadman. It could also offer clues to the region’s future, as the tropics undergo significant transformation due to climate change.


“This is the first time anyone has been able to put a tropical species into an evolutionary context with molecular data,” said Steadman, an ornithology curator at the Florida Museum of Natural History on the UF campus and co-author of the study discussing the finding. “And being able to fit together the tortoise’s evolutionary history together will help us better understand today’s tropical species, many of which are endangered.”

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Study: Induced pluripotent stem cells don't increase genetic mutations

Study: Induced pluripotent stem cells don't increase genetic mutations | Amazing Science |

It's been more than 10 years since Japanese researchers Shinya Yamanaka, M.D., Ph.D., and his graduate student Kazutoshi Takahashi, Ph.D., developed the breakthrough technique to return any adult cell to its earliest stage of development (a pluripotent stem cell) and change it into different types of cells in the body.


Called induced pluripotent stem cells (iPSCs), this technique opens the doors to medical advances, including generating cartilage cell tissue to repair knees, retinal cells to improve the vision of those with age-related macular degeneration and other eye diseases, and cardiac cells to restore damaged heart tissues.

Despite its immense promise, adoption of iPSCs in biomedical research and medicine has been slowed by concerns that these cells are prone to increased numbers of genetic mutations.


A new study by scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, suggests that iPSCs do not develop more mutations than cells that are duplicated by subcloning. Subcloning is a technique where single cells are cultured individually and then grown into a cell line. The technique is similar to the iPSC except the subcloned cells are not treated with the reprogramming factors which were thought to cause mutations. The researchers published their findings on February 6, 2017, in the Proceedings of the National Academy of Sciences.


"This technology will eventually change how doctors treat diseases. These findings suggest that the question of safety shouldn't impede research using iPSC," said Pu Paul Liu, M.D., Ph.D., co-author, senior investigator in NHGRI's Translational and Functional Genomics Branch and deputy scientific director for the Division of Intramural Research.


Dr. Liu and his collaborators examined two sets of donated cells: one set from a healthy person and the second set from a person with a blood disease called familial platelet disorder. Using skin cells from the same donor, they created genetically identical copies of the cells using both the iPSC and the subcloning techniques. They then sequenced the DNA of the skin cells as well as the iPSCs and the subcloned cells and determined that mutations occurred at the same rate in cells that were reprogrammed and in cells that were subcloned.


Most genetic variants detected in the iPSCs and subclones were rare genetic variants inherited from the parent skin cells. This finding suggests that most mutations in iPSCs are not generated during the reprogramming or iPSC production phase and provides evidence that iPSCs are stable and safe to use for both basic and clinical research, Dr. Liu said.

Via Mariaschnee
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Optogenetic Toolbox to Specifically Alter Methylation Pattern of Specific Sites

Optogenetic Toolbox to Specifically Alter Methylation Pattern of Specific Sites | Amazing Science |

Enzymes involved in epigenetic processes such as methyltransferases or demethylases are becoming highly utilized for their persistent DNA or histone modifying efficacy. Scientists now have developed an optogenetic toolbox fused to the catalytic domain (CD) of DNA-methyltransferase3A (DNMT3A-CD) or Ten-Eleven Dioxygenase-1 (TET1-CD) for loci-specific alteration of the methylation state at the promoter of Ascl1 (Mash1), a candidate proneuron gene. Optogenetical protein pairs, CRY2 linked to DNMT3A-CD or TET1-CD and CIB1 fused to a Transcription Activator-Like Element (TALE) locating an Ascl1 promoter region, were designed for site specific epigenetic editing. A differentially methylated region at the Ascl1 promoter, isolated from murine dorsal root ganglion (hypermethylated) and striated cells (hypomethylated), was targeted with these optogenetic-epigenetic constructs. Optimized blue-light illumination triggered the co-localization of TALE constructs with DNMT3A-CD or TET1-CD fusion proteins at the targeted site of the Ascl1 promoter.


