This Is Why You Aren’t Allowed to Use an In-Flight Bathroom Until Takeoff

If your plane is getting ready to take off when that water you downed earlier finally catches up with you, don’t even think about heading to the bathroom. Even if the plane is barely filled, the airline has a very good reason to keep you in your seat.

About 13 percent of fatal plane accidents and onboard deaths happen during takeoff and the initial climb, according to Boeing data from 2007 through 2016. To prevent injury, federal regulations require airlines to light up seatbelt signs before the plane starts to move. And lest you think that’s just the airline’s problem, another law requires passengers to sit down with their seatbelt fastened when the ‘Fasten Seat Belt’ light is on. The plane crew wants you to be safe, and starting to taxi while passengers are out of their seats—including on the toilet, which obviously doesn’t have a seatbelt—could pose a safety threat. In the interest of everyone on the flight’s well-being, here are 18 more things you should never do on a plane.

The law doesn’t require pilots to stop a plane if a passenger stands up during taxiing, but it does encourage it. Federal Aviation Administration rules cite one pilot whose airline pilot certificate was suspended for a week after he taxied to the runway while passengers were in the aisle. There are times when it would be safer to keep moving than to stop taxiing, the FAA clarifies, but it highlights that ‘historically most airlines ensured passengers were seated during movement on the surface.’ If you insist on going, there’s a good chance the plane will stop moving, putting the whole flight off schedule if it loses its place in line. That’s not something your flight crew will appreciate. Don’t miss these other 28 things your pilot wishes you knew.

Next time, try to leave time for a bathroom break before getting on a plane. Better yet, plan your toilet stop around the best time to use the bathroom on a plane. [Source: Southern Living]

Want to live for ever? Flush out your zombie cells

As time passes, the number of damaged, ‘senescent’ cells in our bodies increases. These in turn are responsible for many effects of ageing. Now scientists are working to eliminate them

In a lab just south of San Francisco I am looking at two blown-up images of microscope slides on a computer screen, side by side. The slides are the same cross-sections of mouse knees from a six-month-old and an 18-month-old animal. The older mouse’s image has a splattering of little yellow dots, the younger barely any. That staining indicates the presence of so-called senescent cells – “zombie cells” that are damaged and that, as a defence against cancer, have ceased to divide but are also resistant to dying. They are known to accumulate with age, as the immune system can no longer clear them, and as a result of exposure to cell-damaging agents such as radiation and chemotherapy. And they have been identified as a cause of ageing in mice, at least partially responsible for most age-related diseases. Seeing the slides, it makes me worried about my own knees. “Tell us about it,” says Pedro Beltran who heads the biology team at Unity Biotechnology, a 90 person-strong company trying to halt, slow or reverse age-associated diseases in humans by killing senescent cells. “We think about it all the time… Wait until you see your brain.”

Developing therapies to kill senescent cells is a burgeoning part of the wider quest to defeat ageing and keep people healthier longer. Unity, which was founded in 2011, has received more than $385m in funding to date including investment from big tech names such as Amazon’s Jeff Bezos and PayPal co-founder Peter Thiel. It went public this May and is valued at more than $700m. Its first drug entered early clinical trials in June, aimed at treating osteoarthritis.

Other startups with zombie cells in their sights include Seattle-based Oisín Biotechnologies which was founded in 2016 and has raised around $4m; Senolytic Therapeutics whose scientific development is based in Spain and which was established last September (it won’t disclose its financing other than to say it has a first round, which will allow it to reach clinical trials); and Cleara Biotech, formed this June backed by $3m in funding and based in the Netherlands. In addition, Scottish company CellAge, also founded in 2016, has raised about $100,000 to date, partly through a crowdfunding campaign.

“I myself am a victim to narrative,” says Alex Rosenberg, a Duke University philosophy professor whose new book hopes to convince readers that narratives — and especially narrative history — are flawed as tools of knowledge.

Rosenberg is a philosopher of science and a writer of historical fiction. How History Gets Things Wrong: The Neuroscience of Our Addiction to Stories, out this week from MIT Press, does not deny that stories can be wonderful as art and effective at eliciting emotions that then push action. But, Rosenberg tells The Verge, stories also lull us into a false sense of knowledge and fundamentally limit our understanding of the world.

This interview has been lightly edited for clarity.

You’re a professor of philosophy with appointments in biology and political science, and you’re also a novelist, but you’re not a neuroscientist or a historian. So how did you come to write this book?

