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‘People didn't like women in space': how Sally Ride made history and paid the price

‘People didn't like women in space': how Sally Ride made history and paid the price

Yahoo15-06-2025
A week before Sally – a documentary about the first American woman to fly into space – landed at the Sundance film festival in January, Nasa employees received emails informing them how Donald Trump's diversity, equity and inclusion (DEI) rollbacks would take effect.
Contracts and offices associated with DEI programs were to be terminated. Staff were given Orwellian instruction to inform the government of any attempt to disguise inclusion efforts in 'coded or imprecise language'. In the weeks to follow, Nasa would take back its promise to send the first woman and person of color to the moon's surface. Meanwhile, employees are reported to be hiding their rainbow flags and any other expressions of solidarity with the LGBTQ+ community, allegedly because they were instructed to do so though Nasa denies those claims.
'The pride flag flew in space a couple years ago,' says Cristina Costantini, the director of Sally, on a Zoom call with the Guardian. 'Now all Nasa employees are being asked to take down any representations of pride.'
Related: 'Absolutely shocking': Netflix documentary examines how the Titan sub disaster happened
Costantini calls the developments sad, especially because such harmful silencing contributes to the very atmosphere that made her film's subject hide her own queer identity throughout her celebrated career. Sally Ride, who made history when she rode the space shuttle Challenger into the stars on 18 June 1983, was a lesbian. The public, and so many who knew Ride personally, only found out that part of her legacy after she died of cancer in 2012. Ride's obituary identified Tam O'Shaughnessy as her partner of 27 years.
O'Shaughnessy is a key voice in Sally, a National Geographic documentary revisiting everything we thought we knew about Ride – from her astronomic accomplishments to the infuriating sexism she confronted at Nasa and in the media, with reporters questioning how she would dress, whether space travel would affect her ovaries and if she would buckle and cry in the face of daunting challenges. But now there's the extra dimension, the part of Ride kept tragically buried because of the institutionalized homophobia we see resurfacing today. 'We made this movie not thinking it was particularly controversial,' says Costantini. 'We had no idea it would be this relevant.'
Costantini is speaking from her Los Angeles office in Atwater Village, a photo of a space shuttle and another of Ride on the Challenger mission hovering just behind her. The investigative reporter turned film-maker – who grew up wanting to be a scientist and made her feature debut co-directing the Sundance audience award winner Science Fair – describes Ride as a major influence on her life. She remembers researching the astronaut as a young child on an old Encarta Encyclopedia CD-Rom for a book report. In grade three, Costantini contributed to a class mural where the students in her Milwaukee school painted their heroes on a wall. Ride is drawn standing alongside Brett Favre and Michael Jordan – a small sampling of the heroes that fed childhood aspirations in the mid-90s, says Costantini.
With Sally, Costantini is returning to her icon's story with a canvas bigger than either a book report or mural, but an even more challenging story to tell.
'The film is really two stories interwoven,' says Costantini. 'It's the public and the private Sally. The public Sally is so well-documented that it's a problem. We had to bring in 5,000 reels from the Nasa archive and sort through and sound sync all of them. That was a monumental task.
'And then the other task is the private story, maybe the more interesting story, which has no documentation at all. There are only five really good pictures of [Sally and her partner, Tam] together that we had. You can't build a love story out of showing people the same five pictures over and over again. For that we had to kind of invent our own cinematic romantic language.'
Costantini's doc pairs narrations from O'Shaughnessy and others who were close to Ride with animation and 16mm visuals. They express the love, the excitement of first relationships, the heavy toll from keeping these feelings secret and the sting when Ride – whose noted emotional reserve is making more and more sense – would behave inexplicably.
'Sally is a very confusing central subject in some ways,' says Costantini, remarking on how Ride didn't always make for a picture-perfect feminist hero, the uneasiness going a long way to make her even more compelling. The director refers to a story recounted by fellow astronaut Kathryn Sullivan. During the race to become the first American woman to go to space, Ride sabotaged a Nasa exercise Sullivan was working on. Talking heads mull whether that was an example of Ride's prankster sense of humour, or a cutthroat competitive nature that flew in the face of female solidarity and sisterhood. 'She didn't leave tell all diaries or an audio journal of how she was feeling in every single moment. So we're left to interpret later on what her choices were, and why she did what she did.'