The researchers found that this spatiotemporal association of the fusion proteins selectively alters the methylation state and also regulates gene activity. This proof of concept developed herein holds immense promise for the ability to regulate gene activity via epigenetic modulation with spatiotemporal precision.

Via dromius
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Supercomputing, experiment combine for first look at magnetism of real nanoparticle

Supercomputing, experiment combine for first look at magnetism of real nanoparticle | Amazing Science |

Barely wider than a strand of human DNA, magnetic nanoparticles -- such as those made from iron and platinum atoms -- are promising materials for next-generation recording and storage devices like hard drives. Building these devices from nanoparticles should increase storage capacity and density, but understanding how magnetism works at the level of individual atoms is critical to getting the best performance.


However, magnetism at the atomic scale is extremely difficult to observe experimentally, even with the best microscopes and imaging technologies. That's why researchers working with magnetic nanoparticles at the University of California, Los Angeles (UCLA), and the US Department of Energy's (DOE's) Lawrence Berkeley National Laboratory (Berkeley Lab) approached computational scientists at DOE's Oak Ridge National Laboratory (ORNL) to help solve a unique problem: to model magnetism at the atomic level using experimental data from a real nanoparticle.


"These types of calculations have been done for ideal particles with ideal crystal structures but not for real particles," said Markus Eisenbach, a computational scientist at the Oak Ridge Leadership Computing Facility (OLCF), a DOE Office of Science User Facility located at ORNL.


Eisenbach develops quantum mechanical electronic structure simulations that predict magnetic properties in materials. Working with Paul Kent, a computational materials scientist at ORNL's Center for Nanophase Materials Sciences, the team collaborated with researchers at UCLA and Berkeley Lab's Molecular Foundry to combine world-class experimental data with world-class computing to do something new--simulate magnetism atom by atom in a real nanoparticle.


Using the new data from the research teams on the West Coast, Eisenbach and Kent were able to precisely model the measured atomic structure, including defects, from a unique iron-platinum (FePt) nanoparticle and simulate its magnetic properties on the 27-petaflop Titan supercomputer at the OLCF.


Electronic structure codes take atomic and chemical structure and solve for the corresponding magnetic properties. However, these structures are typically derived from many 2-D electron microscopy or x-ray crystallography images averaged together, resulting in a representative, but not true, 3-D structure.

Via Mariaschnee
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Funnel web spider venom can protect cells from being destroyed by a stroke

Funnel web spider venom can protect cells from being destroyed by a stroke | Amazing Science |

Doctors have stumbled on an unlikely source for a drug to ward off brain damage caused by strokes: the venom of one of the deadliest spiders in the world.


A bite from an Australian funnel web spider can kill a human in 15 minutes, but a harmless ingredient found in the venom can protect brain cells from being destroyed by a stroke, even when given hours after the event, scientists say. If the compound fares well in human trials, it could become the first drug that doctors have to protect against the devastating loss of neurons that strokes can cause.


Researchers discovered the protective molecule by chance as they sequenced the DNA of toxins in the venom of the Darling Downs funnel web spider (Hadronyche infensa) that lives in Queensland and New South Wales. Venom from three spiders was gathered for the study after scientists trapped and “milked exhaustively” three spiders on Orchid beach, about 400km north of Brisbane.


The molecule, called Hi1a, stood out because it looked like two copies of another brain cell-protecting chemical stitched together. It was so intriguing that scientists decided to synthesize the compound and test its powers. “It proved to be even more potent,” said Glenn King at the University of Queensland’s centre for pain research.


Strokes occur when blood flow to the brain is interrupted and the brain is starved of oxygen. About 85% of strokes are caused by blockages in blood vessels in the brain, with the rest due to bleeds when vessels rupture. Approximately six million people a year die from stroke, making it the second largest cause of death worldwide after heart attacks.

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Making CRISPR More Accessible

Making CRISPR More Accessible | Amazing Science |

Researchers have developed a novel computational tool to help design single guide RNAs (sgRNAs) for DNA deletion using the CRISPR-Cas system. The new tool, CRISPETa, was reported in PLOS Computational Biology recently.


