adj. entranced and unsettled by the vastness of the universe, experienced in a jolt of recognition that the night sky is not just a wallpaper but a deeply foreign ocean whose currents are steadily carrying off all other castaways, who share our predicament but are already well out of…
THE WORLD IN PLACE OF ITSELF
February 24, 2012
degrasse
February 19, 2012
howlin’ at a paper moon
December 29, 2011
(Source: trailhikers)
November 6, 2011
"Sometimes when I look at you, I feel I’m gazing at a distant star. It’s dazzling, but the light is from tens of thousands of years ago. Maybe the star doesn’t even exist any more. Yet sometimes that light seems more real to me than anything."
— Haruki Murakami (via cyrtenes)
August 30, 2011
"If you torture data sufficiently, it will confess to almost anything."
— Fred Menger
August 7, 2011
[1105.0183] Shape Dynamics. An Introduction
By Julian Barbour:
Shape dynamics is a completely background-independent universal framework of dynamical theories from which all absolute elements have been eliminated. For particles, only the variables that describe the shapes of the instantaneous particle configurations are dynamical. In the case of Riemannian three-geometries, the only dynamical variables are the parts of the metric that determine angles. The local scale factor plays no role. This leads to a shape-dynamic theory of gravity in which the four-dimensional diffeomorphism invariance of general relativity is replaced by three-dimensional diffeomorphism invariance and three-dimensional conformal invariance. Despite this difference of symmetry groups, it is remarkable that the predictions of the two theories — shape dynamics and general relativity — agree on spacetime foliations by hypersurfaces of constant mean extrinsic curvature. However, the two theories are distinct, with shape dynamics having a much more restrictive set of solutions. There are indications that the symmetry group of shape dynamics makes it more amenable to quantization and thus to the creation of quantum gravity. This introduction presents in simple terms the arguments for shape dynamics, its implementation techniques, and a survey of existing results.
July 17, 2011
NASA’s Stillsuit: Atlantis Crew to Test Pee-Recycling Bag | Wired Science | Wired.com
By Dave Mosher
CAPE CANAVERAL — A textbook-sized kit that can convert urine into drinkable water will accompany NASA’s last space shuttle mission this Friday.
Soldiers already use similar technology to filter out parasites, bacteria, viruses and other contaminants from dirty fluids, including urine, but NASA’s adapted baggie system has yet to prove itself in space.
“This could be a first step toward recapturing the humidity from our sweat, from our breath, even from our urine, and recycling it and making it drinkable,” said NASA project scientist and experiment leader Howard Levine, who made a reference to water-recycling “stillsuits” used on a desert world in the science fiction series Dune.
Astronauts aboard the International Space Station already drink water from a pee-recycling machine delivered several years ago, but it saps power from the orbital laboratory’s limited supply. The space-ready water conversion kit, however, won’t need an external power source because it relies on a passive property of fluids called forward osmosis.
NASA’s recycler will use a sugary solution injected into a semi-permeable inner bag, which is nested inside an outer bag. Dirty fluid that’s pumped into the outer bag will slowly pass through the inner bag and into the sugary solution, leaving behind its contaminants. On Earth, the double-sack system makes about a liter of sports drink-like fluid in four to six hours.
One of the four astronauts aboard space shuttle Atlantis will test the recycler — with an experimental fluid, not their own urine — toward the end of their 12-day mission, scheduled for launch this Friday at 11:26 a.m. EDT.
Levine and engineer Monica Soler of the Bionetics Corporation, who helped NASA retrofit the recycler for space, gave a demonstration here at Kennedy Space Center. We show the steps in this gallery.
July 14, 2011
seophoria
n. the satisfaction of lists, a series of bullet points being fired into the air as if to celebrate victory against the complexity of a universe that bombards us with five exabytes of data that would paralyze us if we didn’t connect random dots into constellations of dippers, hunters, and sexy ways to please your man.
June 24, 2011
NIH researchers find new clues about aging
Telomere shortening is probably a defense mechanism against cancer. So lengthening telomeres (assuming we had a treatment that would do this) might not lower the risk of all-cause mortality. However, throw in some great cures for cancer and telomere lengthening will suddenly become a very appealing idea.
