This Thanksgiving, Reunite along with your Long-Lost Family—Old Videogames

Tucked away in my mom’s household, someplace in room that used to be mine, actually Nintendo GameCube that isn’t mine. My own GameCube is God-knows-where—languishing on some GameStop warehouse rack, or in someone’s garage, buried beneath an electrical drill after an impulsive used-game purchase into the belated 2000s. But this other GameCube, the one that’s there now? I have no concept exactly how it found myself in my space. My stepdad is really a collector of varied types of junk, and another time when I visited it was just there, an apparition from video gaming past.

The part games play within our lives has exploded larger, messier, and much more socially appropriate before 2 decades. Videogames are no more niche tasks; their logic inflects all digital news in one single way or any other, so even if you are not playing directly, you are most likely nevertheless playing in some way. (If social media marketing exposure isn’t a game, I do not know what is.) The thought of games being a countercultural escape is an outdated one in most contexts. They are just a the main material of our lives.

There’s one major exclusion for this sea change, though: the break season. During November and December, which for more and more people involves a pilgrimage to bygone places, videogames accept a renewed and single value.

Home is a messy place. For most folks, oahu is the website of old memories, both negative and positive. The accumulated detritus of longstanding household battles, parental disappointments, grudges and squabbles lasting years, or even decades, accumulates effortlessly in an old home, like dust on the walls. Family gatherings are nostalgia machines, both for good memories and the absolute worst.

Games provides a salve on bad memories and old wounds, pleased places to attend when things get uncomfortable. If that one uncle gets too drunk and starts mentioning when you got endured up for senior prom, well, that’s just what that old Game Boy colors you’ve still got in the closet is for, right?

Those old games can be a way to occupy older variations of ourselves, too. A way of visiting with some body you once knew— keeping, as Joan Didion put it, on nodding terms together with your old self. Choosing the old games kept in cabinet, or just participating in an old pastime inside places you accustomed, can unlock old emotions, old sensory faculties of self, and let you turn them over in new light.

Once I had been younger, I happened to be responsible for starting videogames inside my grandmother’s household every Thanksgiving and xmas. The Super Nintendo and Nintendo 64 devices she owned, when my childhood activity when I visited her, were repurposed right into a way of keeping a whole gaggle of grandkids occupied before and after supper. We’d play Super Smash Bros. and Super Mario World; I still keep in mind what it absolutely was like, sitting in that little corner associated with the dining room with my grandmother, forcing her to learn how to play these Nintendo games so I’d have anyone to play with. (She constantly humored me personally.) Going house now, playing Nintendo games old and brand new in those exact same places, will put me personally both in of those places at once. I’ll imagine myself due to the fact older shepherd as well as the young, extremely enthusiastic nerd, both having controller within my hand.

And games can also be a way of bringing a back-up with us. The week after Thanksgiving, I’m spending a week back home. In preparation, I loaded up my Nintendo change with expanded storage capacity and a bunch of new games—some ports of current games, some games i am meaning to test. It’s a convenience blanket, a method to bring my current straight back with me. To not get back to a previous form of myself completely. A memory trick in a 720p display screen.

Therefore, as corny because it sounds, videogames, and their capacity to both hide us and expose us, are one thing become thankful because of this Thanksgiving. When you go home, check out the cabinet, see if there’s an Atari or perhaps a Sega Genesis tucked within. Pull it down, keep in mind exactly how it felt; invest some time in those old footwear. Me personally, i’ll see if that GameCube still works.

Reactions to Twitter’s brand new Character Limit Top This Week’s Web News

recently in “Your faves are problematic” news, Louis C.K. and Mad guys creator Matthew Weiner, your time and effort has come. But in other news, Eminem possesses new track with Beyoncé, that is offering the internet one thing else to share. Will there be other things that had every person chatting the other day? Why, we’re glad you asked.

Trump’s Merger Mission

Just what occurred: how badly does the president hate CNN? adequate to possibly step over the line and restrict its business dealings? Let’s learn.

Exactly what actually occurred: AT&T has been doing foretells purchase CNN moms and dad business Time Warner for quite some time now—WIRED also arrived on the scene against it greater than a year ago—but this week, apparently away from nowhere, the efforts hit a major, unexpected snag.