Since its initial discovery and subsequent development throughout the last decade, CRISPR has become known as a powerful tool in genomic experiments, both for trying to understand the genome and attempting to treat genetic disorders. Several variants of the system have been developed, such as CRISPRi to influence gene expression at a transcription level and dCas9 to bind to the DNA without cleaving the strand. In 2015, Professor Rory Johnson and his team developed another CRISPR variant, known as DECKO, which was designed specifically to facilitate the removal of selected DNA sequences from the genome.


DECKO uses two distinct sgRNAs to guide the cleavage protein Cas9 to the correct sites in the genome on either side of the material being deleted. When the nuclease cleaves the DNA at both sites, the sequence between the two loci is removed completely from the genome with high accuracy. The nature of CRISPR means that DECKO can be used to remove both coding and non-coding material and as a result has become a popular tool among researchers.


During the initial development of DECKO, the team noticed that one of the most time-consuming parts of their experiments was the sgRNA design process because there was no pre-made design software available. Now, Master’s student Carlos Pulido may have created the solution to this problem with a novel software pipeline called CRISPETa, which can suggest sgRNAs based on the intended target region.

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First results of CRISPR gene editing of human embryos released from China

First results of CRISPR gene editing of human embryos released from China | Amazing Science |

A team in China has corrected genetic mutations in at least some of the cells in three normal human embryos using the CRISPR genome editing technique. The latest study is the first to describe the results of using CRISPR in viable human embryos, New Scientist can reveal.


While this study – which attempted to repair the DNA of six embryos in total – was very small, the results suggest CRISPR works much better in normal embryos than it did in previous tests on abnormal embryos that could not develop into children.

“It is encouraging,” says Robin Lovell-Badge of the Francis Crick Institute in London, who has contributed to several major reports on human genome editing. The numbers are far too low to make strong conclusions though, he cautions.


The CRISPR gene editing technique is a very efficient way of disabling genes, by introducing small mutations that disrupt the code of a DNA sequence. CRISPR can also be used to repair genes, but this is much more difficult.
Until now, results have only been published from experiments in which the CRISPR technique was used in abnormal embryos, made when two sperm fertilize the same egg. The idea behind this work was that it was more ethical to test the technique on embryos that could never fully develop.
In the first attempt to fix genes in human embryos, fewer than 1 in 10 cells were successfully repaired – an efficiency rate that is too low to make the method practical. A second study published in 2016 also had a low rate of efficiency. However, because these embryos were very genetically abnormal, these experiments may not have given an accurate indication of how well the technique would work in healthier embryos.
The Chinese team behind the latest study, at the Third Affiliated Hospital of Guangzhou Medical University, first carried out experiments with abnormal embryos, and found the repair rate was very low. But they had more success when they tried to repair mutations in normal embryos derived from immature eggs donated by people undergoing IVF.
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Study identifies key factor in DNA damage associated with aging 

Study identifies key factor in DNA damage associated with aging  | Amazing Science |

In a recent study, Rochester scientists made two important contributions to DNA damage research. First, though scientists could previously point to an association between DNA damage and aging, the Rochester group has demonstrated a causal relationship between reduced DNA damage and extended lifespan. Second, the researchers have identified a cellular factor—an enzyme called topoisomerase 2, or Top2, implicated in DNA damage—that can be targeted to reduce that damage. The findings are published in the journal Aging.


“This part of the puzzle has been missing from the DNA damage theory of aging,” says David Goldfarb, professor of biology. There are many examples of DNA damage being associated with aging, but never has a reduction in DNA damage been shown to extend lifespan. The study also shows how this information may have therapeutic potential.


Goldfarb’s lab exposed yeast—which ages much like humans—to a lifespan-shortening, drug-like molecule that acts on Top2 and helped the lab uncover Top2’s role. Top2 introduces double strand breaks into DNA as part of its catalytic cycle. The breaks must then be resealed. “Every once in a while Top2 gets trapped on the DNA before it can seal the breaks,” Goldfarb says. “When that happens, at least in young cells, there are a number of back-up systems that recognize the breaks and repair them.”