Genetic splicing mechanism triggers both premature aging syndrome and normal cellular aging
National Institutes of Health researchers have identified a new pathway that sets the clock for programmed aging in normal cells. The study provides insights about the interaction between a toxic protein called progerin and telomeres, which cap the ends of chromosomes like aglets, the plastic tips that bind the ends of shoelaces.
The study by researchers from the National Human Genome Research Institute (NHGRI) appears in the June 13, 2011 early online edition of the Journal of Clinical Investigation.
Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin.
Progerin is a mutated version of a normal cellular protein called lamin A, which is encoded by the normal LMNA gene. Lamin A helps to maintain the normal structure of a cell’s nucleus, the cellular repository of genetic information.
In 2003, NHGRI researchers discovered that a mutation in LMNA causes the rare premature aging condition, progeria, formally known as known as Hutchinson-Gilford progeria syndrome. Progeria is an extremely rare disease in which children experience symptoms normally associated with advanced age, including hair loss, diminished subcutaneous fat, premature atherosclerosis and skeletal abnormalities. These children typically die from cardiovascular complications in their teens.
“Connecting this rare disease phenomenon and normal aging is bearing fruit in an important way,” said NIH Director Francis S. Collins, M.D., Ph.D., a senior author of the current paper. “This study highlights that valuable biological insights are gained by studying rare genetic disorders such as progeria. Our sense from the start was that progeria had a lot to teach us about the normal aging process and clues about more general biochemical and molecular mechanisms.”
Collins led the earlier discovery of the gene mutation responsible for progeria and subsequent advances at NIH in understanding the biochemical and molecular underpinnings of the disease.
In a 2007 study, NIH researchers showed that normal cells of healthy people can produce a small amount of progerin, the toxic protein, even when they do not carry the mutation. The more cell divisions the cell underwent, the shorter the telomeres and the greater the production of progerin. But a mystery remained: What was triggering the production of the toxic progerin protein?
The current study shows that the mutation that causes progeria strongly activates the splicing of lamin A to produce the toxic progerin protein, leading to all of the features of premature aging suffered by children with this disease. But modifications in the splicing of LMNA are also at play in the presence of the normal gene.
The research suggests that the shortening of telomeres during normal cell division in individuals with normal LMNA genes somehow alters the way a normal cell processes genetic information when turning it into a protein, a process called RNA splicing. To build proteins, RNA is transcribed from genetic instructions embedded in DNA. RNA does not carry all of the linear information embedded in the ribbon of DNA; rather, the cell splices together segments of genetic information called exons that contain the code for building proteins, and removes the intervening letters of unused genetic information called introns. This mechanism appears to be altered by telomere shortening, and affects protein production for multiple proteins that are important for cytoskeleton integrity. Most importantly, this alteration in RNA splicing affects the processing of the LMNA messenger RNA, leading to an accumulation of the toxic progerin protein.
Cells age as part of the normal cell cycle process called senescence, which progressively advances through a limited number of divisions in the cell lifetime. “Telomere shortening during cellular senescence plays a causative role in activating progerin production and leads to extensive change in alternative splicing in multiple other genes,” said lead author Kan Cao, Ph.D., an assistant professor of cell biology and molecular genetics at the University of Maryland, College Park.
Telomerase is an enzyme that can extend the structure of telomeres so that cells continue to maintain the ability to divide. The study supplied support for the telomere-progerin link, showing that cells that have a perpetual supply of telomerase, known as immortalized cells, produce very little progerin RNA. Most cells of this kind are cancer cells, which do not reach a normal cell cycle end point, and instead replicate out of control.
The researchers also conducted laboratory tests on normal cells from healthy individuals using biochemical markers to indicate the occurrence of progerin-generating RNA splicing in cells. The cell donors ranged in age from 10 to 92 years. Regardless of age, cells that passed through many cell cycles had progressively higher progerin production. Normal cells that produce higher concentrations of progerin also displayed shortened and dysfunctional telomeres, the tell-tale indication of many cell divisions.
In addition to their focus on progerin, the researchers conducted the first systematic analysis across the genome of alternative splicing during cellular aging, considering which other protein products are affected by jumbled instructions as RNA molecules assemble proteins through splicing. Using laboratory techniques that analyze the order of chemical units of RNA, called nucleotides, the researchers found that splicing is altered by short telomeres, affecting lamin A and a number of other genes, including those that encode proteins that play a role in the structure of the cell.
