Swarms of small earthquakes happen frequently in Yellowstone, but it’s very unusual for so many earthquakes to happen over several days, said Robert Smith, a professor of geophysics at the University of Utah. “They’re certainly not normal,” Smith said. “We haven’t had earthquakes in this energy or extent in many years.”
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“There doesn’t seem to be anything to be alarmed about,” Vallie said. Smith said it’s difficult to say what might be causing the tremors. He pointed out that Yellowstone is the caldera of a volcano that last erupted 70,000 years ago.
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Yellowstone has had significant earthquakes as well as minor ones in recent decades. In 1959, a magnitude 7.5 quake near Hebgen Lake just west of the park triggered a landslide that killed 28 people.
So far the most powerful quake over the last few days has been one at 3.8 on the Richter scale. An earthquake of 4.0-4.9 “Noticeable shaking of indoor items, rattling noises. Significant damage unlikely.” The Richter scale is a logarithmic scale, meaning a measure of 4.0 is 10 times as powerful as 3.0 quake, and 5.0 is 100 times more powerful than a 3.o quake.
It seems that Attercopus is a missing link, capable of producing silk but not of weaving it. “The thing that had been called the oldest known spider we have now shown is in fact more primitive than a true spider,” Professor Selden told BBC News.
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“They’re all microscopic fragments. What you’ve got is a jigsaw puzzle, with half the pieces and no picture on the box lid,” Professor Selden said. “You don’t know what it’s going to be if you haven’t got all the pieces, so having these additional pieces means it changed the idea of what it was.” The finding is important for evolutionary biologists trying to unravel the origin of spider silk.
“The puzzle about silk was this: we knew that it wasn’t used for making webs initially, for catching insects, because there were no flying insects when the earliest spiders were around,” Professor Selden said.
“Here we clearly have a spider-like animal that could produce silk but didn’t yet have these flexible spinnerets for weaving it into webs; we think that this sort of spider would leave a trail of silk as it moved along, using it to find its way back to its burrow.”
Another great example of scientists incorporating new information and adjusting their understanding of what they are studying.
The theory that the recycled universe was based on, called loop quantum cosmology (LQC), had managed to illuminate the very birth of the universe – something even Einstein’s general theory of relativity fails to do.
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LQC is in fact the first tangible application of another theory called loop quantum gravity, which cunningly combines Einstein’s theory of gravity with quantum mechanics. We need theories like this to work out what happens when microscopic volumes experience an extreme gravitational force, as happened near the big bang, for example.
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If LQC turns out to be right, our universe emerged from a pre-existing universe that had been expanding before contracting due to gravity. As all the matter squeezed into a microscopic volume, this universe approached the so-called Planck density, 5.1 × 1096 kilograms per cubic metre. At this stage, it stopped contracting and rebounded, giving us our universe.
In classical cosmology, a phenomenon called inflation caused the universe to expand at incredible speed in the first fractions of a second after the big bang. This inflationary phase is needed to explain why the temperature of faraway regions of the universe is almost identical, even though heat should not have had time to spread that far – the so-called horizon problem. It also explains why the universe is so finely balanced between expanding forever and contracting eventually under gravity – the flatness problem. Cosmologists invoke a particle called the inflaton to make inflation happen, but precious little is known about it.
In a recent study 20 individuals from the great ape species were unable to transfer their knowledge from the trap-table and trap-tube or vice versa, despite the fact that both these puzzles work in the same way. Strikingly the crows in The University of Auckland study were able to solve the trap-table problem after their experience with the trap-tube.
“The crows appeared to solve these complex problems by identifying causal regularities,” says Professor Russell Gray of the Department of Psychology. “The crows’ success with the trap-table suggests that the crows were transferring their causal understanding to this novel problem by analogical reasoning. However, the crows didn’t understand the difference between a hole with a bottom and one without. This suggests the level of cognition here is intermediate between human-like reasoning and associative learning.”
“It was very surprising to see the crows solve the trap-table,” says PhD student Alex Taylor. “The trap table puzzle was visually different from the trap-tube in its colour, shape and material. Transfer between these two distinct problems is not predicted by theories of associative learning and is something not even the great apes have so far been able to do.”
Since the first antibiotics reached the pharmacy in the 1940s, researchers discovered that they target various pieces of machinery in bacterial cells, disrupting the bacteria’s ability to build new proteins, DNA, or cell wall. But these effects alone do not cause death, and a complete explanation of what actually kills bacteria after they are exposed to antibiotics has eluded scientists.
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The group found that all bactericidal antibiotics, regardless of their initial targets inside bacteria, caused E. coli to produce unstable chemicals called hydroxyl radicals. These compounds react with proteins, DNA, and lipids inside cells, causing widespread damage and rapid death for the bacteria.
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With the results of these two experiments, the researchers were able to identify three major processes implicated in gentamicin-induced cell death: protein transport, a stress response triggered by abnormal proteins in the cell membrane, and a metabolic stress response.
There’s another important downside to scale. When we look at large quantities of information, what we’re really doing is searching for patterns. And being the kind of creatures that we are, and given the nature of the laws of probability, we are going to find patterns. Distinguishing between a real legitimate pattern, and something random that just happens to look like a pattern can be somewhere between difficult and impossible. Using things like Bayesian methods to screen out the false positives can help, but scale means that scientists need to learn new methods – both the new ways of doing things that they couldn’t do before, and the new ways of recognizing when they’ve screwed up.
There’s the nature of scale. Tasks that were once simple have become hard or even impossible, because they can’t be done at scale. Tasks that were once impossible have become easy because scale makes them possible. Scale changes everything.