Costantini also points to Ride's five-year marriage to fellow astronaut Steve Hawley. The union in retrospect can be seen as a betrayal of who she was, and the LGTBQ+ movement that she never publicly aligned with. But it was also a necessary and sacrificial career move to make her dream possible, deflecting any suspicions about sexual orientation while making Ride a more ideal candidate to make history and inspire young women. 'People didn't like women in space,' says Costantini. 'And they especially didn't like single women in space. Some of the male astronauts were, like: 'Well, it was a good look for her not to be single and in space.''
When Ride does climb above the atmosphere on her historic mission, there's a cathartic moment where the tense conflicts within her – or put upon her – are either resolved or abandoned, if only temporarily.
Related: Liza: A Truly Terrific Absolutely True Story review – dazzling glamour and true grit
'I loved being weightless,' says Ride, while in space, her recorded words packing new mean considering all the burdens we now understand. 'It's a feeling of freedom.'
'She escaped Earth's orbit – Earth's gravity – metaphorically too,' says Costantini, on that pivotal moment in American history and Ride's personal life. 'Looking at the Earth from space, she started to, for the first time, really think about the imaginary lines that we have. She was struck by the fact that all these countries have known borders around them. These are human constructions. As Tam says in the film, the lines between genders, the lines between race, the lines between countries, who we're allowed to love, those are meaningless constructs.
'Space was transformative for her. When she came back to Earth, she finally allowed herself to be who she really is, and love who she really loved.'
Sally premieres on National Geographic on 16 June and is available on Hulu and Disney+ on 17 June
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These People ‘Convinced' Their Partner To Have Kids. Here's How That Worked Out For Them.
These People ‘Convinced' Their Partner To Have Kids. Here's How That Worked Out For Them.

Yahoo

time14 minutes ago

  • Yahoo

These People ‘Convinced' Their Partner To Have Kids. Here's How That Worked Out For Them.

We all know — or know of — a couple who broke up because only one of them wanted children, even if that couple is just Sofía Vergara and Joe Manganiello. Whether or not to become parents is one of the most important issues for couples to align on, and when they disagree, it can understandably be their undoing. But life is never that straightforward, and in some cases, one person in the couple can sometimes change their mind about having kids. The other may even make the case to try and 'convince' them to reconsider. This sometimes works out for them and sometimes doesn't, but it's certainly a fine line to tread. Related: 'Deciding to have children isn't something anyone should be pushed into,' Teresha Young, an international wellness and relationship coach told HuffPost. 'If a couple talks things through openly and honestly, and a partner decides of their own accord that they now want children, it can be a natural, healthy and positive shift. 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How human hibernation could revolutionize medicine and get us to Mars
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National Geographic

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Putting people into sleep mode is a sci-fi concept that's a lot closer to becoming real than you might think. Erin Belback is part of an ongoing human trial backed by NASA that aims to replicate the effects of hibernation in humans—a potential tool for overcoming some of the physiological problems of long-duration spaceflight. Scientists at the University of Pittsburgh plan to monitor her exhaled breath and body temperature to study her metabolic rate for their research. Photograph by Rebecca Hale, National Geographic Photographs by Corey Arnold The test subject had slipped into what physician Clifton Callaway describes as a 'twilight kind of sleep.' Eighteen hours after Callaway's team at the University of Pittsburgh's Applied Physiology Lab started the man on a sedative that suppressed his body's natural shivering response, his internal temperature had sunk from 98.6°F to 95°F. His heart rate and blood pressure had dropped. 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This would be an encouraging boost for the viability of extended travel through space, where radiation is as much as 200 times greater than on Earth. In fact, when it comes to achieving the dream of crew missions to Mars, says ESA's chief exploration scientist Angelique Van Ombergen, space radiation 'is a big showstopper.' Robert Foote, a volunteer in the NASA-supported trial in Pittsburgh, is monitored by scientists after being asleep for 20 hours. By achieving hibernation on demand, researchers could potentially unlock a wide range of medical benefits, including extending the time that doctors have to treat strokes and heart attacks. Photograph by Tim Betler, UPMC Scientists aren't studying hibernation just so we can ship astronauts ever deeper into space, though. Its physiological superpowers could save countless lives here on Earth, if we can unlock the secrets to the mysterious molecular-level changes that shift animals in and out of a state of hibernation, or 'torpor'—a miraculously reversible state of dormancy characterized by extreme lethargy, a lowered body temperature and metabolic rate, and a host of other remarkable changes. 