- Senior Russian official Pyotr Kucherenko mysteriously dies after decrying ‘fascist invasion’ of Ukraine New York Post
- Death of Russian minister on return from Cuba is latest unexplained incident involving Moscow’s elites CNN
- Russian Deputy Minister Dies Suddenly After Slamming ‘Fascist Invasion’ of Ukraine The Daily Beast
- Mystery As Russian Official Dies Mid-Flight After Becoming Seriously Ill Newsweek
- Senior Russian Official Dies After Privately Bemoaning ‘Fascist’ Invasion The Moscow Times
- View Full Coverage on Google News
Tag Archives: mysteriously
This mutant Venus flytrap mysteriously lost its ability to “count” to 5
Comparing stimulation of a Venus flytrap and the mutant DYSC. Credit: Ines Kreuzer, Rainer Hedrich, Soenke Scherzer
In 2011, a horticulturist named Mathias Maier stumbled across an unusual mutant of a Venus flytrap, a carnivorous plant that traps and feeds on insects. Scientists recently discovered that the typical Venus flytrap can actually “count” to five, sparking further research on how the plant manages this remarkable feat. The mutant flytrap might hold the key. According to a new paper published in the journal Current Biology, this mutant flytrap doesn’t snap closed in response to stimulation like typical Venus flytraps.
“This mutant has obviously forgotten how to count, which is why I named it Dyscalculia (DYSC),” said co-author Rainer Hedrich, a biophysicist at Julius-Maximilians-Universität Würzburg (JMU) in Bavaria, Germany. (It had previously been called “ERROR.”)
As we’ve reported previously, the Venus flytrap attracts its prey with a pleasing fruity scent. When an insect lands on a leaf, it stimulates the highly sensitive trigger hairs that line the leaf. When the pressure becomes strong enough to bend those hairs, the plant will snap its leaves shut and trap the insect inside. Long cilia grab and hold the insect in place, much like fingers, as the plant begins to secrete digestive juices. The insect is digested slowly over five to 12 days, after which the trap reopens, releasing the dried-out husk of the insect into the wind.
In 2016, Hedrich led the team of German scientists who discovered that the Venus flytrap could actually “count” the number of times something touches its hair-lined leaves—an ability that helps the plant distinguish between the presence of prey and a small nut or stone, or even a dead insect. The scientists zapped the leaves of test plants with mechano-electric pulses of different intensities and measured the responses. It turns out that the plant detects that first “action potential” but doesn’t snap shut right away, waiting until a second zap confirms the presence of actual prey, at which point the trap closes.
But the Venus flytrap doesn’t close all the way and produces digestive enzymes to consume the prey until the hairs are triggered three more times (for a total of five stimuli). The German scientists likened this behavior to performing a rudimentary cost-to-benefit analysis, in which the triggering stimuli help the Venus flytrap determine the size and nutritional content of any potential prey struggling in its maw and whether it’s worth the effort. If not, the trap will release whatever has been caught within 12 hours or so.
In 2020, Japanese scientists genetically altered a Venus flytrap so that it glows green in response to outside stimulation, yielding important clues about how the plant’s short-term “memory” works. They introduced a gene for a calcium sensor protein called GCaMP6, which glows green whenever it binds to calcium. That green fluorescence allowed the team to visually track the changes in calcium concentrations in response to stimulating the plant’s sensitive hairs with a needle.
Enlarge / Stimulation of the Venus flytrap by touch triggers electrical signals and calcium waves. The calcium signature is decoded; this causes the trap to shut quickly. But the DYSC mutant has lost the ability to read and decode the calcium signature correctly.
Ines Kreuzer / University of Wuerzburg
The results supported the hypothesis that the first stimulus triggers the release of calcium, but the concentration doesn’t reach the critical threshold that signals the trap to close without a second influx of calcium from a second stimulus. That second stimulus has to occur within 30 seconds, however, since the calcium concentrations decrease over time. If it takes longer than 30 seconds between the first and second stimuli, the trap won’t close. So the waxing and waning of calcium concentrations in the leaf cells really do seem to serve as a kind of short-term memory for the Venus flytrap, though precisely how calcium concentrations work with the plant’s electrical network remains unclear.
That doesn’t seem to be the case with DYSC, even though it is otherwise “essentially indistinguishable” from Venus flytraps in the wild. DYSC does not close in response to two sensory stimuli, nor does it process its prey in response to additional stimuli. Naturally, Hedrich et al. wanted to find out why. They purchased wild Venus flytraps and the mutant DYSC flytraps and performed parallel experiments: both mechanically stimulating the plants and measuring the action potentials, and spraying the plants with a contact hormone called jasmonic acid, which is crucial for the processing of prey.
