Samsung seems to have a bit of an odd fascination with gigantic tablets (albeit one that the buying public doesn’t appear to share). In 2015, it launched a huge 18.4-inch Android slate, the Galaxy View, that weighed nearly six pounds. Undeterred by consumer’s shift from tablets to smartphones for content consumption, the company is back at it with a new large-scale tablet that has a slightly smaller screen but a much bigger battery.
While Samsung sold the original Galaxy View through its normal channels, the Galaxy View 2 is currently available through AT&T, which has a couple of compelling reasons to offer the device to its customers — namely, its existing DirecTV service and the streaming video service it has planned to launch later this year. These and other streaming video alternatives can be accessed through a TV Mode button and viewed on a 17.3-inch full HD touchscreen. A built-in kickstand provides support to hold the View 2 while you’re watching it, as you may not want a 4.9-pound inanimate object sitting on your lap for long amounts of time.
That’s especially true as the 12,000mAh battery probably produces a not insufficient amount of warmth, more than doubling the power of the Galaxy View’s 5,700mAh battery. It’s also upgraded to an Exynos 7884 chip from an Exynos 7580 processor, and 3GB of RAM from 2 gigs of memory. You get 64GB of onboard storage — with a microSD card slot to add up to 400GB more — as well as a 5-megapixel front-facing camera and a quartet of speakers equipped with Dolby Atmos Sound technology.
Because it’s being made available through AT&T, you obtain the Galaxy View 2 via monthly contract. In particular, you’ll pay $37 per month for 20 months, or over $700, which is nearly $200 less than the original View costs at Amazon.com or Walmart.com. Do you think it’s worth the cost to have a giant viewing surface for your binge watching, whether the original or its successor? Let us know in the Comments section below.
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Around 400 million years ago, the ancestor of all four-limbed creatures took its first steps onto dry land. Fast-forward about 350 million years, and a descendant of these early landlubbers did an about-face: It waded back into the water. With time, the back-to-the sea creatures would give rise to animals vastly different from their land-trotting kin: They became the magnificent whales, dolphins, and porpoises that glide through the oceans today.
Going back to being aquatic was a drastic move that would change the animals inside and out, in the space of about 10 million years—an eyeblink in evolutionary terms. Members of this group, now called cetaceans, dropped their hind limbs for powerful flukes and lost nearly all their hair. For decades, their bizarre body plans perplexed paleontologists, who speculated they might have arisen from creatures as varied as marine reptiles, seals, marsupials like kangaroos, and even a now-extinct group of wolf-like carnivores.
“The cetaceans are on the whole the most peculiar and aberrant of mammals,” one scientist wrote in 1945.
Then, in the late 1990s, genetic data confirmed that whales were part of the same evolutionary line that spawned cows, pigs, and camels—a branch called Artiodactyla. Fossils from modern-day India and Pakistan later fleshed out that family tree, identifying the closest ancient relatives of cetaceans as small, wading deer-like creatures.
But their body plans are just the start of cetaceans’ weirdness. To survive in the sea, they also had to make internal modifications, altering their blood, saliva, lungs, and skin. Many of those changes aren’t obvious in fossils, and cetaceans aren’t easily studied in the lab. Instead it was, once again, genetics that brought them to light.
With an increasing availability of cetacean genomes, geneticists can now look for the molecular changes that accompanied the back-to-water transition. While it’s impossible to be certain about the influence of any particular mutation, scientists suspect that many of the ones they see correspond to adaptations that allow cetaceans to dive and thrive in the deep blue sea.
Diving into the depths
The first cetaceans lost a lot more than legs when they went back to the water: Entire genes became nonfunctional. In the vast of book of genetic letters that make up a genome, these defunct genes are among the easiest changes to detect. They stand out like a garbled or fragmented sentence, and no longer encode a full protein.
Such a loss could happen in two ways. Perhaps having a particular gene was somehow detrimental for cetaceans, so animals that lost it gained a survival edge. Or it could be a “use it or lose it” situation, says genomicist Michael Hiller of the Senckenberg Research Institute in Frankfurt, Germany. If the gene had no purpose in the water, it would randomly accumulate mutations and the animals would be no worse off when it didn’t function anymore.
Hiller and colleagues dove into the back-to-water transition by comparing the genomes of four cetaceans—dolphin, orca, sperm whale and minke whale—with those of 55 terrestrial mammals plus a manatee, a walrus, and the Weddell seal. Some 85 genes became nonfunctional when cetaceans’ ancestors adapted to the sea, the team reported in Science Advances in 2019. In many cases, Hiller says, they could guess why those genes became defunct.
For example, cetaceans no longer possess a particular gene—SLC4A9—involved in making saliva. That makes sense: What good is spit when your mouth is already full of water?
Cetaceans also lost four genes involved in the synthesis of and response to melatonin, a hormone that regulates sleep. The ancestors of whales probably discovered pretty quickly that they couldn’t surface to breathe if they shut off their brains for hours at a time. Modern cetaceans sleep one brain hemisphere at a time, with the other hemisphere staying alert. “If you don’t have the regular sleep as we know it anymore, then you probably do not need melatonin,” says Hiller.