'It's a well-established principle,' Callaway explains, 'that at low temperatures, like in hibernating animals, you tolerate lack of oxygen, lack of blood flow better and longer.' But why? Why don't bears' muscles atrophy while they sleep? How come their blood doesn't clot? And what triggers the process to begin with? In their hunt for answers, scientists are now inching closer to their most ambitious discovery yet: a central switch in the brains of hibernating animals that activates the various beneficial phenomena of hibernation, all at once. Mimicking the colder body temperature of bears during hibernation, for instance, could lessen the severity of 'reperfusion injuries,' the often devastating damage that occurs after cardiac arrest when blood flow is restored to the oxygen-deprived tissues of the body, setting off massive inflammation, oxidative stress, and cell death. It could also help extend the narrow window of time that doctors have to provide critical care during strokes and heart attacks. A clearer understanding of how hibernating bears preserve muscle mass and turn on and off insulin resistance could have other benefits: It might help us treat chronic obesity and diabetes in humans. ICU patients can lose more than 10 percent of their muscle mass in seven days. Could an induced state of hibernation stall or even stop the decline? Scientists are searching beyond bears for the answers because, of course, bears aren't the only animals that hibernate. A team at Colorado State University is investigating how the 13-lined ground squirrel can rapidly fatten and then switch off its appetite before hibernation for clues to combating obesity. UCLA researchers examining the genes of yellow--bellied marmots have recently found that 'epigenetic aging' is 'essentially stalled' during the seven to eight months they hibernate each year. Experts in Germany are exploring how bats maintain blood circulation at low temperatures, with an eye to human hibernation applications. And biologists at the University of Alaska Fairbanks are studying a squirrel that can drop its body temperature by 70 degrees and heart rate down to five beats per minute and survive eight months in subzero temperatures. Their goal is to develop a 'hibernation mimetic' drug that might safely allow clinicians to place humans into an immediate state of hibernation—without a long prep time, in a rural hospital lacking advanced equipment, or even in an ambulance racing through the streets. It would instantly dial down cellular metabolism, slow cell death, and catalyze a whole host of other biological processes associated with hibernation. (New bat discovery could help humans hibernate during space travel.) To decode hibernation's mysteries, biologists like Heiko Jansen are carefully studying the world's most notorious hibernators: bears. The 11 grizzlies housed at the Washington State University Bear Center are onetime 'trouble' bears from Yellowstone National Park and their offspring. Today they are sleeping for the benefit of science. The center's grizzlies are monitored in camera-equipped dens as they snooze through the late stages of their hibernation. For the five months they rest, their metabolism slows dramatically, reducing their need for food and oxygen. Callaway's twilight sleep experiment provides a glimpse into what might be possible for humans, but what happens in the lab and in the wild are clearly two different things. Bears don't need drugs to settle in for the winter—they have a natural 'torpor switch,' he says, which is flipped through some process that we don't fully understand. And though they're unruly, bears still offer a good comparison for our own potential: They're at least closer to us in size than a rodent, and, perhaps most critically, their temperature drop during deep sleep is well within the range of human survivability. One bright afternoon in late March, biologist Heiko Jansen stood outside a fenced-in pasture at the Washington State University Bear Research, Education, and Conservation Center in Pullman and watched as a shaggy 300-pound female grizzly bear named Kio struggled to eat a marshmallow. Other than a serious case of bedhead and the glacial pace of Kio's chewing, there were few visible clues that the dangerous, disheveled giant with the four-inch claws was undergoing a profound metamorphosis. Looking from the outside, little about Kio's metabolic process seems applicable to humans. Ten