However, a number of researchers have shown that DNA damage repair systems decline as cells age, causing the unrepaired DNA breaks created by Top2 to persist. The unrepaired double strand breaks cause aging, diseases like cancer, and, ultimately, death.

Via Integrated DNA Technologies
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DNA sequencing gives clues to why woolly mammoth died out

DNA sequencing gives clues to why woolly mammoth died out | Amazing Science |

The last woolly mammoths to walk the Earth were so wracked with genetic disease that they lost their sense of smell, shunned company, and had a strange shiny coat. That's the verdict of scientists who have analyzed ancient DNA of the extinct animals for mutations. The studies suggest the last mammoths died out after their DNA became riddled with errors. The knowledge could inform conservation efforts for living animals.


There are fewer than 100 Asiatic cheetahs left in the wild, while the remaining mountain gorilla population is estimated at about 300. The numbers are similar to those of the last woolly mammoths living on Wrangel Island in the Arctic Ocean around 4,000 years ago.


Dr Rebekah Rogers of the University of California, Berkeley, who led the research, said the mammoths' genomes "were falling apart right before they went extinct". This, she said, was the first case of "genomic meltdown" we have seen in a single species.


Woolly mammoths were once common in North America and Siberia. They were driven to extinction by environmental factors and possibly human hunting about 10,000 years ago. Small island populations clung on until about 4,000 years ago.

"There was this huge excess of what looked like bad mutations in the genome of the mammoth from this island," said Dr Rogers.

"We found these bad mutations were accumulating in the mammoth genome right before they went extinct."


Knowledge of the last days of the mammoth could help modern species on the brink of extinction, such as the panda, mountain gorilla and Indian elephant. The lesson from the woolly mammoth is that once numbers drop below a certain level, the population's genetic health may be beyond saving. Genetic testing could be one way to assess whether levels of genetic diversity in a species are enough to give it a chance of survival. A better option is to stop numbers falling too low.


"When you have these small populations for an extended period of time they can go into genomic meltdown, just like what we saw in the mammoth," said Dr Rogers.


"So if you can prevent these organisms ever being threatened or endangered then that will do a lot more to help prevent this type of genomic meltdown compared to if you have a small population and then bring it back up to larger numbers because it will still bear those signatures of this genomic meltdown."

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Full operating system and movie was stored on DNA and recovered without errors

Full operating system and movie was stored on DNA and recovered without errors | Amazing Science |

The world is churning out so much data that hard-drives may not be able to keep up, leading researchers to look at DNA as a possible storage medium. DNA is ultra compact, and doesn’t degrade over time like cassettes and CDs. In a new study, Yaniv Erlich and Dina Zielinski demonstrate DNA’s full potential and reliability for storing data. The researchers wrote six files—a full computer operating system, a 1895 French film, an Amazon gift card, a computer virus, a Pioneer plaque, and a study by information theorist Claude Shannon—into 72,000 DNA strands, each 200 bases long. They then used sequencing technology to retrieve the data, and software to translate the genetic code back into binary. The files were recovered with no errors. We spoke with Erlich about the results, and what they mean for the future of data storage.

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Electrons Use DNA Like a Wire for Signaling DNA Replication 

Electrons Use DNA Like a Wire for Signaling DNA Replication  | Amazing Science |

A Caltech-led study has shown that the electrical wire-like behavior of DNA is involved in the molecule's replication.


In the early 1990s, Jacqueline Barton, the John G. Kirkwood and Arthur A. Noyes Professor of Chemistry at Caltech, discovered an unexpected property of DNA—that it can act like an electrical wire to transfer electrons quickly across long distances. Later, she and her colleagues showed that cells take advantage of this trait to help locate and repair potentially harmful mutations to DNA.


Now, Barton's lab has shown that this wire-like property of DNA is also involved in a different critical cellular function: replicating DNA. When cells divide and replicate themselves in our bodies—for example in the brain, heart, bone marrow, and fingernails—the double-stranded helix of DNA is copied. DNA also copies itself in reproductive cells that are passed on to progeny.