The researchers suggest that the combination of telomere fraying and loss with progerin production together induces cell aging. This finding lends insights into how progerin may participate in the normal aging process.
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For more about Hutchinson-Gilford progeria syndrome, go to http://www.genome.gov/11007255.
NHGRI is one of the 27 institutes and centers at the NIH, an agency of the Department of Health and Human Services. The NHGRI Division of Intramural Research develops and implements technology to understand, diagnose and treat genomic and genetic diseases. Additional information about NHGRI can be found at its website, www.genome.gov.
The National Institutes of Health (NIH) - The Nation’s Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
June 22, 2011
Human Gene May Sense Magnetic Field, Researchers Suggest - NYTimes.com
By NICHOLAS WADE:
A researcher studying how monarch butterflies navigate has picked up a strong hint that people may be able to sense the earth’s magnetic field and use it for orienting themselves.
Many animals rely on the magnetic field for navigation, and researchers have often wondered if people, too, might be able to detect the field; that might explain how Polynesian navigators can make 3,000-mile journeys under starless skies. But after years of inconclusive experiments, interest in people’s possible magnetic sense has waned.
That may change after an experiment being reported last week by Steven M. Reppert, a neurobiologist at the University of Massachusetts Medical School, and his colleagues Lauren E. Foley and Robert J. Gegear. They have been studying cryptochromes, light-sensitive proteins that help regulate the daily rhythm of the body’s cells, and how they help set the sun compass by which monarchs navigate.
But the butterflies can navigate even when the sun is obscured, so they must have a backup system. Since physical chemists had speculated the cryptochromes might be sensitive to magnetism, Dr. Reppert wondered if the monarch butterfly was using its cryptochromes to sense the earth’s magnetic field. He first studied the laboratory fruit fly, whose genes are much easier to manipulate, and showed three years ago that the fly could detect magnetic fields, but only when its cryptochrome gene was in good working order.
He then showed that the monarch butterfly’s two cryptochrome genes could each substitute for the fly’s gene in letting it sense magnetic fields, indicating the butterfly uses the proteins for the same purpose.
One of the monarch’s two cryptochrome genes is similar in its DNA sequence to the human cryptochrome gene. That prompted the idea of seeing whether the human gene, too, could restore magnetic sensing to fruit flies whose own gene had been knocked out. In the journal Nature Communications, Dr. Reppert reports that this is indeed the case. “A reassessment of human magnetosensitivity may be in order,” he and his colleagues write.
The human cryptochrome gene is highly active in the eye, raising the possibility that the magnetic field might in some sense be seen, if the cryptochromes interact with the retina.
Dr. Reppert said the focus on human use of the magnetic field for navigation might be misplaced. Following an idea proposed last year by John B. Phillips of Virginia Tech, he said the primary use of magnetic sensing might be for spatial orientation.
“It could be providing a spherical coordinate system that the animal could use for spatial positioning,” he said.
Dr. Phillips said that Dr. Reppert’s work was of interest but that he had been surprised by an experiment in which Dr. Reppert disrupted the part of the cryptochrome thought to interact with the magnetic field, yet the flies had still detected the magnetism. “It’s 50-50 whether he’s really studying what he thinks he is,” Dr. Phillips said.
Dr. Reppert replied that he had already ruled out the alternative explanation suggested by Dr. Phillips.
But both scientists agreed on the possibilities opened up by the cryptochrome system. Depending on how the proteins are aligned in the eye, insects may perceive objects as being lighter or darker as they orient themselves in relation to the magnetic field, Dr. Phillips said.
In fact, the cryptochrome system might supply a grid imposed on all the landmarks in a visual scene, helping a squirrel find a buried acorn, or a fox integrate its visual scene with what it hears. “This is the fun stage where we are not constrained by many facts,” Dr. Phillips said.
If butterflies, birds and foxes possess such a wonderful system, why would it ever have died out in the human lineage?
“It may be that our electromagnetic world is interfering with our ability to do this kind of stuff,” Dr. Phillips said.
As for Dr. Reppert, he is now planning his next step, that of understanding how the cryptochrome proteins sense the magnetic field and how they convey that information to the fruit fly’s and monarch’s brain.
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