days earlier, she rose from her bed of straw and began to slowly work through a feast of bear kibble, apples, and elk bones and leg meat. It was her first meal in five months. Her salivary glands were still sluggish. Then she pooped out a 'fecal plug' composed of plants, dried feces, dead cells, and hair lodged in her lower intestine. Those three key activities—rise, eat, poop out the plug—seem to have helped flip a series of microscopic genetic switches inside her cells, catalyzing the slow-motion reversal of a host of bizarre biological cycles her body had entered into over the winter. Kio's metabolism, which had been operating at one-quarter its normal speed, kicked into gear, more than doubling by the time she was struggling with the marshmallow. Her core body temperature, hovering about 12 degrees below normal, began to rise. Two of her heart's four chambers, which had all but shut down for the winter, reopened for business. Her fat cells, for months miraculously resistant to insulin, the hormone that tells the body when to absorb sugar, started to respond to it again. Her appetite, absent for months, rumbled to life. When the grizzlies begin to stir, in March, they are awake but drowsy—their bodies beginning the process of reversing their metabolic slowdown. This bear, Adak, will be rewarded with honey and other treats after presenting his legs for a blood draw. Five months earlier, back in November, when Kio lay down and packed it in for the winter, she stopped eating, her gut entered 'stasis,' her saliva glands shut down, and she began living on her own body fat. Over the following months, she burned roughly 20 percent, or 70 pounds, of her body weight. To facilitate this, her body became resistant to insulin, a good thing for hibernators. Humans who become insulin resistant often develop diabetes—clearly a bad thing. Bears can switch that resistance on and off, depending on the season, without health consequences. If we could understand how, maybe we could figure out a way for humans to do it too? (Hibernating bears could hold a clue to treating diabetes.) The notion got a boost of confidence in 2018, when a Canadian group published the first complete grizzly bear DNA sequence. A year later, Jansen headed up a team that used a technique known as RNA sequencing to identify which genes are activated in bear muscle, fat, and liver tissue samples before, during, and after hibernation. They found seasonal changes in more than 10,000 of a grizzly's 30,723 genes. Now, in order to decode how bears switch insulin resistance on and off, Jansen has been extracting stem cells from blood samples collected from Pullman's bears at different times of year, methodically eliminating individual genes and then growing colonies of fat cells in petri dishes to see what happens. 'We're not saying that we'll find something that can reverse diabetes,' Jansen offers. 'But at least by looking at a model system, the cells that change their sensitivity, we can begin to develop some clues as to what's going on.' Kio's cardiac function might also yield insights that help treat human blood--clotting disorders. While Kio was hibernating, her heart rate slowed from 80 to 100 beats per minute to about 10. Normally this would cause her blood to clot into dangerous blockages and induce a stroke—'if that happened to us,' says Jansen, 'we'd be dead'—but hibernating bears also experience a remarkable drop in their blood-clotting platelets. It was Kio's ability to maintain muscle tone, however, that particularly transfixed some of her researchers. Unlike humans, who begin to lose muscle mass within a week of inactivity, Kio rose from her hibernation bed as fit as if she'd spent the winter chasing chipmunks. Up in Alaska, researchers Vadim Fedorov and Anna Goropashnaya are trying to unlock the mystery of how bears do this—and test the hypothesis that humans might be able to as well. The Russian-born husband-and-wife team specialize in evolutionary genetics at the University of Alaska's Institute of Arctic Biology (IAB), in Fairbanks. When they began analyzing gene expression patterns in tissue samples collected from captive black bears nearly 20 years ago, the results shocked them. Seeing as how bears stop eating and slow their metabolism during hibernation, Fedorov and Goropashnaya assumed the gene activity involved in building new muscles would be dialed down to preserve energy. Instead, the genes were just as active and even appeared to ramp up. 'We checked it several times,' says Goropashnaya. 