The long periods of time that whales must hold their breath to dive and hunt also seem to have spurred genetic changes. Diving deep, as scuba divers know, means little bubbles of nitrogen can form in the blood and seed clots — something that was probably detrimental to early cetaceans. As it happens, two genes (F12 and KLKB1) that normally help kick off blood clotting are no longer functional in cetaceans, presumably lowering this risk. The rest of the clotting machinery remains intact so whales and dolphins can still seal up injuries.
Another lost gene—and this one surprised Hiller—encodes an enzyme that repairs damaged DNA. He thinks this change has to do with deep dives as well. When cetaceans come up for a breath, oxygen suddenly floods their bloodstreams, and as a result, so do reactive oxygen molecules that can break DNA apart. The missing enzyme—DNA polymerase mu—normally repairs this kind of damage, but it does so sloppily, often leaving mutations in its wake. Other enzymes are more accurate. Perhaps, Hiller thinks, mu was just too sloppy for the cetacean lifestyle, unable to handle the volume of reactive oxygen molecules produced by the constant diving and resurfacing. Dropping the inaccurate enzyme and leaving the repair job to more accurate ones that cetaceans also possess may have boosted the chances that oxygen damage was repaired correctly.
Cetaceans aren’t the only mammals that returned to the water, and the genetic losses in other aquatic mammals often parallel those in whales and dolphins. For example, both cetaceans and manatees have deactivated a gene called MMP12, which normally degrades the stretchy lung protein called elastin. Maybe that deactivation helped both groups of animals develop highly elastic lungs, allowing them to quickly exhale and inhale some 90 percent of their lungs’ volume when they surface.
Deep-diving adaptations aren’t all about loss, though. One conspicuous gain is in the gene that carries instructions for myoglobin, a protein that supplies oxygen to muscles. Scientists have examined myoglobin genes in diving animals from tiny water shrews all the way up to giant whales, and discovered a pattern: In many divers, the surface of the protein has a more positive charge. That would make the myoglobin molecules repel each other like two north magnets. This, researchers suspect, allows diving mammals to maintain high concentrations of myoglobin without the proteins glomming together, and thus high concentrations of muscle oxygen when they dive.
Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body.
The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.
For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.
Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said.
Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.
Amid that lingering uncertainty, scientists are discussing how to proceed from here. Antivirals or drugs that target infected cells, some of which are already in development, might help MS patients. Vaccines against EBV are in development, too. The authors of the Science paper say widespread vaccination could prevent most instances of MS. But other researchers aren’t so sure the case is closed, and they suggest putting more emphasis on understanding how the virus might interact with social factors such as stress.
“Patients often want to know why this disease happened to them,” said Lindsey Wooliscroft, a neurologist and associate director of research for the VA’s Multiple Sclerosis Center of Excellence in Portland, Oregon. “It’s frustrating when I can’t tell them.”
Epstein-Barr most often strikes in early childhood, with few or no noticeable symptoms. After the initial infection, the virus lurks inside certain immune cells for the rest of a person’s life.
If someone avoids EBV until adolescence or adulthood, the virus is more likely to cause mononucleosis, an illness characterized by fever and fatigue. Mono is more common in Western countries, where kids encounter fewer germs early in life, said Alberto Ascherio, a professor of epidemiology and nutrition at the Harvard T. H. Chan School of Public Health and senior author of the Science paper.
Like mono, multiple sclerosis is most prevalent in the U.S. and parts of Europe. Scientists first suggested more than four decades ago that the two conditions might be linked. In the following years, the evidence piled up: Nearly everyone with multiple sclerosis has latent EBV in their cells. People who recall being sick with mono have a heightened risk of MS. Immune cells harboring the virus are more prevalent in the brains of MS patients.
“We’ve long suspected that Epstein-Barr virus had a role” in the development of MS, Wooliscroft said. “But it’s just been very hard to prove.”
The surest way to prove causation would be to start with a group of healthy, uninfected adults and divide them at random into two groups. Researchers would infect just one group with the virus and then monitor both groups afterward to see who develops MS.
In the real world, such an experiment isn’t ethical. Ascherio and his coauthors wanted to do the closest possible thing: find a group of people who hadn’t yet been infected with EBV at a given time point, then see whether those who eventually did get infected were more likely to develop MS. “Conceptually, our study is very simple,” Ascherio said. “In practice, it seemed virtually impossible to conduct.”
That’s because the scientists would need a large number of study participants to monitor over the course of years, as MS can be slow to develop and diagnose. For help, the research team turned to the US military, which collects regular blood samples from active service members for HIV screening. In the end, it took two decades for the team to accrue enough data to perform its statistical analysis.