Media straight away began jumping in the news, because the media really really loves talking about itself. At the same time, other people begun to explore Trump’s feasible participation.

It is here an alternative undertake this story making it look like it is being done to harm the president? As being a matter of fact…

Always remember exactly how magical the web could be for anyone hunting for … almost anything, really.

The Takeaway: Of course, maybe there are legitimate known reasons for the Department of Justice to be concerned with enough time Warner deal…

…well, not those reasons, obviously.

Therefore, About This Roy Moore Story…

What occurred: Remember when electability and morality had been real things people cared about? The US Senate race in Alabama might convince you that’s no more the scenario.

Just what Really took place: In order to get you up to speed as fast as possible, let’s just focus on this tweet from Thursday.

That did not seem good on at the very least several levels, and when the Washington Post story finally dropped the story in regards to the allegations against Roy Moore, it in fact was a big deal.

How dreadful could it be? Well, it depended in your political allegiance and your location, it seems, as you reporter found out when he called Alabama Republican figures to generally share the allegations.

It absolutely wasnot only Republican officials in Alabama who had been dismissive of this tale, some people on Twitter had been besides.

That types of response hasn’t gone unnoticed, specially after the White House offered a less full-throated protection. At the same time, somewhere else on Twitter, viewpoints were not equivalent.

Man, 2017 sure is just a 12 months and a half, huh?

The Takeaway: Still, it’s not want it could easily get any more extreme, right?

Oh, that is correct. 2017.

Twitter: Now with Two Times the Characters!

What took place: It finally arrived: Twitter now let’s every person state two times as much.

Just what actually occurred: It is a thing that everybody else literally knew had been coming—really, it’d been anticipated since September—but Twitter officially rolled out its new 280-character limit wide the other day, unleashing all method of coverage from the media enthusiastic about the illusion of modification. But just how did the latest character limit look at on Twitter it self?

Well. Yes.

However the final word in the switch, in accordance with many whom quoted this for truth—or, about, activity value—was, evidently, this:

The Takeaway: Thankfully, someone was willing to talk truth to power.

(We additionally didn’t need 50-character display names, but which also occurred the other day.)

A Verified Debacle

Just what occurred: evidently, being truly a white supremacist is newsworthy in and of itself.

Exactly what actually took place: Doubling the quantity of characters per tweet was not the actual only real hot water Twitter squeezed itself in last week, because it proved. You realize that whole “verification check mark” thing which has been a thorn in the organization’s side since it began being rolled out a year ago? Well…

Whilst the backlash got entirely swing, Twitter attempted to use those 280 figures to dig itself out of the gap that was rapidly forming. Somewhat unsuccessfully.

Twitter boss Jack Dorsey got myself involved.

But did that assistance…? Let’s choose “no.”

The upshot of all with this? Well, at the least everybody knows that verification is trash…? It is a start. A start of what, we cannot quite tell, but it’s surely beginning something.

The Takeaway: inside of all days, Twitter’s position is not the most effective appearance.

Cannot Bore Us, Reach the Chorus

What took place: possibly it’s time for musical interlude. Simply never tune in to the words, what you may do.

Just what Really occurred: Look, it’s been an extended, exhausting week. Let us end with something stupid. Or, at the very least, something which’s much less smart because it believes it really is.

Yeah. This is the ticket. I mean, it isn’t clear anyway from that tweet what is in fact being said or be it an recommendation or something like that else, but nevertheless, it is positively a admission. Maybe some body wish to explain, maybe?

Oh, OK. That is clearly a small bit a lot more of a conclusion, but what’s the hot subject under consideration? Perhaps Not the store, clearly…

Oh. Oh. Actually, let us save the “oh”s until after you’ve listened to the track for yourself, as it’s certainly one thing. Hey, Twitter, why not reveal that which you think?

Something’s without a doubt, nonetheless; regardless of how good or bad the track is (it’s bad), this is certainly probably the most mainstream attention for Keith Urban track in… forever? Don’t simply take this as a foolproof method to go back to relevance, faded music movie stars of yore.

The Takeaway: for individuals who had been already preparing to ask “But when do the males get their track?” don’t worry, you are currently covered. (outside, like, the remainder history of popular music.)