'We couldn't believe it.' At the university's Institute for Arctic Biology, Anna Goropashnaya and Vadim Fedorov are investigating how muscle tissue of squirrels and bears (squirrel tissue is projected on their lab wall for this image) is preserved in hibernation when the animals don't eat and barely move. The findings were 'illogical' but somehow correct. Scores of genes known to be part of muscle protein biosynthesis were turned up in what appeared to be a coordinated—and metabolically costly—frenzy of activity. The two presented their first paper on the phenomenon in 2011. Now, with the aid of newer DNA sequencing technologies, they're able to study twice as many genes and with far more specificity, which is what led them to the mTOR pathway, a well-known cellular 'dial' that also plays a key role in controlling the rate of cell division. Typically, when mammals are starved of nutrients, their bodies dial mTOR down to suppress cell regeneration and steer energy to protect existing cells. But in the muscles of hibernating bears, the researchers confirmed what they'd first observed years earlier: mTOR increased instead. Fedorov and Goropashnaya were stumped. If hibernating bears are building new muscle, where are they getting the nutrients to make it? Researchers at the Universities of Wisconsin and Montreal have explored one possibility: microbes. Early findings in other hibernators indicate that instead of producing urine when hibernating, animals recycle the nitrogen in urea, and microbes in their guts could be ingesting and metabolizing it into amino acids, which make new muscles. If Fedorov and Goropashnaya can identify a single, extra-powerful 'upstream' gene responsible for switching on this muscle regeneration, it could have profound medical implications. The muscles of bedbound ICU patients wouldn't melt away within weeks, and astronauts could build muscles while resting. But what if all the disparate and remarkable processes of hibernation could be globally activated all at once—with a drug? To find out, scientists are looking deeper into the animal kingdom to unlock the secrets of the most extreme hibernator of all. (It's not just bears: These hibernating animals may surprise you.) The arctic ground squirrel, a diminutive rodent with gold-tinted fur, a button nose, and a tiny pair of Bugs Bunny-like front incisors, can drastically drop its body temperature and heart rate, slow to one breath per minute, and survive months in subzero conditions. The squirrels are also, for the most part, far easier to study than bears. An arctic ground squirrel remains in hibernation in a lab at the Institute of Arctic Biology at the University of Alaska Fairbanks. 'Until they open their eyes,' says Kelly Drew, the affable, silver-haired neuroscientist who directs the Center for Transformative Research in Metabolism at the IAB, after digging through a nest of cotton and wood shavings to pull out a frozen, furry snowball. 'Then they can bite.' In the early 2000s, Drew persuaded the U.S. military to fund a search for the brain chemicals that trigger hibernation in the squirrels. If she could identify those chemicals, she suggested, she could then test them on humans, in hopes of developing new ways to cool wounded soldiers on the battlefield. Drew's first breakthrough with the squirrels arrived in 2005 when an undergraduate research assistant chanced upon a paper from a Japanese lab while combing through scientific literature. The Japanese group had actually achieved the opposite of what Drew hoped to do. They'd found a drug that woke hibernating hamsters by blocking their brain cells' response to a specific chemical called adenosine. Drew assigned a graduate student to inject a synthetic version of adenosine, a drug called 6-Cyclohexyladenosine, or CHA, directly into the brains of her squirrels. Rather than blocking adenosine, which is how the caffeine in your coffee works its magic, CHA replicates its effects. When the graduate student dosed a squirrel's brain in the summer, outside of hibernation season, nothing happened. But when he repeated it closer to hibernation season, the CHA put the animal into such a deep state of torpor, the student initially thought he had killed it. 'He was super sad because that's a big deal,' Drew recalls. 'He takes the animal out for the vet to do the necropsy. The vet gets the tools out, he's going to start cutting open this dead animal, and it starts to move.' Her lab had done it. They'd found a way to put a squirrel in hibernation mode, like flipping a switch. Temporarily removed from its refrigerated hibernation den and settled on a bed of wood shavings, this arctic ground squirrel remained in a state of torpor for over an hour before beginning to stir. The squirrels survive their long hibernation by warming up for short periods every few weeks. On the opposite side of the world, at the University of Bologna in Italy, around the same time Drew's grad student stumbled on that Japanese paper about adenosine, another grad student named Domenico Tupone was charting a similar path. The focus of his laboratory research wasn't hibernation per se but a component of it: identifying the brain circuits that regulate body temperature during sleep. His team suspected that a small patch of neurons at the base of an ordinary rat's brain helped convey temperature-control signals to the periphery of the body. They temporarily immobilized those neurons with an injection, then placed the rat in a cold, dark cage. The experiment validated