Hedrich and his team found that the mutation did not seem to affect either the action potential or the underlying calcium signal in the first two-count stage of the process. The action potentials fire, yet the trap doesn’t snap shut, suggesting that the touch-activation of calcium signaling is being suppressed. Furthermore, the scientists suspected a defect that affected the decoding of the calcium signal. Administering jasmonic acid didn’t fix the problem with the failure of the rapid trap closure, but it did restore the ability to process prey.
Co-author Ines Kreuzer next examined gene expression patterns in the mutant genes to spot any changes that might account for this. She was able to narrow the likely suspects down to a few decoding components, which bind to calcium and subsequently modify certain effector proteins—most notably an enzyme called LOX3, which plays a vital role in the biosynthesis of jasmonic acid. The next step is to look more closely at the modified proteins and change their activity when prey comes into contact with DYSC. “In this way, we want to close the circle and find out what the plant does to distinguish numbers from each other—i.e., how it counts,” said Hedrich.
DOI: Current Biology, 2023. 10.1016/j.cub.2022.12.058 (About DOIs).
Listing image by Naturfoto Honal | Getty
The Color of Wolves Mysteriously Changes Across America. We Finally Know Why : ScienceAlert
Guessing the color of the coat of a gray wolf seems like a no-brainer. But the canines, whose habitats are spread across North America and Eurasia, aren’t always actually gray.
On the North American continent, specifically, the farther south you go, the more wolves there are with dark, black-hued coats. The phenomenon was unexplained for a long time, but now scientists have determined that the culprit is one of the biggest drivers of natural selection: disease.
An international team led by ecologist Sarah Cubaynes of the University of Montpellier in France has determined that the often fatal canine distemper virus is the trigger that produces a higher number of black-coated wolves (Canis lupus).
“In most parts of the world black wolves are absent or very rare, yet in North America, they are common in some areas and absent in others,” explains biologist Tim Coulson of the University of Oxford.
“Scientists have long wondered why. We now have an explanation based on wolf surveys across North America, and modeling motivated by extraordinary data collected by co-authors who work in Yellowstone.”
Evolutionary pressure can result in some peculiar consequences, especially when it comes to disease. Some individuals can be more likely to survive based on the presence of genes that confer resistance to that disease. The survivors then produce offspring with those genetic variations, and the genetic profile of a population can change over time.
The genetic configurations that confer resistance, however, don’t always have just one function. As we recently learned, genetic variants that conferred resistance against the Black Plague also increase susceptibility to autoimmune disorders such as rheumatoid arthritis, meaning we are still feeling its effects centuries later.
In the case of these wolves, coat color is determined by a gene called CPD103, which historically made their coats gray. However, a CPD103 mutation emerged in dogs and crossed over to wolves, producing a black coat.
Each wolf has two copies of CPD103, one inherited from each parent. Unlike red hair in humans, though, it takes just one copy of the black coat gene to produce a black coat.
Scientists suspected that the canine distemper virus may play a role in the numbers of black-coated wolves across North America since the DNA region in which CPD103 resides is also involved in encoding a protein that protects against lung infections like canine distemper.
This would mean that if wolves with black coats are more likely to survive the disease, they’ll reproduce and pass their CPD103 variant on to their cubs.
So, the team set about testing this hypothesis. Researchers analyzed 12 wolf populations across North America to see if the presence of canine distemper antibodies – a sign of having had, and surviving, the virus – was strongly correlated with black-coated wolves.
They found that wolves with the antibodies were, indeed, more likely to have black coats – especially in older wolves. Black wolves were also more common in areas in which outbreaks had occurred.
Next, the team studied 20 years’ worth of wolf population data from Yellowstone National Park, where wolves were reintroduced in the 1990s.
There, the population consists of 55 percent gray wolves and 45 percent black wolves. Of those black wolves, just 5 percent had two copies of the black-coat CPD103 variant. This suggests that wolves choosing mates of the opposite color have a better chance of reproductive success, and their offspring surviving canine distemper.
However, it only works in regions that have experienced canine distemper outbreaks. According to the team’s mathematical modeling, the competitive advantage of choosing an opposite color mate disappears if canine distemper isn’t a problem.
The research not only gives a fascinating reason for the greater prevalence of black wolves in some areas, but it also offers a tool for studying historic canine distemper outbreaks, as well as disease resistance.
The team notes that their results are likely to apply to a broad range of species. In a broad range of insects, mammals, amphibians, reptiles, and birds, color variation can be associated with disease resistance; this coloration may act as a signal to help animals choose mates that will give their offspring a survival advantage.
“When coloration is genetically determined and disease resistance is heritable and associated with coloration, a preference for a mate of a specific color will enhance fitness by maximizing the chances of producing resistant offspring in environments with frequent and virulent enough pathogens,” the researchers write in their paper.