What Protects Elephants from Cancer?

Elephants and other large animals have a lower incidence of cancer than would be expected statistically, suggesting that they have evolved ways to protect themselves against the disease. A new study reveals how elephants do it: An old gene that was no longer functional was recycled from the vast “genome junkyard” to increase the sensitivity of elephant cells to DNA damage, enabling them to cull potentially cancerous cells early.

Quanta Magazine

author photo


Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.

In multicellular animals, cells go through many cycles of growth and division. At each division, cells copy their entire genome, and inevitably a few mistakes creep in. Some of those mutations can lead to cancer. One might think that animals with larger bodies and longer lives would therefore have a greater risk of developing cancer. But that’s not what researchers see when they compare species across a wide range of body sizes: The incidence of cancer does not appear to correlate with the number of cells in an organism or its lifespan. In fact, researchers find that larger, longer-lived mammals have fewer cases of cancer. In the 1970s, the cancer epidemiologist Richard Peto, now a professor of medical statistics and epidemiology at the University of Oxford, articulated this surprising phenomenon, which has come to be known as Peto’s paradox.

The fact that larger animals like elephants do not have high rates of cancer suggests that they have evolved special cancer suppression mechanisms. In 2015, Joshua Schiffman at the University of Utah School of Medicine and Carlo Maley at Arizona State University headed a team of researchers who showed that the elephant genome has about 20 extra duplicates of p53, a canonical tumor suppressor gene. They went on to suggest that these extra copies of p53 could account, at least in part, for the elephants’ enhanced cancer suppression capabilities. Currently, Lisa M. Abegglen, a cell biologist at the Utah School of Medicine who contributed to the study, is leading a project to find out whether the copies of p53 have different functions.

Vincent Lynch, a geneticist at the University of Chicago, has shown that part of what enabled elephants to grow so big was that one of their pseudogenes—a broken duplicate of an ancestral gene—suddenly acquired a new function.

Courtesy of Vincent J. Lynch

Yet extra copies of p53 are not the elephants’ only source of protection. New work led by Vincent Lynch, a geneticist at the University of Chicago, shows that elephants and their smaller-bodied relatives (such as hyraxes, armadillos and aardvarks) also have duplicate copies of the LIF gene, which encodes for leukemia inhibitory factor. This signaling protein is normally involved in fertility and reproduction and also stimulates the growth of embryonic stem cells. Lynch presented his work at the Pan-American Society for Evolutionary Developmental Biology meeting in Calgary in August 2017, and it is currently posted on

Lynch found that the 11 duplicates of LIF differ from one another but are all incomplete: At a minimum they all lack the initial block of protein-encoding information as well as a promoter sequence to regulate the activity of the gene. These deficiencies suggested to Lynch that none of the duplicates should be able to perform the normal functions of a LIF gene, or even be expressed by cells.

The eminent biologist Richard Peto, now at the University of Oxford, pointed out in the 1970s that elephants and other large-bodied animals ought to be at great statistical risk for cancer.

Cathy Harwood

But when Lynch looked in cells, he found RNA transcripts from at least one of the duplicates, LIF6, which indicated that it must have a promoter sequence somewhere to turn it on. Indeed, a few thousand bases upstream of LIF6 in the genome, Lynch and his collaborators discovered a sequence of DNA that looked like a binding site for p53 protein. It suggested to them that p53 (but not any of the p53 duplicates) might be regulating the expression of LIF6. Subsequent experiments on elephant cells confirmed this hunch.

To discover what LIF6 was doing, the researchers blocked the gene’s activity and subjected the cells to DNA-damaging conditions. The result was that the cells became less likely to destroy themselves through a process called apoptosis (programmed cell death), which organisms often use as a kind of quality control system for eliminating defective tissue. LIF6 therefore seems to help eradicate potentially malignant cells. Further experiments indicated that LIF6 triggers cell death by creating leaks in the membranes around mitochondria, the vital energy-producing organelles of cells.

To find out more about the evolutionary history of LIF and its duplicates, Lynch found their counterparts in the genomes of closely related species: manatees, hyraxes and extinct mammoths and mastodons. His analysis suggested that the LIF gene was duplicated 17 times and lost 14 times during the evolution of the elephant’s lineage. Hyraxes and manatees have LIF duplicates, but the p53 duplicates appear only in living and extinct elephants, which suggests that the LIF duplications happened earlier in evolution.