their hypothesis. As Tupone and his colleagues watched, the rat sank into a state of hypothermia so extreme it should have proved fatal. That's when things got weird. Six hours and four injections later, the hypothermic rat was still alive. And when the team finally removed it from its cage and warmed it up, the rat behaved, at least outwardly, as if nothing had happened. Afterward, as Tupone and his colleagues examined the brain waves picked up by a web of electrodes attached to the rodent's skull, scientist Matteo Cerri made an observation that altered the course of Tupone's future research. The peaks and valleys of the brain waves looked familiar. Cerri had seen the same patterns in hibernating animals. But there was one crucial difference. Unlike arctic ground squirrels, rats do not naturally hibernate. Tupone had to know: If a non-hibernating animal could be safely induced into hibernation, then maybe humans could do it too? In the years that followed, Tupone obsessed over scraps of paper in dimly lit bars, sketching out what a brain circuit capable of triggering hibernation in humans might look like. In bed, he tossed and turned, fantasizing about a 'revolutionary' IV-administered drug akin to Drew's 'hibernation mimetic' that paramedics could use to slow cell death on the way to the hospital. He became convinced that if it could be accomplished safely, inducing natural torpor in humans would upend basic science. The next step for both researchers, though—human trials—presented their stiffest obstacle yet. In order to administer Drew's 'hibernation mimetic' to ground squirrels, her team often had to perform invasive brain surgeries. For humans, the drug would need to be delivered via IV. The trouble is, adenosine receptors are present throughout the body, and activating them globally can trigger unwanted side effects, including cardiac arrest. After four more years of frustrating trial and error, Drew paired the drug with a compound that fixed the heart attack problem, and she's currently trying to solve the additional obstacle of fluctuating blood glucose levels, which in extreme cases can cause seizures in lab animals and even death. 'It works; it definitely cools them,' Drew says. 'We're just trying to tweak it so it's as safe as possible.' Clinicians have lots of devices to regulate temperature, 'but the human body typically fights it. By avoiding that cold defense response, which is what our hibernation mimetic does, then the clinician has the ability to dial in whatever temperature they want.' In minutes, not hours. Tupone, meanwhile, was working on parallel tracks at Portland's Oregon Health & Science University under Shaun Morrison, one of the world's experts on the brain circuits that control body temperature. Tupone's primary focus was on extending the map of temperature--related circuits into new parts of the brain, but in his spare time, he continued to hunt for the elusive hibernation switch. Around 2016, he stumbled upon a curious biological phenomenon that convinced him he was getting close. He and Morrison were attempting to confirm their map of the brain's thermoregulatory control system, in an experiment similar to the one in which the unexpected survival of those hypothermic Italian rats had blown his mind. This time, Tupone used a small knife to sever the bundle of nerves running to the rat's brain stem, cutting off the pathway that relays temperature--control signals down to the body's periphery. Once again, though, Tupone's results seemed to flip the expected rule of mammalian physiology. Rather than disabling the ability of the rat to respond to heat or cold, Tupone's incision somehow enhanced it. When Tupone wrapped the rat in a plastic blanket and ran hot water over it, its body began generating even more heat. When he used freezing cold water, the rat's brain seemed to allow its body temperature to fall even faster. An arctic ground squirrel emerges from a burrow in the foothills of Alaska's Brooks Range shortly after its eight-month hibernation. Each fall, Colorado State University scientists working at the nearby Toolik Field Station collar squirrels with devices to track body temperature data and light, which tells them if a squirrel is in or out of its burrow. In the spring, new squirrels are ear-tagged and weighed before their summer of foraging begins. The long-term study is revealing how climate change is affecting the biology of these important hibernators. Tupone and Morrison quickly concluded they had discovered something profound. The results suggested that a second, previously undiscovered brain circuit capable of modulating body temperature existed—one that facilitated the transition in and out of hibernation. They named the phenomenon 'thermoregulatory inversion' (TI). But where exactly was this circuit, and how could it be activated? After eight years of trial and error, Tupone and Morrison published a paper this past January announcing they'd found a small patch of neurons in the rat's hypothalamus—the ventromedial periventricular area (VMPeA)—that, when activated, not only seems to slow metabolism, lower body temperature, and induce brain waves and cardiac patterns unique to hibernation but also sets in motion phenomena that flip the body's normal temperature-control system on its head, facilitating the transition into and out of the torpor state. They'd found it: the elusive 'torpor switch.' Tupone believes the switch is connected to an incomplete version of the hibernation circuitry that still exists in many animals. To disable it, he hypothesizes, evolution did the most efficient thing. It simply removed the connection between the circuitry and the switch that would flip it on automatically. 