“It is possible that we have significantly underestimated the role of pathogens in generating the diversity of morphological and behavioral traits observed in nature.”
Isn’t that an intriguing notion?
The research has been published in Science.
This mysteriously deleted video suggests the Metal Gear Solid 3 remake may be announced at The Game Awards
Update 7.41pm: After discovering the footage used in the mysterious video has been taken from an Unreal Engine 5 assets pack, it now appears that the video is a hoax.
Whilst it’s unclear where the story originated – or why – for now, it’s best to presume this isn’t true until Konami, Virtuos, or TGA confirm otherwise. Original story follows.
I’ve just found that the video comes from here tho’
A free UE5 assets pack.
This doesn’t confirms or denies anything ofc, but it’s weird they used this instead of some actual work of their own.https://t.co/lfiUz2FWmV— GGFTL (@GGFTL1) October 30, 2022
Original story: It looks like the long-rumoured Metal Gear Solid 3: Snake Eater remake may be announced at the upcoming The Game Awards.
The news comes via a now-deleted video that reportedly popped up on Chinese studio Virtuos’ YouTube channel earlier today.
You can never delete something quicker than someone can save a copy of it, though; Virtuos’ video – regardless of whether it had been published intentionally or otherwise – is now doing the rounds, and has Metal Gear fans speculating that the remake may soon be formally confirmed.
It looks as though the teaser – which seems to be getting scrubbed as quickly as it’s being reuploaded – includes Morse code for the phrase “December 8, 1964”. 8th December is when the awards are set to be broadcast, whilst 1964 is the year in which Snake Eater is set (thanks, MP1st).
Seems Virtuous’ Metal Gear Solid 3 Remake may be getting announced at the Game Awards. First preview of it. Virtuous themselves uploaded this teaser, but then deleted it, but people saved it. The Morse Code spells out December 8th, IE the Game Awards. https://t.co/pHYjNvyt48
— AestheticGamer aka Dusk Golem (@AestheticGamer1) October 30, 2022
More interestingly still, this strange video kerfuffle coincides with the recent release of a recruitment video in which Virtuos shares “a day in the life of Virtuos Montreal”. Within the video, an artist can be seen with The Art of Metal Gear Solid coyly on display on the side.
This all comes a year after a remake of Metal Gear Solid 3 was first reported to be in the works, with Konami reportedly handing development to Virtuos Studios.
ICYMI, actor Oscar Isaac has revealed that he’s still “hopeful” that the long-awaited Metal Gear Solid movie will happen.
In a recent interview about his upcoming graphic novel, Isaac was asked for an update about the movie, and kindly obliged, albeit without offering any firm information about the film’s progress.
“We want it to happen,” said Isaac. “Be excited. What’s the script? What’s the story? What’s the take? […] But hopeful that comes to fruition because there’s so much potential for that.
“It’s an incredible game. It’s my favourite,” he confirmed.
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California Quakes Mysteriously Preceded by Shifts in Earth’s Magnetic Field : ScienceAlert
When the next big earthquake strikes somewhere around the world, it will arrive without warning, destroying infrastructure and putting lives at risk.
Yet for days leading up to the event, titanic geological forces will already be at work, warping the crust in subtle ways that could, in theory, predict the coming catastrophe.
One possible sign could involve flickers in the magnetic field that ebbs and flows around our planet. For decades, researchers have debated the merits of hunting for magnetic signatures to imminent tremors, for want of convincing evidence.
A new case-controlled study by QuakeFinder, a humanitarian research project within systems engineering services company Stellar Solutions, in collaboration with the Google Accelerated Science team, concludes there just might be a good reason to continue the search.
Applying machine learning to ground-based measurements of local magnetic changes in the lead-up to a number of significant earthquakes across California between 2005 and 2019, the researchers found signs of a pattern that demands further study.
This isn’t to say the effect they observed could necessarily be used to predict earthquakes, but it’s nonetheless a fascinating lead for future study.
“We are not claiming that this signal exists before every earthquake,” QuakeFinder director Dan Schneider told Joshua Rapp Learn at Eos.
Yet the findings could be enough to keep the controversial topic of electromagnetic forecasts of major tremors alive for a little longer.
Premises behind hypothetical fluctuations in the magnetic field prior to earthquakes sound reasonable enough. Some argue the massive build-up of pressure in the crust prior to a quake could, in theory, change the properties of the rock layers enough to influence their conductivity.
Other studies hint at pockets of trapped gas building up prior to release creating the necessary electrical currents to affect magnetic activity.
Spotting the resulting ultra-low frequency shifts in the magnetic field would give authorities warning that something big is going to pop, providing time to prepare in the same way communities might do for a growing hurricane.
