thats how Satan gets yaI don't normally listen to the metal you post. But because of the Tolkien passage I took a little listen. 30 seconds worth.
[DOUBLEPOST=1521102953][/DOUBLEPOST]https://fivethirtyeight.com/feature...digits-were-still-no-closer-to-the-end-of-pi/Spending a year in space not only changes your outlook, it transforms your genes.
Preliminary results from NASA's Twins Study reveal that 7% of astronaut Scott Kelly's genes did not return to normal after his return to Earth two years ago.
The study looks at what happened to Kelly before, during and after he spent one year aboard the International Space Station through an extensive comparison with his identical twin, Mark, who remained on Earth.
NASA has learned that the formerly identical twins are no longer genetically the same.
The transformation of 7% of Scott's DNA suggests longer-term changes in genes related to at least five biological pathways and functions.
The newest preliminary results from this unique study of Scott, now retired from NASA, were released at the 2018 Investigator's Workshop for NASA's Human Research Program in January. Last year, NASA published its first round of preliminary results at the 2017 Investigator's Workshop. Overall, the 2018 findings corroborated those from 2017, with some additions.
To track physical changes caused by time in space, scientists measured Scott's metabolites (necessary for maintaining life), cytokines (secreted by immune system cells) and proteins (workhorses within each cell) before, during and after his mission. The researchers learned that spaceflight is associated with oxygen-deprivation stress, increased inflammation and dramatic nutrient shifts that affect gene expression.
In particular, Chris Mason of Weill Cornell Medicine reported on the activation of Scott's "space genes" while confirming the results of his separate NASA study, published last year.
To better understand the genetic dynamics of each twin, Mason and his team focused on chemical changes in RNA and DNA. Whole-genome sequencing revealed that each twin has more than expected unique mutations in his genome -- in fact, hundreds.
Although 93% of Scott's genetic expression returned to normal once he returned to Earth, a subset of several hundred "space genes" remained disrupted. Some of these mutations, found only after spaceflight, are thought to be caused by the stresses of space travel.
As genes turn on and off, change in the function of cells may occur.
Looking to Mars
Mason's work shows that one of the most important changes to Scott's cells was hypoxia, or a deficient amount of tissue oxygenation, probably due to a lack of oxygen and high levels of carbon dioxide. Possible damage to mitochondria, the "power plants of cells," also occurred in Scott's cells, as indicated by mitochondrial stress and increased levels of mitochondria in the blood.
Mason's team also saw changes in the length of Scott's telomeres, caps at the end of chromosomes that are considered a marker of biological aging. First, there was a significant increase in average length while he was in space, and then there was a decrease in length within about 48 hours of his landing on Earth that stabilized to nearly preflight levels. Scientists believe that these telomere changes, along with the DNA damage and DNA repair measured in Scott's cells, were caused by both radiation and calorie restrictions.
Additionally, the team found changes in Scott's collagen, blood clotting and bone formation due, most likely, to fluid shifts and zero gravity. The researchers discovered hyperactive immune activity as well, thought to be the result of his radically different environment: space.
The Twins Study helps NASA gain insight into what happens to the human body in space beyond the usual six-month International Space Station missions previously studied in other astronauts. Ten groups of researchers, including Mason's team, are looking at a wide variety of information about the Kelly twins' health, including how gut bacteria, bones and the immune system might be affected by living off planet.
Kelly's one-year mission is a scientific stepping stone to a planned three-year mission to Mars, NASA said. Research into how the human body adjusts to weightlessness, isolation, radiation and the stress of long-duration spaceflight is needed before astronauts are sent on journeys that would triple the time humans have spent in space so far.
Depending on your philosophical views on time and calendars and so on, today is something like the 4.5 billionth Pi Day that Earth has witnessed. But that long history is nothing compared to the infinity of pi itself.
A refresher for those of you who have forgotten your seventh-grade math lessons
">1: Pi, or the Greek letter π" role="presentation">π
, is a mathematical constant equal to the ratio of a circle’s circumference to its diameter — C/d. It lurks in every circle, and equals approximately 3.14. (Hence Pi Day, which takes place on March 14, aka 3/14.)
But the simplicity of its definition belies pi’s status as the most fascinating, and most studied, number in the history of the world. While treating pi as equal to 3.14 is often good enough, the number really continues on forever, a seemingly random series of digits ambling infinitely outward and obeying no discernible pattern — 3.14159265358979…. That’s because it’s an irrational number, meaning that it cannot be represented by a fraction of two whole numbers (although approximations such as 22/7 can come close).
But that hasn’t stopped humanity from furiously chipping away at pi’s unending mountain of digits. We’ve been at it for millennia.
People have been interested in the number for basically as long we’ve understood math. The ancient Egyptians, according to a document that also happens to be the world’s oldest collection of math puzzles, knew that pi was something like 3.1. A millennium or so later, an estimate of pi showed up in the bible: The Old Testament, in 1 Kings, seems to imply that pi equals 3: “And he made a molten sea, ten cubits from the one brim to the other: it was round all about … and a line of thirty cubits did compass it round about.”