Linda Chalker-Scott, an associate professor at Washington State University, is the author of The Informed Gardener and producer of the column “Horticultural Myths.” In The Truth About Garden Remedies: What Works, What Doesn’t, and Why, Jeff Gillman, associate professor at the University of Minnesota, is just as rational and informative
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Do go ahead and dig in soil improvements, Chalker-Scott advises, for vegetable gardens or annual flowerbeds, in which nutrients need replacing yearly. But there’s really no need to dig organic amendments—manure and peat moss, etc.—into landscapes that are permanent. Treat those plantings of trees and shrubs as if they were forest ecosystems, not agricultural fields—wood chips and decaying leaves on top, no tilling-in of fertilizer.
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It must drive both authors nuts to hear people say, “I’m an organic gardener. I never use chemicals.” Everything on earth is composed of chemicals.
A new study by Harvard Medical School researchers reveals that the biochemical mechanism that makes yeast grow old has a surprising parallel in mice, suggesting it may be a universal cause of aging in all organisms.
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In young organisms, SIRT1 effectively doubles as a gene-expression regulator and a DNA repairer. But when DNA damage accumulates—as it does with age—SIRT1 becomes too busy fixing broken DNA to keep the expression of hundreds of genes in check. This process is so similar to what happens in aging yeast that its discoverers believe it may represent a universal mechanism of aging.
Aging may be a case of neglect — an absentee landlord at the cellular level that allows gene activity to go awry, according to a study published today.
Scientists have long known that aging causes gene expression to change, and DNA damage to accumulate. But now, research led by Harvard Medical School scientists explains the connection between the two processes in mammals.
The paper, published in the journal Cell, found that a multi-tasking protein called SIRT1 that normally acts as guardian of the genome gets dragged away to DNA fix-it jobs. When the protein abandons its normal post to work as a genetic handyman, order unravels elsewhere in the cell. Genes that are normally under its careful watch begin to flip on.
“What this paper actually implies is that aspects of aging may be reversible,” said David Sinclair, a Harvard Medical School biologist who led the research. “It sounds crazy, but in principle it should be possible to restore the youthful set of genes, the patterns that are on and off.”
The study is just the latest to draw yet more attention to sirtuins, proteins involved in the aging process
Aging is fascinating. By and large people just accept it. We see it happen to those all around us, without exception. But what causes biological aging? It is an interesting area of research.
investigating the ability of living neurons to act as a set of neuronal weights which were used to control the flight of a simulated aircraft. These weights were manipulated via high frequency stimulation inputs to produce a system in which a living neuronal network would “learn” to control an aircraft for straight and level flight.
A system was created in which a network of living rat cortical neurons were slowly adapted to control an aircraft’s flight trajectory. This was accomplished by using high frequency stimulation pulses delivered to two independent channels, one for pitch, and one for roll. This relatively simple system was able to control the pitch and roll of a simulated aircraft.
When Dr. Thomas DeMarse first puts the neurons in the dish, they look like little more than grains of sand sprinkled in water. However, individual neurons soon begin to extend microscopic lines toward each other, making connections that represent neural processes. “You see one extend a process, pull it back, extend it out — and it may do that a couple of times, just sampling who’s next to it, until over time the connectivity starts to establish itself,” he said. “(The brain is) getting its network to the point where it’s a live computation device.”
To control the simulated aircraft, the neurons first receive information from the computer about flight conditions: whether the plane is flying straight and level or is tilted to the left or to the right. The neurons then analyze the data and respond by sending signals to the plane’s controls. Those signals alter the flight path and new information is sent to the neurons, creating a feedback system.
“Initially when we hook up this brain to a flight simulator, it doesn’t know how to control the aircraft,” DeMarse said. “So you hook it up and the aircraft simply drifts randomly. And as the data come in, it slowly modifies the (neural) network so over time, the network gradually learns to fly the aircraft.”
Although the brain currently is able to control the pitch and roll of the simulated aircraft in weather conditions ranging from blue skies to stormy, hurricane-force winds, the underlying goal is a more fundamental understanding of how neurons interact as a network, DeMarse said.
Matz says the protists probably move by sending leg-like extensions, called pseudopodia, out of their cells in all directions. The pseudopodia then grab onto mud in one direction and the organism rolls that way, leaving a track. Hr says the giant protists’ bubble-like body design is probably one of the planet’s oldest macroscopic body designs, which may have existed for 1.8 billion years.
“I personally think now that the whole Precambrian may have been exclusively the reign of protists,” says Matz. “Our observations open up this possible way of interpreting the Precambrian fossil record.”
He says the appearance of all the animal body plans during the Cambrian explosion might not just be an artifact of the fossil record. There are likely other mechanisms that explain the burst-like origin of diverse multicellular life forms.
Slowly rolling across the ocean floor, a humble single-celled creature is poised to revolutionize our understanding of how complex life evolved on Earth.
A distant relative of microscopic amoebas, the grape-sized Gromia sphaerica was discovered once before, lying motionless at the bottom of the Arabian Sea. But when Mikhail Matz of the University of Texas at Austin and a group of researchers stumbled across a group of G. sphaerica off the coast of the Bahamas, the creatures were leaving trails behind them up to 50 centimeters (20 inches) long in the mud.
The trouble is, single-celled critters aren’t supposed to be able to leave trails. The oldest fossils of animal trails, called ‘trace fossils’, date to around 580 million years ago, and paleontologists always figured they must have been made by multicellular animals with complex, symmetrical bodies.