Unfortunately, what sounds like a promising idea runs into a number of obstacles in application.
For one thing, plenty of things can create low-frequency wobbles in local patches of a magnetic field. Even increases in nearby traffic or small shifts in solar activity can introduce a buzz that might be mistaken for a geological disturbance.
Unweaving a reliable signal from this noise requires having accurate measuring equipment at fixed locations near sizable tremors. Even where that occurs, enough quakes of the right size need to be recorded for a statistical sample.
With research sites located near faults all over the state of California, Quakefinder is in a solid position to overcome these hurdles.
Magnetometers buried at the different research sites provided the researchers with a sizable amount of data on quakes greater than magnitude 4.5.
After selecting quakes for which there were measurements from two close sites, and excluding pairs of sites without suitable recordings, the researchers were left with measurements on 19 earthquakes.
This sample was then divided into two groups, one serving as the basis of a machine-learning study that attempted to sift out potential patterns from known influences, with the second group serving as a test for any possible discoveries.
The signal-to-noise ratio identified by the process and confirmed in the test run wasn’t exactly strong. As the researchers admit in their published report, obvious electromagnetic anomalies prior to quakes “would have been observed, documented, and accepted much earlier” in previous investigations.
But they do suggest something intriguing is lurking in the electromagnetic shimmer like a suspicious cry in the rainstorm, one that could be present up to three days before an earthquake hits. Fine-tuning of the researchers’ method using a larger sample might be able to identify what’s going on.
Should future studies land upon a reliable hum of impending doom in the magnetic field of one area, it might still not be a universal tune, demanding even further testing at multiple sites around the globe.
For now, the idea of using tiny changes in the planet’s magnetic field to forecast tremors remains controversial. But buoyed by results like these, further investigations might finally uncover the secret whispers of a fault at breaking point.
This research was published in the Journal of Geophysical Research: Solid Earth.
Earth’s Days Are Mysteriously Getting Longer, Scientists Say
Atomic clocks, combined with precise astronomical measurements, have revealed that the length of a day is suddenly getting longer, and scientists don’t know why.
This has critical impacts not just on our timekeeping, but also things like GPS and other technologies that govern our modern life.
Over the past few decades, Earth’s rotation around its axis – which determines how long a day is – has been speeding up. This trend has been making our days shorter; in fact, in June 2022 we set a record for the shortest day over the past half a century or so.
But despite this record, since 2020 that steady speedup has curiously switched to a slowdown – days are getting longer again, and the reason is so far a mystery.
While the clocks in our phones indicate there are exactly 24 hours in a day, the actual time it takes for Earth to complete a single rotation varies ever so slightly. These changes occur over periods of millions of years to almost instantly – even earthquakes and storm events can play a role.
It turns out a day is very rarely exactly the magic number of 86,400 seconds.
The ever-changing planet
Over millions of years, Earth’s rotation has been slowing down due to friction effects associated with the tides driven by the Moon. That process adds about about 2.3 milliseconds to the length of each day every century. A few billion years ago an Earth day was only about 19 hours.
For the past 20,000 years, another process has been working in the opposite direction, speeding up Earth’s rotation. When the last ice age ended, melting polar ice sheets reduced surface pressure, and Earth’s mantle started steadily moving toward the poles.
Just as a ballet dancer spins faster as they bring their arms toward their body – the axis around which they spin – so our planet’s spin rate increases when this mass of mantle moves closer to Earth’s axis. And this process shortens each day by about 0.6 milliseconds each century.
Over decades and longer, the connection between Earth’s interior and surface comes into play too. Major earthquakes can change the length of day, although normally by small amounts.
For example, the Great Tōhoku Earthquake of 2011 in Japan, with a magnitude of 8.9, is believed to have sped up Earth’s rotation by a relatively tiny 1.8 microseconds.
Apart from these large-scale changes, over shorter periods weather and climate also have important impacts on Earth’s rotation, causing variations in both directions.
The fortnightly and monthly tidal cycles move mass around the planet, causing changes in the length of day by up to a millisecond in either direction. We can see tidal variations in length-of-day records over periods as long as 18.6 years.
The movement of our atmosphere has a particularly strong effect, and ocean currents also play a role. Seasonal snow cover and rainfall, or groundwater extraction, alter things further.
Why is Earth suddenly slowing down?
Since the 1960s, when operators of radio telescopes around the planet started to devise techniques to simultaneously observe cosmic objects like quasars, we have had very precise estimates of Earth’s rate of rotation.
A comparison between these estimates and an atomic clock has revealed a seemingly ever-shortening length of day over the past few years.