Archimedes, the greatest mathematician of antiquity, got as far as 3.141 by around 250 B.C. Archimedes approached his calculation of pi geometrically, by sandwiching a circle between two straight-edged regular polygons. Measuring polygons was easier than measuring circles, and Archimedes measured pi-like ratios as the number of the polygons’ sides increased, until they closely resembled circles.
Meaningful improvement on Archimedes’s method wouldn’t come for hundreds of years. Using the new technique of integration, mathematicians like Gottfried Leibniz, one of the fathers of calculus, could prove such elegant equations for pi as:
The right-hand side, just like pi, continues forever. If you add and subtract and add and subtract all those simple fractions, you’ll inch ever closer to pi’s true value. The problem is that you’ll inch very, very slowly. To get just 10 correct digits of pi, you’d have to add about 5 billion fractions together.
But more efficient formulas were discovered. Take this one, from Leonhard Euler, probably the greatest mathematician ever, in the 18th century:
And Srinivasa Ramanujan, a self-taught mathematical genius from India, discovered the totally surprising and bizarre equation below in the early 1900s. Each additional term in this sum adds eight correct digits to an estimate of pi:
Much like with the search for large prime numbers, computers blasted this pi-digit search out of Earth orbit and into deep space starting in the mid-1900s. ENIAC, an early electronic computer and the only computer in the U.S. in 1949, calculated pi to over 2,000 places, nearly doubling the record.
As computers got faster and memory became more available, digits of pi began falling like dominoes, racing down the number’s infinite line, impossibly far but also never closer to the end. Building off of Ramanujan’s formula, the mathematical brothers Gregory and David Chudnovsky calculated over 2 billion digits of pi in the early 1990s using a homemade supercomputer housed in a cramped and sweltering Manhattan apartment. They’d double their tally to 4 billion digits after a few years.
The current record now stands at over 22 trillion digits — thousands of times more than the Chudnovskys’ home-brewed supercomputer — worked out after 105 days of computation on a Dell server using a freely available program called y-cruncher. That program, which uses both the Ramanujan and Chudnovsky formulas, has been used to find record numbers of digits of not only pi, but other endless, irrational numbers, including e, 2" role="presentation">2–√
, log⁡2" role="presentation">log2
and the golden ratio.
But maybe 22 trillion digits is just a bit of overkill. NASA’s Jet Propulsion Laboratory uses only 15 digits of pi for its highest-accuracy calculations for interplanetary navigation. Heck, Isaac Newton knew that many digits 350 years ago. “A value of π" role="presentation">π
to 40 digits would be more than enough to compute the circumference of the Milky Way galaxy to an error less than the size of a proton,” a group of researchers wrote in a useful history of the number. So why would we ever need 22 trillion digits?
Sure, we’ve learned a bit of math theory while digging deep into pi: about fast Fourier transforms and that pi is probably a so-called normal number. But the more satisfying answer seems to me to have nothing to do with math. Maybe it has to do with what President John F. Kennedy said about building a space program. We do things like this “not because they are easy, but because they are hard; because that goal will serve to organize and measure the best of our energies and skills.”
But there’s one major difference: The moon is not infinitely far away; we can actually get there. Maybe this famous quote about chess is more apt: “Life is not long enough for chess — but that is the fault of life, not of chess.”
Pi is too long for humankind. But that is the fault of humankind, not of pi. Happy Pi Day.
A theory explaining how we might detect parallel universes and a prediction for the end of the world was completed by Stephen Hawking shortly before he died, it has emerged.
The renowned theoretical physicist was working right up until his death last week on his final work – A Smooth Exit from Eternal Inflation – which is currently being reviewed by a leading scientific journal. In it he predicted that the universe would eventually end when stars run out of energy.
But Hawking also theorised in his final work that scientists could find alternate universes using probes on space ships, allowing humans to form an even better understanding of our own universe, what else is out there and our place in the cosmos.
The physicist’s final work was published alongside his co-author, Professor Thomas Hertog, of KU Leuven University in Belgium.
“He has often been nominated for the Nobel and should have won it. Now he never can,” Prof Hertog told The Sunday Times, arguing that Hawking could have won that prize for his work on this final paper.
He “would have won a Nobel Prize”, Prof Hertog said.
us not good brains to think pictures of time with no timeToo sciency
[DOUBLEPOST=1521549119][/DOUBLEPOST]Gregor Mendel discovered fundamental rules of genetics by raising pea plants. He realized that hidden factors — we now know them to be genes — were passed down from parents to offspring.
It wasn’t until the early 1900s, long after Mendel’s death, that doctors discovered that humans weren’t so very different. Some diseases, it turns out, are inherited — they’re Mendelian.