I’ve always been besotted by history, but it’s not part of my academic credentials in any way. I am a philosopher of science, and, at one point, I went back to graduate school to study molecular biology, anatomy and physiology, and evolutionary biology. These are fields that have the tools and data and theories that have burgeoned over the last 30 years and which have begun to be able to finally shed light on the brain and human cognitive capacities and abilities. My interests have been carried along by developments of sciences that have been increasingly employed in areas like neuroscience to address some very traditional questions that philosophers have been interested in.

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A single gene mutation may have helped humans become optimal long-distance runners

Two to three million years ago, the functional loss of a single gene triggered a series of significant changes in what would eventually become the modern human species, altering everything from fertility rates to increasing cancer risk from eating red meat.

In a new paper, published in the September 12 issue of the Proceedings of the Royal Society B, researchers at University of California San Diego School of Medicine report on studies of mice engineered to lack the same gene, called CMAH, and resulting data that suggest the lost gene may also have contributed to humanity’s well-documented claim to be among the best long-distance runners in the animal kingdom.

At roughly the same time as the CMAH mutation took hold, human ancestors were transitioning from forest dwellers to life primarily upon the arid savannahs of Africa. While they were already walking upright, the bodies and abilities of these early hominids were evolving dramatically, in particular major changes in skeletal biomechanics and physiology that resulted in long, springy legs, big feet, powerful gluteal muscles and an expansive system of sweat glands able to dissipate heat much more effectively than other larger mammals.

Such changes, say scientists, helped fuel the emergence of the human ability to run long distances relatively tirelessly, allowing ancestors to hunt in the heat of the day when other carnivores were resting and to pursue prey to their point of exhaustion, a technique called persistence hunting.

“We discovered this first clear genetic difference between humans and our closest living evolutionary relatives, the chimpanzees, more than 20 years ago,” said senior author Ajit Varki, MD, Distinguished Professor of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine and co-director of the UC San Diego/Salk Center for Academic Research and Training in Anthropogeny.

Given the approximate timing of the mutation and its documented impact on fertility in a mouse model with the same mutation, Varki and Pascal Gagneux, Ph.D., professor of anthropology and pathology, began investigating how the genetic difference might have contributed to the origin of Homo, the genus that includes modern Homo sapiens and extinct species like Homo habilis and Homo erectus.

“Since the mice were also more prone to muscle dystrophy, I had a hunch that there was a connection to the increased long distance running and endurance of Homo,” said Varki, “but I had no expertise on the issue and could not convince anyone in my lab to organize this long-shot experiment.”

Read more at: https://phys.org/news/2018-09-gene-mutation-humans-optimal-long-distance.html#jCp

NASA chief excited about prospects for exploiting water on the moon

(Reuters) – NASA Administrator Jim Bridenstine has a vision for renewed and “sustainable” human exploration of the moon, and he cites the existence of water on the lunar surface as a key to chances for success.

FILE PHOTO: NASA Administrator Jim Bridenstine (L) makes remarks as US Strategic Command Commander Gen. John Hyten listens during the House Armed Services Strategic Forces Subcommittee’s joint hearing with the House Science, Space and Technology Committee, in Washington, U.S., June 22, 2018. REUTERS/Mike Theiler/File Photo

“We know that there’s hundreds of billions of tons of water ice on the surface of the moon,” Bridenstine said in a Reuters TV interview in Washington on Tuesday, a day after NASA unveiled its analysis of data collected from lunar orbit by a spacecraft from India.

The findings, published on Monday, mark the first time scientists have confirmed by direct observation the presence of water on the moon’s surface – in hundreds of patches of ice deposited in the darkest and coldest reaches of its polar regions.

The discovery holds tantalizing implications for efforts to return humans to the moon for the first time in half a century. The presence of water offers a potentially valuable resource not only for drinking but for producing more rocket fuel and oxygen to breathe.

Bridenstine, a former U.S. Navy fighter pilot and Oklahoma congressman tapped by President Donald Trump in April as NASA chief, spoke about “hundreds of billions of tons” of water ice that he said were now known to be available on the lunar surface.

But much remains to be learned.

Scientists calculate the speed of death in cells, and it’s surprisingly slow

Regular, programmed “cellular suicide” keeps us healthy.

Cells in our bodies die all the time, and now we know just how fast.

Scientists found that death travels in unremitting waves through a cell, moving at a rate of 30 micrometers (one-thousandth of an inch) every minute, they report in a new study published Aug. 10 in the journal Science. That means, for instance, that a nerve cell, whose body can reach a size of 100 micrometers, could take as long as 3 minutes and 20 seconds to die.