But there’s a surprising reveal once we take away the rotation speed fluctuations we know happen due to the tides and seasonal effects. Despite Earth reaching its shortest day on 29 June 2022, the long-term trajectory seems to have shifted from shortening to lengthening since 2020. This change is unprecedented over the past 50 years.
The reason for this change is not clear. It could be due to changes in weather systems, with back-to-back La Niña events, although these have occurred before. It could be increased melting of the ice sheets, although those have not deviated hugely from their steady rate of melt in recent years.
Could it be related to the huge volcano explosion in Tonga injecting huge amounts of water into the atmosphere? Probably not, given that occurred in January 2022.
Scientists have speculated this recent, mysterious change in the planet’s rotational speed is related to a phenomenon called the “Chandler wobble” – a small deviation in Earth’s rotation axis with a period of about 430 days.
Observations from radio telescopes also show that the wobble has diminished in recent years; the two may be linked.
One final possibility, which we think is plausible, is that nothing specific has changed inside or around Earth. It could just be long-term tidal effects working in parallel with other periodic processes to produce a temporary change in Earth’s rotation rate.
Do we need a ‘negative leap second’?
Precisely understanding Earth’s rotation rate is crucial for a host of applications – navigation systems such as GPS wouldn’t work without it. Also, every few years timekeepers insert leap seconds into our official timescales to make sure they don’t drift out of sync with our planet.
If Earth were to shift to even longer days, we may need to incorporate a “negative leap second” – this would be unprecedented, and may break the internet.
The need for negative leap seconds is regarded as unlikely right now. For now, we can welcome the news that – at least for a while – we all have a few extra milliseconds each day.
Matt King, Director of the ARC Australian Centre for Excellence in Antarctic Science, University of Tasmania and Christopher Watson, Senior Lecturer, School of Geography, Planning, and Spatial Sciences, University of Tasmania.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Earth’s Days Have Been Mysteriously Increasing in Length – Scientists Don’t Know Why
Precise measurements show that Earth’s rotation has been mysteriously slowing down since 2020, making the day longer.
Precise astronomical observations, combined with atomic clocks, have revealed that the length of a day is suddenly getting longer. Scientists don’t know why.
This has critical impacts not just on our timekeeping, but also on things like GPS and other precision technologies that govern our modern life.
Earth’s rotation around its axis has been speeding up over the past few decades. Since this determines how long a day is, this trend has been making our days shorter. In fact, in June 2022 we set a record for the shortest day over the past half a century or so.
However, despite this record, since 2020 that steady speedup has curiously switched to a slowdown. Now, days are getting longer again, and the reason so far remains a mystery.
While the clocks in our phones indicate there are exactly 24 hours in a day, the actual time it takes for Earth to complete a single rotation can vary ever so slightly. These changes sometimes occur over periods of millions of years, and other times almost instantly. For example, even earthquakes and storm events can play a role.
It turns out that a day is very rarely exactly the magic number of 86,400 seconds.
The ever-changing planet
Earth’s rotation has been slowing down over millions of years due to friction effects associated with the tides driven by the Moon. That process adds about 2.3 milliseconds to the length of each day every 100 years. A few billion years ago, an Earth day was only about 19 hours.
For the past 20,000 years, another process has been working in the opposite direction, speeding up Earth’s rotation. When the last ice age ended, melting polar ice sheets reduced surface pressure, and Earth’s mantle started steadily moving toward the poles.
Just as a ballet dancer spins faster as they bring their arms toward their body – the axis around which they spin – our planet’s spin rate increases when this mass of mantle moves closer to Earth’s axis. This process has been shortening each day by about 0.6 milliseconds each century.
Over decades and longer, the connection between Earth’s interior and surface comes into play too. Major earthquakes can change the length of day, although normally by small amounts. For example, the Great Tōhoku Earthquake of 2011 in Japan, with a magnitude of 8.9, is believed to have sped up Earth’s rotation by a relatively tiny 1.8 microseconds.
Apart from these large-scale changes, over shorter periods weather and climate also have important impacts on Earth’s rotation, causing variations in both directions.
The fortnightly and monthly tidal cycles move mass around the planet, causing changes in the length of day by up to a millisecond in either direction. We can see tidal variations in length-of-day records over periods as long as 18.6 years. The movement of our atmosphere has a particularly strong effect, and ocean currents also play a role. Seasonal snow cover and rainfall, or groundwater extraction, alter things further.
Why is Earth suddenly slowing down?
Since the 1960s, when operators of radio telescopes around the planet started to devise techniques to simultaneously observe cosmic objects like quasars, we have had very precise estimates of Earth’s rate of rotation.