Today, scientists have identified over 7,000 Mendelian diseases, and many are discovered with screenings of children and adults. But a new study suggests that many disorders go undetected.
With a database of electronic health records and DNA samples, a team of scientists has found that 3.7 percent of patients in a hospital system carried a genetic variant linked to a disease. It’s possible that as many as 4.5 percent of cases of apparently nongenetic diseases, from infertility to kidney failure, are the result of such mutations.
The study also suggests that it may be possible to catch more of these hidden disorders with a computer program that flags suspicious clusters of symptoms in groups of patients. That would be an enormous step forward for patients coping with unexplained ailments.
The study, published Thursday in Science, represents the first large-scale search of electronic health records for hidden Mendelian diseases. But Dr. Joshua C. Denny, a biomedical informatics researcher at the Vanderbilt University School of Medicine and co-author of the new study, suspected that it only revealed the tip of a genetic iceberg. Much larger databases including DNA and records for hundreds of thousands of people are being built, and searching them may uncover many more hidden mutations.
“I’m sure there’s a whole bunch else out there that we will discover,” Dr. Denny said.
He and his colleagues gathered data from Vanderbilt’s massive electronic health records system, which includes more than two million patients. More than 225,000 have signed up as volunteers for genetic research, allowing scientists to analyze their DNA.
The researchers picked out 21,701 patients from the database and surveyed all the symptoms recorded for each one. They then compared the symptoms to those seen in 1,204 Mendelian diseases.
It was a difficult task. These disorders can produce a number of symptoms, and each patient may have a different combination of them.
And some symptoms linked to a Mendelian disease may also be signs of other diseases. Cystic fibrosis can cause asthma and recurrent infections, for instance — but those symptoms alone aren’t enough to diagnose the disease.
Dr. Denny and his colleagues developed a scoring system to determine how likely it was that each patient in their study suffered each Mendelian disease. If a patient had a rare symptom linked to a disease, she scored a lot of points. A common symptom earned her far fewer points.
The researchers identified groups of people with symptoms strongly suggesting they shared a Mendelian disease. The researchers went on to examine the DNA of these patients to see if they also shared a mutation.
Dr. Denny would have been happy just to find a few undiagnosed patients. Instead, the team found 807 patients carrying mutations in genes linked to 17 different diseases, such as cystic fibrosis or hemochromatosis, a disorder that causes iron to build up in the blood.
Only eight of these patients had gotten a test that revealed the mutation. In other cases, doctors had tested for the wrong disease and gotten a negative result. Many times, the doctors hadn’t ordered any genetic tests at all.
Typically, these disorders can be passed down in one of two ways. A dominant disease, like Huntington’s, requires inheriting just one defective copy of a gene from a parent. Recessive diseases, such as sickle cell anemia, usually require two defective copies of the same gene.
The mutations that the scientists discovered often didn’t fit the standard profile for the diseases. Many of the patients had conditions that are considered recessive, yet they carried a just single defective copy of the gene.
A single defective copy may cause milder versions of Mendelian diseases, Dr. Denny suspects.
The researchers identified 36 people, for example, who carried only one defective version of a gene called AGXT. Two copies of the gene cause a disease known as primary hyperoxaluria, which can result in kidney failure in toddlers. The patients identified in the new study also suffered kidney problems — but not in the first few years of life.
One patient who turned up in their search had kidney stones at age 15. That’s unusual — but apparently not enough to lead the patient’s doctors to suspect primary hyperoxaluria.
“It’s not as simple as what we learned in high school genetics,” Dr. Denny said.
These results are all the more surprising given how modest Dr. Denny’s search was. He only looked for a limited number of mutations in a relatively small group of people, all of whom were of European descent. (Much of what is known about gene variants that cause disease was discovered by researching predominantly white populations.)
“I’m kind of surprised we found anything. The fact that we did means there’s maybe a lot out there that we don’t know,” Dr. Denny said.
Heidi L. Rehm, a molecular geneticist at Brigham and Women’s Hospital who was not involved in the study, said many doctors do not suspect that their patients are suffering from a Mendelian disorder unless they suffer severe textbook symptoms.
“They simply never order any genetic testing, and then you never develop an understanding that it’s genetic to begin with,” she said.
Overlooking the genetic causes of diseases can seriously harm patients. “There are people here who had kidney and liver transplants that could potentially have been avoided,” Dr. Denny said.
Undiagnosed hemochromatosis, for example, can lead to liver failure. Of the 40 people Dr. Denny and his colleagues identified with hemochromatosis, four needed liver transplants.
Yet hemochromatosis can be readily treated by having patients donate blood on a regular basis, which helps rid them of excess iron.
The strategy employed by the research team was startlingly effective at identifying potential causes of disease. In the long run, Dr. Denny and Dr. Rehm agreed, the best solution might be to sequence the entire genome of every patient — in childhood, or even at birth.
But such a policy would create an unmanageable glut of genetic data.
“I don’t think we’re ready to do that,” Dr. Denny said.