'It is like you have all the cables inside your walls to turn on a light,' he says, but you've removed the connection to the switch that controls that light. 'We think humans have all the circuitry.' Our switch, he believes, just isn't connected anymore. To back up his findings, Tupone is now collaborating with Kelly Drew's lab to find the analogous circuitry—and the switch—in arctic ground squirrels. And he's laying the groundwork for a drug of his own that can flip the switch in his rats without invasive brain surgery. Each advance, though, generates more mysteries. To flip their switch on and off in the study they published in January, Tupone and Morrison had to use invasive brain surgery and manually apply a drug to the general area where it was located. Even that infinitesimally small patch of the brain still contained millions of neurons, including an entire neighborhood of unrelated neurons surrounding it. To find a drug specific enough to give to humans without immense side effects, Tupone will need to identify the precise neurons around the switch and design a drug that will target only those involved in hibernation. That's just the tip of the iceberg, though. To suppress the shivering response in humans, anesthesiologists typically administer muscle relaxants or paralyzing drugs, which suppress breathing, so doctors have to intubate patients … which requires putting them into a medically induced coma. This is why induced hypothermia is not available outside hospitals. It's also not currently an option for stroke patients, because of the dangerous drop in blood pressure that often occurs during the gap between administering anesthesia and intubating a patient, which can deprive the brain of even more oxygen at a moment when dangerous blockages are already suffocating its cells. Rats don't hibernate. But what if they could? Neurologist Domenico Tupone and fellow researchers from the University of Oregon say they've identified a 'torpor switch' in rat brain neurons (projected on the wall) that can be activated to send the rodents into a deep state of hibernation. Identifying this circuitry in non-hibernators could be a breakthrough in the human hibernation effort. 'It can actually worsen a stroke,' says researcher Cal-laway, from the University of Pittsburgh. 'But boy, it sure would be nice to lower your body temperature and let your brain tolerate the stroke longer until I can get you to the cath lab and take that blood clot out.' As an emergency physician, Callaway understands better than most the potential applications for humans, as well as the challenges presented by making the leap from bears and squirrels to humans. He's been researching and refining the techniques used to induce hypothermia in cardiac and brain-injured patients since the 1990s, and he's also a former chair of the American Heart Association's Emergency Cardiovascular Care Committee, which is why NASA awarded him a grant through the Translational Research Institute for Space Health to explore whether his techniques can be applied to the metabolic needs of astronauts. So far, there are problems. The drop in blood pressure and heart rate in his five healthy volunteers was so extreme that those with cardiovascular or other medical conditions might not be able to tolerate it. And within days, all five of the 'pretend astronauts' had developed a tolerance to his sedative, suggesting, among other things, that its effectiveness would fade over time. Those are solvable problems, Callaway says. 'This is just the first step' in a process that he believes will take 10 to 15 years—a mere nap for Rip Van Winkle. 'There's a lot of science to be done,' he says. But he's excited by the progress: 'I don't think it's pie-in-the-sky anymore.' To keep the pretend astronauts inspired during the human trial, Callaway's team had plastered the walls of their lab with posters: a satellite floating in space above the swirling blues and whites of Earth; the cratered, gleaming surface of a moonlike planet; the rainbow-hued burst of starlight, radiating from a distant galaxy. For now, such destinations are accessible only in our dreams. But someday in the not too distant future, a real astronaut might awaken from a hibernation-like slumber to gaze on the real thing.

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