Elephants are closely related to large animals such as manatees (left), but also to smaller ones like hyraxes (right), aardvarks and armadillos. Elephants only began to develop their immense size about 30 million years ago.

Jim P. Reid, USFWS / Bjørn Christian Tørrissen

Lynch found that most duplicates of the LIF gene are pseudogenes—old, mutated, useless copies of genes that survive in the genome by chance. The exception, however, is the LIF6 gene sequence, which unlike the others has not accumulated random mutations, implying that natural selection is preserving it.

“We think that LIF6 is a refunctionalized pseudogene,” Lynch said. That is, the elephant LIF6 re-evolved into a functional gene from a pseudogene ancestor. Because it came back from the dead and plays a role in cell death, Lynch called it a “zombie gene.”

Although manatees and hyraxes also have extra copies of LIF, only modern and extinct elephants have LIF6, which suggests that it evolved only after the elephants branched away from those related species. And when Lynch’s group dated the origin of LIF6 by molecular clock methods, they found that the pseudogene regained a function about 30 million years ago, when the fossil record indicates that elephants were evolving large body sizes.

Lucy Reading-Ikkanda/Quanta Magazine

“Refunctionalizing a pseudogene is not something that happens every day,” explained Stephen Stearns, an evolutionary biologist at Yale University, in an email to Quanta. Being able to show that it happened at roughly the same time that elephants evolved a large body, he wrote, “supports, but does not prove, that the refunctionalizing of the gene was a precondition for the evolution of large body size.”

Evolving protections against cancer would seem to be in the interest of all animals, so why don’t they all have a refunctionalized LIF6 gene? According to the researchers, it’s because this protection comes with risks. LIF6 suppresses cancer, but extra copies of LIF6 would kill the cell if they accidentally turned on. “There’s a bunch of toxic pseudogenes sitting there” in the genome, Lynch explained in an email. “If they get inappropriately expressed, it’s basically game over.”

There also appears to be a trade-off between cancer suppression mechanisms and fertility. A study published in 2009 suggested that LIF is critical for implantation of the embryo in the uterus. Because LIF activity is controlled by p53, LIF and p53 jointly regulate the efficiency of reproduction. When the same set of genes has two functions (such as reproduction and cancer suppression), it is possible that those functions will be in direct conflict—a phenomenon that geneticists call antagonistic pleiotropy.

The elephants may have solved the problem of antagonistic pleiotropy by duplicating p53 and LIF and splitting up those functions, according to Maley. “Some copies of p53 and LIF are doing what’s necessary for fertility, while other pairs of LIF and p53 are doing what’s necessary for cancer suppression,” he said. Maley speculated that the gene duplicates “allowed the elephants to get better at cancer suppression and still maintain their fertility, which would allow them to grow a larger body.” That hypothesis, however, still needs to be tested, he said.

Bats are not large animals, but some species live for decades. Scientists are investigating whether they have their own protective adaptations against cancer.

Ann Froschauer, USFWS

Evolving extra copies of p53 and LIF may have helped elephants overcome Peto’s paradox, but that can’t be the only solution: Other large animals like whales have only one copy of p53 and one version of LIF. Lynch and his team are currently exploring how whales and bats solve Peto’s paradox. Although not large-bodied, some bat species live up to 30 years, and the longer-lived ones might have evolved cancer suppression mechanisms that the shorter-lived ones lack.

Maley is also working on how whales solve Peto’s paradox. Even though whales don’t have extra copies of p53, he said, “we do think there has been a lot of selection and evolution on genes in the p53 pathway.” Maley believes that understanding how diverse large-bodied animals solve Peto’s paradox may have applications in human health. “That is the end goal,” he said. “The hope is that by seeing how evolution has found a way to prevent cancer, we could translate that into better cancer prevention in humans.”

“Every organism that evolved large body size probably has a different solution to Peto’s paradox,” Maley said. “There’s a bunch of discoveries that are just waiting for us out there in nature, where nature is showing us the way to prevent cancer.”

Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.