Using radio telescopes to measure Earth’s rotation involves observations of radio sources like quasars. Credit:
Scientists have speculated this recent, mysterious change in the planet’s rotational speed is related to a phenomenon called the “Chandler wobble” – a small deviation in Earth’s rotation axis with a period of about 430 days. Observations from radio telescopes also show that the wobble has diminished in recent years. Perhaps the two are linked.
One final possibility, which we think is plausible, is that nothing specific has changed inside or around Earth. It could just be long-term tidal effects working in parallel with other periodic processes to produce a temporary change in Earth’s rotation rate.
Do we need a ‘negative leap second’?
Precisely understanding Earth’s rotation rate is crucial for a host of applications – navigation systems such as GPS wouldn’t work without it. Also, every few years timekeepers insert leap seconds into our official timescales to make sure they don’t drift out of sync with our planet.
If Earth were to shift to even longer days, we may need to incorporate a “negative leap second” – this would be unprecedented, and may break the internet.
The need for negative leap seconds is regarded as unlikely right now. For now, we can welcome the news that – at least for a while – we all have a few extra milliseconds each day.
Written by:
- Matt King – Director of the ARC Australian Centre for Excellence in Antarctic Science, University of Tasmania
- Christopher Watson – Senior Lecturer, School of Geography, Planning, and Spatial Sciences, University of Tasmania
This article was first published in The Conversation.
Her Lungs Mysteriously Shut Down. How Could This Have Happened?
The 21-year-old woman gasped as she read the headline: “The 16-Year-Old Girl Who Walks and Eats Tacos While on Life Support.” She scanned the article about a girl who had a mysterious illness that destroyed her lungs and who now needed a machine to breathe for her. “I need to do something,” she told herself once she finished the article. She believed she knew what was killing this young girl, because the story could have been her own, six years earlier.
Back then, she was a high school junior on the starting lineup of the girls’ volleyball team. Just days into the new school year, she developed a 103-degree fever and sore throat. Her doctor, in tiny Thief River Falls, Minn., figured she had some type of viral infection and predicted she would feel better after a few days of rest. He was wrong. The fever resolved but was replaced with the most profound fatigue the girl had ever known. Just getting out of bed left her breathless. Her mother took her to the nearest emergency room, 25 miles away.
As the nurse checked the young woman’s vital signs, she looked alarmed. The patient’s oxygen saturation, which would normally be well over 90 percent, was in the 60s, dangerously low. The nurse slapped an oxygen mask over her nose and mouth and reached out to the doctor in charge. A chest X-ray showed a gray cloud invading her lungs. Minutes later she was in an ambulance headed for the Sanford Medical Center in Fargo, N.D., the closest hospital with a pediatric intensive-care unit.
In Fargo she was started on several broad-spectrum antibiotics. The doctors there didn’t know which bug was causing this pneumonia, but until they did, they figured these antibiotics should protect her. But she continued to worsen, and within days needed to be put on a ventilator.
When even that wasn’t enough, the doctors at Sanford contacted the Mayo Clinic in Rochester, Minn. Eight days after she walked into the E.R., the patient’s lungs were hardly working at all. The next step was an artificial-heart-and-lung machine known familiarly as ECMO — short for extracorporeal membrane oxygenation. This device, about the size of a refrigerator, acts as a lung to remove the carbon-dioxide waste product from the blood and replace it with oxygen and then as a heart to recirculate the oxygenated blood back through the body. The ECMO team from the Mayo Clinic flew out to Fargo with their machine, attached the young woman to the device and flew back with her to the Mayo Clinic Hospital. That machine breathed for her for the next 116 days.
Months on the Transplant List
Like the girl in the article, she, too, had walked while connected to the massive machine. She, too, had eaten while on the machine, though not tacos. The first thing to pass her lips was a communion wafer when she finally felt well enough to walk at least part of the way to the hospital chapel surrounded by a squad of doctors, nurses and technicians. They never figured out why her lungs failed. She spent months on the transplant list, waiting for a new heart and lungs to replace the ones her doctors thought would never recover. But they did. And finally, after seven months in the hospital, she was able to go home.
For a few years afterward she returned to Mayo every six months for a checkup. During those visits, she always stopped by the pediatric intensive-care unit to see the nurses who had become a second family to her in the months she hovered near death. At one visit, two years after her own time in the hospital, several nurses told her about a child whose illness seemed remarkably like her own.
Hours later she and her parents met with this child’s parents, who told the story of their daughter, just 12 years old, whose lungs had simply stopped working after what looked like a viral illness. The families compared notes to see if there were any similarities between the two children’s lives and exposures. They lived in different environments — one rural, one urban — in different parts of the state. Nothing seemed to match, until finally the child’s parents reported that in the weeks before coming to the hospital, their daughter had been taking an antibiotic: trimethoprim-sulfamethoxazole (TMP-SMX), known under the brand name Bactrim. The young woman gasped. She had been taking this antibiotic (in her case to treat acne) — right up to the day she went to the E.R.