That may sound morbid, but it’s precisely this lethal tide that keeps us alive and healthy. Apoptosis — or programmed cell death — is necessary for clearing our bodies of unnecessary or harmful cells, such as those that are infected by viruses. It also helps shape organs and other features in a developing fetus. (There is a second way cells can die, called necrosis, which is a different process that occurs as an unplanned response to a stressful event.)

If this process doesn’t work properly, the consequences can be dire. For example, cancerous cells, happily living on, having slipped the grasp of the Grim Reaper, begin to spread instead of dying off. [5 Ways Your Cells Deal With Stress]

“Sometimes our cells die when we really don’t want them to — say, in neurodegenerative diseases. And sometimes our cells don’t die when we really do want them to — say, in cancer,” senior author Dr. James Ferrell, a professor of chemical and systems biology and biochemistry at Stanford University, said in a statement. “And if we want to intervene, we need to understand how apoptosis is regulated.”

Apoptosis is also sometimes called “cellular suicide,” because it is a process of self-destruction. It begins with a signal either from the inside or the outside that informs enzymes within the cells called caspases to start cleaving the cell. But it had been unclear how apoptosis, after being triggered, actually spread through the cell.

To figure this out, Ferrell and his team observed the process in one of the larger cells present in nature: egg cells of Xenopus laevis,or African clawed frogs. They filled test tubes with fluid from the eggs and triggered apoptosis, which they watched unfold by tagging involved proteins with fluorescent light. If they saw fluorescent light, it meant apoptosis was taking place.

They found that the fluorescent light traveled through the test tubes at a constant speed. If apoptosis had carried on due to simple diffusion (the spreading of substances from an area of high concentration to one of low concentration), the process would have slowed down toward the end, according to the study.

Since it didn’t, the researchers concluded that the process they observed must be “trigger waves,” which they likened to “the spread of a fire through a field.” The caspases that are first activated, activate other molecules of caspases, which activate yet others until the entire cell is destroyed.

“It spreads in this fashion and never slows down, never peters out,” Ferrell said in the statement. “It doesn’t get any lower in amplitude because every step of the way it’s generating its own impetus by converting more inactive molecules to active molecules until apoptosis has spread to every nook and cranny of the cell.”

The team then wanted to watch this process occur inside the egg itself, as it would in nature. They noticed that when frog eggs died, they darkened in color. So, they initiated conditions that would naturally lead to the death of a frog egg and imaged what happened. Similarly, the cell darkened at the average rate of 30 micrometers per minute.

Such trigger waves are actually pervasive in nature, Ferrell said. Trigger waves also help cells reproduce, neurons propagate signals through the brain and viruses spread from cell to cell. Ferrell and his team hope to find out where else in biology trigger waves occur.

Originally published on Live Science.
Source: NBCNEWS.COM

Petrichor: why does rain smell so good?

It turns out it’s not just gratitude that makes rain smell so appealing after a long period of dry weather.

There’s actually some chemistry involved too.

Bacteria, plants and even lightning can all play a role in the pleasant smell we experience after a thunderstorm; that of clean air and wet earth.

Known as petrichor, the scent has long been chased by scientists and even perfumers for its enduring appeal.

Wet earth

First named by two Australian researchers in the 1960s, the warm, earthy fragrance we experience when rain hits dry ground is produced by bacteria.

“These critters are abundant in soil,” explained Prof Mark Buttner, head of molecular microbiology at the John Innes Centre.

“So when you’re saying you smell damp soil, actually what you’re smelling is a molecule being made by a certain type of bacteria,” he told the BBC.

That molecule, geosmin, is produced by Streptomyces. Present in most healthy soils, these bacteria are also used to create commercial antibiotics.

Drops of water hitting the ground cause geosmin to be released into the air, making it much more abundant after a rain shower.

“Lots of animals are sensitive but human beings are extremely sensitive to it,” added Prof Buttner.

“This is the kind of stuff you don’t want to be right about.”
Poring over four decades of satellite data, climate scientists have concluded for the first time that humans are pushing seasonal temperatures out of balance – shifting what one researcher called the very “march of the seasons themselves.”
Ever-mindful of calculable uncertainty and climate deniers, the authors give “odds of roughly 5 in 1 million” of these changes occurring naturally, without human influence.

Like homicide detectives, climate scientists are continually sifting through evidence looking for what they also call “fingerprints”.

Over the years, they’ve teased out the human signal from Earthly noise in annual and decade-spanning temperature records, marine chemistry, rapid Arctic change, and more.