The new Caltech-led study, based on work by graduate student Elizabeth O'Brien in collaboration with Walter Chazin's group at Vanderbilt University, shows that a key protein required for replicating DNA depends on electrons traveling through DNA.


"Nature is the best chemist and knows exactly how to take advantage of DNA electron-transport chemistry," says Barton, who is also the Norman Davidson Leadership Chair of Caltech's Division of Chemistry and Chemical Engineering. "The electron transfer process in DNA occurs very quickly," says O'Brien, lead author of the study, appearing in the February 24 issue of Science. "It makes sense that the cell would utilize this quick-acting pathway to regulate DNA replication, which necessarily is a very rapid process."


The researchers found their first clue that DNA replication might involve the transport of electrons through the double helix by taking a closer look at the proteins involved. Two of the main players in DNA replication, critical at the start of the process, are the proteins DNA primase and DNA polymerase alpha. DNA primase typically binds to single-stranded, uncoiled DNA to begin the replication process. It creates a "primer" made of RNA to help DNA polymerase alpha start its job of copying the single strand of DNA to create a new segment of double-helical DNA.


DNA primase and DNA polymerase alpha molecules both contain iron-sulfur clusters. Barton and her colleagues previously discovered that these metal clusters are crucial for DNA electron transport in DNA repair. In DNA repair, specific proteins send electrons down the double helix to other DNA-bound repair proteins as a way to "test the line," so to speak, and make sure there are no mutations in the DNA. If there are mutations, the line is essentially broken, alerting the cell that mutations are in need of repair. The iron-sulfur clusters in the DNA repair proteins are responsible for donating and accepting traveling electrons.

Via Integrated DNA Technologies
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Consensus statement: Virus taxonomy in the age of metagenomics

Consensus statement: Virus taxonomy in the age of metagenomics | Amazing Science |

Viruses are obligate intracellular parasites that probably infect all cellular lifeforms. Although virologists have traditionally focused on viruses that cause disease in humans, domestic animals and crops, the recent advances in metagenomic sequencing, in particular high-throughput sequencing of environmental samples, have revealed a staggeringly large virome everywhere in the biosphere. At least 10^31 virus particles exist globally at any given time in most environments, including marine and freshwater habitats and metazoan gastrointestinal tracts, in which the number of detectable virus particles exceeds the number of cells by 10–100-fold1, 2, 3, 4, 5.


To help conceptualize the sheer number of viruses in existence, their current biomass has been estimated to equal that of 75 million blue whales (approximately 200 million tons) and, if placed end to end, the collective length of their virions would span 65 galaxies6. In addition to their remarkable abundance, viruses are spectacularly diverse in the nature and organization of their genetic material, gene sequences and encoded proteins, replication mechanisms, and interactions with their cellular hosts, whether they are antagonistic, commensal or mutualistic7.


Aquatic environments contain particularly diverse forms of viruses, including single-stranded (ss) and double-stranded (ds) DNA and RNA viruses with genomes that range in size from less than 2,000 bases to more than 2 million bases4. Although dsDNA viruses that infect bacteria (bacteriophages) are the best studied viruses to date, recent work suggests that around 50% of marine viruses have ssDNA or RNA genomes8.


Metagenomic data are changing our views on virus diversity and are therefore challenging the way in which we recognize and classify viruses9. Historically, the description and classification of a new virus by the International Committee on Taxonomy of Viruses (ICTV) have required substantial information on host range, replication cycle, and the structure and properties of virus particles, which were then used to define groups of viruses. However, high-throughput sequencing and metagenomic approaches have radically changed virology, with many more viruses now known solely from sequence data than have been characterized experimentally. For example, the family Genomoviridae currently comprises a single classified virus, whereas more than 120 possible members have been sequenced from diverse environments. However, these sequenced viruses lack information about their hosts and other biological properties that would guide their assignment into species and genera in the family10.