Ketchup is one of the most popular condiments in the US, along with mayonnaise, but getting those few last dollops out of the bottle often results in a sudden splattering. “It’s annoying, potentially embarrassing, and can ruin clothes, but can we do anything about it?” Callum Cuttle of the University of Oxford said during a press conference earlier this week at an American Physical Society meeting on fluid dynamics in Indianapolis, Indiana. “And more importantly, can understanding this phenomenon help us with any other problems in life?”
The answer to both questions, per Cuttle, is a resounding yes. Along with his Oxford colleague, Chris MacMinn, he conducted a series of experiments to identify the forces at play and develop a theoretical model for ketchup splatter. Among the most interesting findings: squeezing the bottle more slowly and doubling the diameter of the nozzle helps prevent splatter. There is also a critical threshold where the flow of ketchup shifts suddenly from not splattering to splattering. A preprint paper has been posted to arXiv and is currently undergoing peer review.
Isaac Newton identified the properties of what he deemed an “ideal liquid.” One of those properties is viscosity, loosely defined as how much friction/resistance there is to flow in a given substance. The friction arises because a flowing liquid is essentially a series of layers sliding past one another. The faster one layer slides over another, the more resistance there is, and the slower one layer slides over another, the less resistance there is.
But not all liquids behave like Newton’s ideal liquid. In Newton’s ideal fluid, the viscosity is largely dependent on temperature and pressure: water will continue to flow — i.e., act like water — regardless of other forces acting upon it, such as being stirred or mixed. In a non-Newtonian fluid, the viscosity changes in response to an applied strain or shearing force, thereby straddling the boundary between liquid and solid behavior. Physicists like to call this a “shearing force”: stirring a cup of water produces a shearing force, and the water shears to move out of the way. The viscosity remains unchanged. But the viscosity of non-Newtonian fluids changes when a shearing force is applied.
Ketchup is a non-Newtonian fluid. Blood, yogurt, gravy, mud, pudding, and thickened pie fillings are other examples, along with hagfish slime. They aren’t all exactly alike in terms of their behavior, but none of them adhere to Newton’s definition of an ideal liquid.
Ketchup, for instance, is comprised of pulverized tomato solids suspended in liquid, making it more of a “soft solid” rather than a liquid, according to Anthony Strickland of the University of Melbourne in Australia. The solids connect to create a continuous network, and one must overcome the strength of that network in order to get the ketchup to flow—typically by tapping or whacking the bottle. Once that happens, the viscosity decreases, and the more it decreases, the faster the ketchup flows. Scientists at Heinz have pegged the optimal flow rate or ketchup at 0.0045 per hour.
When there’s only a little ketchup left in the bottle, you need to whack it that much harder, thereby increasing the risk of splatter. “By the time you get to the end, much of what’s inside is air,” said Cuttle. “So when you squeeze, what you’re doing is compressing air inside the bottle, which build up pressure that drags the [ketchup] out.” The nozzle provides a viscous drag force that counters the viscous flow of the ketchup, and the balance between them determines the flow rate. As the bottle empties, the viscosity decreases because there is less and less ketchup to push. And the outflow of liquid means there is more and more room for the air to expand inside the bottle, decreasing the driving force over time.
Understanding the complicated dynamics of why the smooth flow suddenly shifts to a splatter started with simplifying the problem. Cuttle and MacMinn created an analog of a ketchup bottle, filling syringes (basically capillary tubes) with ketchup and then injecting different amounts of air (from 0 to four milliliters) at fixed compression rates to see how changing the amount of air impacted the flow rate and whether the ketchup splattered. They repeated the experiments with syringes filled with silicon oil in order to better control the viscosity and other key variables.
The result: the syringes with 1 milliliter or more of air injected produced splatter. “This tells us that you need some air in the syringe or bottle to generate a splatter and create that unsteady burst of flow,” said Cuttle. That constitutes a “sauce splatter” critical threshold where the ketchup shifts from smooth flow to splatter, depending on such factors as the amount of air, the rate of compression, and the diameter of the nozzle. Below that threshold, the driving force and liquid outflow are balanced, so the flow is smooth. Above the threshold, the driving force decreases faster than the outflow. The air becomes over-compressed, like a pent-up spring, and the last bit of ketchup is forced out in a sudden burst.
“The splattering of a ketchup bottle can come down to the finest of margins: squeezing even slightly too hard will produce a splatter rather than a steady stream of liquid,” said Cuttle. One handy tip is to squeeze more slowly, thereby reducing the rate at which the air is compressed. Widening the diameter of the nozzle would help even more, since the rubber valve at the spout can exacerbate the risk of splatter. Granted, the valves help avoid leads, but they also force you to build up a certain amount of pressure to get the ketchup to start flowing form the bottle. Cuttle recommends just taking the cap off the bottle when it’s nearly empty as a practical hack, squeezing the last bits of ketchup out of the broader neck.
“It’s common sense, but now there’s a rigorous mathematical framework to back it up,” said Cuttle. “And a gas pushing a liquid out of the way is something that happens in a lot of other contexts.” That includes aquifers for storing captured carbon dioxide, certain types of volcanic eruptions, and re-inflating collapsed lungs.