Since then, another family contacted her with a familiar story: A healthy, active adolescent gets desperately sick, with lungs so damaged that he needed life support. She asked these parents if their son was taking TMP-SMX when he got sick. Yes, came the amazed reply. That made a total of three cases. Maybe she had found a real connection.
And now there was this young woman in the news. Her name was Zei Uwadia. The article named Dr. Jenna Miller as the pediatric I.C.U. specialist at Children’s Mercy Hospital in Kansas City, Mo., who was taking care of Uwadia. The young woman found an email address for the doctor and immediately sent her a note. “I began taking Bactrim for acne about 3-4 weeks prior to [my] acute lung failure,” she wrote. “This happened to at least 3 children between 12-20 years [old]. … The similarities between our cases are uncanny.” She asked if Uwadia had been taking TMP-SMX too.
The Same Unusual Pattern
Miller was astonished. Indeed, the girl was taking TMP-SMX when she got sick. Could there be a link? Miller reached out to a friend, Dr. Jennifer Goldman, who was a pediatrician trained in infectious disease and clinical pharmacology. She had been doing research on adverse reactions to this drug for years. TMP-SMX is an effective, safe and inexpensive drug and, because of that, is the sixth-most-prescribed antibiotic in the country. It could be a coincidence that these four people, a tiny fraction of the millions on this medicine on any given day, got sick. Still, the doctors agreed that they should investigate. The two pediatricians collected the medical records of the patient who sent the email and the other cases she had found. All were healthy young people who developed a devastating lung injury after a brief flulike illness often with a fever, sore throat or cough. And all had taken TMP-SMX.
What convinced the doctors that there was a link were the biopsies of the affected lungs. Each showed the same unusual pattern of focused destruction: The only cells within the lung that were affected were those in which carbon dioxide was taken up and oxygen supplied — the cells that do the most important work of breathing. In two, including the patient who first noted the connection between her illness and the drug, these essential cells eventually grew back, allowing them to once again breathe on their own. Others whose lung tissue did not recover needed a lung transplant. Of those first cases, two died: the 12-year-old that the young woman met at Mayo and Uwadia, the girl in the news story.
In the four years since Miller received the patient’s email, she and Goldman have identified a total of 19 patients, most under age 20, who had this reaction after being treated with TMP-SMX. Six died. It is still unclear how the antibiotic triggers this rare but devastating destruction. Goldman thinks it is probably some kind of allergic reaction. But they still cannot predict who is at risk, or why.
As an I.C.U. doctor, Miller tells me, she uses this drug frequently. And although these cases are rare, the devastation caused is terrible. “Most of these people,” she says, referring to the 19 cases, “were not getting treated for a life-threatening illness, and yet they were given this ordinary drug — and it ended their life or changed it forever.”
This original patient shares Miller’s mixed feelings. She is 26 now and is a nurse who cares for patients who have just had a heart-and-lung transplant. She regularly gives her patients TMP-SMX. And they need it — to treat diseases they have and to prevent diseases they might get. Yet she knows that, because of her reaction to that drug, her lungs will never be the same. She can play a friendly game of volleyball but gets winded after climbing a couple flights of stairs. Still, she has a good life. And she is proud to have made a contribution to the science that she hopes will, one day, prevent this from happening to anyone else.
Lisa Sanders, M.D., is a contributing writer for the magazine. Her latest book is “Diagnosis: Solving the Most Baffling Medical Mysteries.” If you have a solved case to share, write her at Lisa.Sandersmdnyt@gmail.com.
A rocket mysteriously crashed on the Moon. The military intel world has no idea who sent it
Imagine, if you will, a rocket crash on the lunar surface. The crash site is peculiar, unlike others. The rocket itself comes from an unknown place. It’s not The Twilight Zone, it’s reality. This past month NASA revealed that a rocket of some kind crashed into the Moon, with a strange impact crater.
On June 24, NASA released images of the lunar crash site, taken by the Lunar Reconnaissance Orbiter in May. According to the space agency, whatever did hit the Moon’s surface did so on March 4, after being detected on a trajectory with the Moon in late 2021. The Moon is covered in craters, several from past rocket component impacts, but this new one is unique because it’s two separate, overlapping points of impact. Whatever hit the Moon did so in a way that made an 18-meter crater overlapping a 16-meter one. As NASA noted, that implies that each end of the rocket had a large amount of mass, uncommon for these kinds of impacts.