What they discovered is an uneven pace of seasonal change in the atmosphere above the Northern and Southern Hemispheres’ temperate zones.

While warming is famously global, summers in the troposphere are heating faster than winters, in a way physics would dictate if greenhouse gases were the culprit.

The satellite data and computer models for seasonal temperature change used by the study agree with each other even more closely than they do when gauging average annual temperature.

Ben Santer, an atmospheric scientist at Lawrence Livermore National Laboratory and the study’s lead author, likens the temperature results to a wave washing up on a beach.

For every year in the 38-year satellite record, the team captured the monthly temperature lows (troughs) and highs (crests).

In the early years, the “waves” came in small. By the end of the data set under study, 2016, the waves crashed ashore with higher troughs – and much higher crests.

The study, published Thursday in the journal Science, also calls attention to a persistent disconnect between findings that attribute warming to humanity and how the same research has been characterized in testimony before the US Congress.

Santer has previously referenced congressional hearings in peer-reviewed journal articles, dedicating a May 2017 article in Nature Scientific Reports to fact-checking claims made by then-US Environmental Protection Administrator Scott Pruitt in a written supplement to his confirmation hearings.

“To me when incorrect claims are elevated to the level of formal congressional testimony and are part of the Congressional Record, then it is important to address them,” Santer said.

Santer’s newest paper comes during a busy week for climate politics, as several Republicans back a resolution opposing carbon taxes, another Republican congressman preps a long-shot carbon-tax bill, and several research groups led by Columbia University’s Center on Global Energy Policy publish studies of new scenarios analyzing US pricing of carbon dioxide emissions.

Climate models are famously imperfect. The authors indicate where simulated warming has been known to outrun actual temperatures, the focus of much attention in recent years.

They walk briefly through several possible explanations and dismiss concern among some scientific critics that models overestimate how fast the world will warm.

“The claim that overestimation of warming is solely due to a large error in climate model sensitivity has been tested elsewhere and is not credible,” the authors write.

In the end, five of six satellite data sets show that the warming signal has risen above the natural noise, according to the research. Changes miles above the ground are part of the same puzzle visible from your kitchen window.

“There are a lot of observations that the seasonal cycle is changing, and it is also one of the things that is most noticeable in everyday life with trees flowering earlier,” said Friederike Otto, an associate professor at the University of Oxford’s Climate Research Programme.

“But so far this has been tricky to disentangle formally and with high statistical significance from natural variability.”

Santer sees the work as an uncomfortable reminder of the overall climate trend.

“The piling on of evidence is worrying me,” he said.

“This is the kind of stuff you don’t want to be right about.”
ERIC ROSTON, BLOOMBERG
23 JUL 2018

At least 10 dead after 6.4 earthquake hits Indonesia island

JAKARTA — A powerful 6.4 magnitude earthquake struck the popular tourist destination of Lombok in Indonesia on Sunday, killing 10 people and damaging many buildings, authorities said.

The quake hit Lombok island early in the morning when many people were still sleeping. Around 40 people were injured and many fled into open fields away from collapsed buildings.

“We jumped out of our beds to avoid anything falling on our heads,” said Jean-Paul Volckaert who was woken by the quake while sleeping in the Puncak Hotel near Senggigi on Lombok.

“I’ve been walking around but so far there is no damage. We were very surprised as the water in the pools was swaying like a wild sea. There were waves in the pools but only for 20 to 30 seconds,” he told Reuters via telephone.

A group of scientists in Russia claim to have revived a pair of frozen nematodes, or roundworms, that were between 30,000 and 42,000 years old. One of the specimens was found in a soil sample collected from a ground squirrel burrow located around 100 feet underground, and other burrows nearby have been radiocarbon dated to be around 32,000 years old. A second viable nematode was found in a permafrost sample approximately 41,700 years old collected around 11 feet below the surface.

The samples were stored in a laboratory at around -4 degrees Fahrenheit. Isolated nematodes were then later brought up to 68 degrees and surrounded by food. After several weeks of cultivation, the nematodes began showing signs of life and reportedly began moving and eating. “Thus, our data demonstrate the ability of multicellular organisms to survive long-term (tens of thousands of years) cryobiosis under the conditions of natural cryoconservation,” the researchers said in a study published in Doklady Biological Sciences.

While other studies have shown that some species of nematodes can survive extreme environments — such as 25.5 years in below-freezing temperatures and 39 years of dessication — this study appears to be the first to demonstrate nematode survival after such an extreme length of time.

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