Indeed, vast numbers of complete, or nearly complete, genome sequences have been assembled and characterized from metagenomic data for viruses with small11, 12, 13, 14, medium15, 16, 17, 18 and even large19, 20genomes. The identification of entirely new groups of viruses from such analyses emphasizes the power of metagenomic approaches in discovering viruses, some of which could have key functions in the regulation of ecosystems, whereas others could coexist with their hosts without causing recognizable disease or may even be mutualists7. However, realistically, few of these viruses are ever likely to receive the same level of experimental characterization as pathogens that cause human disease or influence the global economy.


The question of whether viruses that are identified by metagenomics can, and should, be incorporated into the official ICTV taxonomy scheme on the basis of sequence data alone is pressing. In response to this question, a workshop of invited experts in the field of virus discovery and environmental surveillance, and members of the ICTV Executive Committee, took place in June 2016 to discuss this possibility and to develop a framework for appropriate approaches to virus classification.


Via Niklaus Grunwald
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Diabetes in your DNA? Scientists zero in on the genetic signature of risk

Diabetes in your DNA? Scientists zero in on the genetic signature of risk | Amazing Science |

Why do some people get Type 2 diabetes, while others who live the same lifestyle never do?


For decades, scientists have tried to solve this mystery – and have found more than 80 tiny DNA differences that seem to raise the risk of the disease in some people, or protect others from the damagingly high levels of blood sugar that are its hallmark.

But no one “Type 2 diabetes signature” has emerged from this search. Now, a team of scientists has reported a discovery that might explain how multiple genetic flaws can lead to the same disease.


They’ve identified something that some of those diabetes-linked genetic defects have in common: they seem to change the way certain cells in the pancreas “read” their genes. The discovery could eventually help lead to more personalized treatments for diabetes. But for now, it’s the first demonstration that many Type 2 diabetes-linked DNA changes have to do with the same DNA-reading molecule. Called Regulatory Factor X, or RFX, it’s a master regulator for a number of genes.


The team reporting the findings in a new paper in the Proceedings of the National Academy of Sciences(link is external) comes from the University of Michigan, National Institutes of Health, Jackson Laboratory for Genomic Medicine, University of North Carolina, and the University of Southern California.

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Self-assembly of fully addressable DNA nanostructures from double crossover tiles

Self-assembly of fully addressable DNA nanostructures from double crossover tiles | Amazing Science |

Two recently developed approaches in DNA self-assembly, DNA origami (1–11) and single-stranded tile (SST) (12–15), are capable of producing finite-size mega-Dalton structures by encoding programmable DNA complementarity. In DNA origami approach, a long scaffold (e.g. M13 viral genome) is folded, by hundreds of short synthetic strands with distinct sequences, into a complex structure. More recently, SSTs, uniquely sequenced short synthetic strands serving as tiles, are designed to self-assemble into finite-size 2-dimensional (2-D) and 3-dimensional (3-D) shapes with comparable complexity to that of DNA origami structures.


Tracing back to the earlier development in the DNA nanotechnology, there reveals that similar structural elements appeared in DNA origami and SST structures can also be found in those self-assembled from multi-stranded tiles, including junction tiles (16–31), planar tiles (31–42) and other tiles (43–58). Among a vast collection of tiles that have been developed, double crossover (DX) tile (32,33) was the first rigid tile introduced to the field. It was one of the early milestones in the field that successfully showed the feasibility of using rigid tile to build 2-D lattice.


In a recent study, scientists have designed finite-size lattices with different DX tiles. Four species of DX tiles were used to construct four different types of finite-size lattices respectively. One of four types was also constructed hierarchically in two consecutive steps, with the first step to form individual tiles separately and the second step to form the desired lattice from the mixture of individual tiles. Furthermore, a larger lattice with more component tiles and the corresponding patterns were built. Lastly, infinite-size AB stripe lattices were formed with unpurified DNA strands.

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New genetic engineering method indispensable biotechnological tool 

New genetic engineering method indispensable biotechnological tool  | Amazing Science |

Research by Professor of Chemical and Biomolecular Engineering Huimin Zhao and graduate student Behnam Enghiad is pioneering a new method of genetic engineering for basic and applied biological research and medicine. Their work, reported in ACS Synthetic Biology on February 6 [DOI:10.1021/acssynbio.6b00324], has the potential to open new doors in genomic research by improving the precision and adherence of sliced DNA.