But no one knows where the rocket came from. NASA is able to say the rocket was at least in space late last year, on its way to a hard crash with the Moon. But as to who sent it or why? That’s a mystery. And outside of NASA, U.S. Space Command, Space Force, even the wider Department of Defense, all are quiet. There are theories but nothing is confirmed.
“Since the origin of the rocket body remains uncertain, the double nature of the crater may indicate its identity,” NASA said in its statement.
And no, it’s likely not aliens. This isn’t Independence Day.
Why doesn’t NASA know? It’s NASA, plus the Moon is relatively close. The United States and its allies have satellites, telescopes and enough tracking software to keep an eye on what is going into space and from where. Rocket launches are traceable – every time North Korea tests out a ballistic missile the intelligence and military world is pretty quick to identify the path, range and possible launch point. This particular incident looks like a job for Space Force. The service branch has guardians monitoring satellites and rockets in lower orbit and keeping track of their paths. The Moon is a bit farther out, but Space Force is looking to expand its patrols farther out. But so far, Space Force isn’t saying anything.
So why is the origin of this rocket unclear? Different branches of the military and government have historically been rivals or at odds, but rocket launches cross over different areas and seem like the kind of topic that would prompt information sharing. Dozens of pieces of rockets, from boosters to other components, have impacted onto the lunar surface. In 2009 NASA even intentionally bombarded the Moon as part of an experiment looking at potential water on the satellite. But this case appears to be more accident than experiment.
There is a likely theory however. The March 4 crash was reported on at the time. The leading theory from scientists is that it was the third-stage rocket booster from the Chinese CHANG’E 5-T1 rocket, which launched in 2014. The 18th Space Control Squadron, which handles space satellite tracking had initially reported the rocket booster as burnt up, but has since changed its status to still in orbit. In March, the squadron gave a statement to The Verge, saying that the rocket piece had not de-orbited but it was unclear if that was what hit the lunar surface.
So is the Chinese rocket the source of this weird double crater? Space watching officials have yet to confirm or deny the theory. Neither the 18th Space Control Squadron nor the wider Space Force have commented on NASA’s images and releases as of press time. But if it was the CHANG’E 5-T1, how it created the double crater is also unclear.
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‘Sudden Adult Death Syndrome’: Young, Healthy People Are Mysteriously Dying
Experts and families of healthy, young people who have suddenly died are speaking out about Sudden Adult Death Syndrome, or Sudden Arrhythmic Death Syndrome, known more commonly as SADS.
SADS, according to the Royal Australian College of General Practitioners (RACGP), “is an umbrella term to describe unexpected deaths in young people (usually 40 years of age), whose cause of death following post mortem examination is ‘undetermined’ or ‘unascertained.’”
“She worked for an advertising company and was doing really well,” said Margherita Cummins, whose daughter Catherine Keane died suddenly at age 31. “She went to the gym and walked 10,000 steps every day.”
Cummins told the Irish Mirror last month that her daughter’s flatmates found Catherine’s dead body after she didn’t come down for breakfast.
“They sent her a text at 11.20am and when she didn’t reply, they checked her room and found she had passed,” the mother recalled. “Her friend heard a noise in her room at 3.56am and believes now that is when she died.”
Another family lost their healthy 19-year-old son from the mysterious disease in April of 2021, 7News.com.au highlighted.
“As most of you know on the 2nd of April 2021 we tragically lost our beautiful Son and Brother Liam to Sudden Adult Death Syndrome,” a fundraising page for the teen said. “Liam was just 19 years of age a vibrant, fit, healthy young man.”
“Liam had everything going for him in life he was learning to drive, looking forward to planned concerts with his friends, many a road trip out and planning the new University life, when everything was cruelly taken from him,” the post continued. “All his hopes and dreams gone and stolen from us as well!”
Dr. Elizabeth Paratz, from Melbourne’s Baker Heart and Diabetes Institute, said the Victorian registry shows “there are approximately 750 cases per year of people aged under 50 in Victoria suddenly having their heart stop.”
“Of these, approximately 100 young people per year will have no cause found even after extensive investigations such as a full autopsy,” she added.
Paratz noted that “the numbers had remained tragically consistent over the years,” according to 7News.com.au.
Medical Daily noted that approximately 210,000 people “die suddenly and unexpectedly each year due to sudden cardiac arrest in the United States,” citing the American Heart Association.
RACGP says on their webpage that “the most common SADS conditions include genetic arrhythmia syndromes such as long QT syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT) and Brugada syndrome.”
“These conditions follow an autosomal dominant inheritance pattern,” RACGP details. “Therefore, first-degree relatives (ie parents, siblings, children) of an individual who has a genetic arrhythmogenic disorder are at a 50% risk of also having a gene variant for the condition, and thus, at risk of developing the condition. All these conditions show considerable clinical variability within families and have incomplete penetrance.”