“Using our technology, we can create highly active artificial restriction enzymes with virtually any sequence specificity and defined sticky ends of varying length,” said Zhao. “This is a rare example in biotechnology where a desired biological function or reagent can be readily and precisely designed in a rational manner.”


Restriction enzymes are essential tools for recombinant DNA technology that have revolutionized modern biological research, however have limited sequence specificity and availability. The Pyrococcus furiosus Argonaute (PfAgo) based platform for generating artificial restriction enzymes (AREs) is capable of recognizing and cleaving DNA sequences at virtually any arbitrary site and generating defined sticky ends of varying length.


Restriction enzymes are an important tool in genomic research: by cutting DNA at a specific site, they create a space wherein foreign DNA can be introduced for gene-editing purposes. This process is not only achieved by naturally-occurring restriction enzymes; other artificial restriction enzymes, or AREs, have risen to prominence in recent years. CRISPR-Cas9, a bacterial immune system used for “cut-and-paste” gene editing, and TALENs, modified restriction enzymes, are two popular examples of such techniques.


Though useful in genetic engineering, no AREs generate defined “sticky ends”—an uneven break in the DNA ladder-structure that leaves complementary overhangs, improving adhesion when introducing new DNA. “If you can cleave two different DNA samples with the same restriction enzyme, the sticky ends that are generated are complementary,” explained Enghiad. “They will hybridize with each other, and if you use a ligase, you can stick them together.”


However, restriction enzymes themselves have a critical drawback: the recognition sequence which prompts them to cut is very short—usually only four to eight base pairs. Because the enzymes will cut anywhere that sequence appears, researchers rely on finding a restriction enzyme whose cut site appears only once in the genome of their organism or plasmid—an often difficult proposition when the DNA at hand might be thousands of base pairs long.


This problem has been partially solved simply by the sheer number of restriction enzymes discovered: more than 3600 have been characterized, and over 250 are commercially available. “Just in our freezer, for our other research, we have probably over 100 different restriction enzymes,” said Enghiad. “We look through them all whenever we want to assemble something … the chance of finding the unique restriction site is so low.


“Our new technology unifies all of those restriction enzymes into a single system consisting of one protein and two DNA guides. Not only have you replaced them, but you can now target sites that no available restriction enzymes can.”


Enghiad and Zhao’s new technique creates AREs through the use of an Argonaute protein (PfAgo) taken from Pyrococcus furiosus, an archeal species. Led by two DNA guides, PfAgo is able to recognize much longer sequences when finding its cut site, increasing specificity and removing much of the obstacles posed by restriction enzymes. Further, PfAgo can create longer sticky ends than even restriction enzymes, a substantial benefit as compared to other AREs.

Via Integrated DNA Technologies
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Super-resolution microscopy reveals mechanics of tiny ‘DNA walkers’ 

Super-resolution microscopy reveals mechanics of tiny ‘DNA walkers’  | Amazing Science |

Researchers have introduced a new type of “super-resolution” microscopy and used it to discover the precise walking mechanism behind tiny structures made of DNA that could find biomedical and industrial applications.


The researchers also demonstrated how the “DNA walker” is able to release an anticancer drug, representing a potential new biomedical technology, said Jong Hyun Choi, an associate professor of mechanical engineering at Purdue University.


Synthetic nanomotors and walkers are intricately designed systems that draw chemical energy from the environment and convert it into mechanical motion. However, because they are too small to be observed using conventional light microscopes, researchers have been unable to learn the precise steps involved in the walking mechanisms, knowledge essential to perfecting the technology.


“If you cannot resolve or monitor these walkers in action, you will be unable to understand their mechanical operation,” Choi said.

He led a Purdue team that has solved this problem by developing a super-resolution microscopy system designed to study the DNA walkers. The new findings appeared in the journal Science Advances on Jan. 20, 2017.

Via Integrated DNA Technologies
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