By March, the child’s doctors were no closer to figuring out why he wasn’t getting better. So they reached out to Trine Mogensen, a professor of immunology at Aarhus University in Denmark. “It was really unclear what this infection was. And there was no evidence of bacterial infection or tuberculosis,” Mogensen says. Stumped, she and her team sequenced the child’s genome to see if this uncovered any clues. “It came out, surprisingly, that there was a genetic mutation,” she says.

What they had found was a mutation in the gene that codes for IFNAR2, a protein that binds to type I interferons. Interferons are a family of proteins that play an essential role in fighting off viral infections. Without type I interferons working well, the child would be unable to mount any kind of immune response to viruses such as Covid-19 and the flu. 

Yet what virus the child was facing was still unclear. So Mogensen got in contact with Christopher Duncan, a clinician-scientist who studies viral immunity and interferons at Newcastle University in the United Kingdom. Duncan had been researching the very same genetic mutation for several years, first documenting it in a 2015 paper in the journal Science Translational Medicine. In that paper, he and his colleagues had found the genetic variant in a family from Ireland. A 13-month-old infant had suffered a severe case of encephalitis—inflammation of the brain—after receiving the MMR vaccine, which contains live (but weakened) forms of the measles, mumps, and rubella viruses. The child’s illness ultimately proved to be fatal. 

Following the publication of that paper, Duncan and his colleagues had been contacted by researchers in Alaska, who had identified a couple of children—unrelated—who had run into major problems with multiple viruses and had the same genetic variant. He was also alerted to two children in northern Canada with a similar condition. 

Knowing this, Mogensen and Duncan went back to the child from Greenland—and finally uncovered the root of his condition. They discovered that three weeks before falling ill, he had also been vaccinated with the live MMR vaccine. (The child survived and is now healthy.) Duncan and Mogensen published their findings in April in the Journal of Experimental Medicine. 

But now the team wanted to know if there were more people carrying this uncatalogued genetic mutation. They had noted that the boy from Greenland and the children from Alaska were all of Inuit or Alaska Native heritage. They trawled through the genetic records of 5,000 Inuit and found the variant was surprisingly common: In fact, 1 in 1,500 people in the Inuit population were carrying it. “That was hugely surprising,” Duncan says. 

The sheer prevalence of this variant in the Inuit population, and the fact it had gone under the radar for so many years, is the fascinating part of the puzzle. The genetic variant probably arose through the “founder effect,” whereby multiple people end up carrying a mutation that originated in a common ancestor. The effect tends to be seen in populations that descend from relatively small groups of people and that don’t mix much with outsiders. “Because these populations were quite secluded or isolated for centuries, then such a mutation can become more prevalent,” explains Mogensen.

It’s likely that many more children died from carrying this genetic variant before it was discovered. “It’s only recently that we do genetic investigations,” Mogensen explains. And we could see more and more of these genetic mutations emerge from the woodwork as genetic sequencing becomes cheaper and more popular, especially in remote populations. “I think that will uncover a lot of explanations for this huge inter-individual variation we see in how sick people become.” (The findings also emphasize the importance of cataloging the genomes of people other than Europeans.) 

Mogensen now wants to look into more samples from the past to get a clearer picture of just how common this genetic mutation is. If it is prevalent enough, there could be a rationale to add the genetic mutation to newborn screening in countries with Inuit populations. It would mean the children carrying the mutation wouldn’t be given the live MMR vaccine, for instance. The team is now in talks with the chief medical officer in Greenland, Mogensen says.

Much of the existing immunology knowledge has been achieved through work on animal models, a less-than-perfect replica of the intricacies of the human immune machinery. Cases like those documented by Duncan and Mogensen can uncover how immune proteins, like interferons, work and fight infection—and highlight just how indispensable they are. When you can see what happens in humans who lack a part of the immune system, says Duncan, “that’s basically the absolute definitive evidence of what it does.”

The discovery slots into a growing field of immunology that searches for a genetic basis for immune deficiencies—what are known as inborn errors of immunity. Scientists have only just begun to unravel how many immunological mysteries can be explained by a genetic mutation. To date, more than 400 “inborn errors of immunity” have been documented, with no signs of that number slowing down. “Every day, we discover more,” says Ivan Zanoni, an immunologist at Harvard Medical School and Boston Children’s Hospital. 

Jean-Laurent Casanova, head of the St. Giles Laboratory of Human Genetics of Infectious Diseases at the Rockefeller University, has been one of those spearheading the movement. In the same issue of the journal that published Mogensen and Duncan’s findings, Casanova and his colleagues describe a similar genetic variant in seven children with heritage from another remote population: West Polynesians. All of the children were of Samoan descent. “We thought that this could hardly be coincidental,” he says. 

However, this time the mutation was in the gene that codes for IFNAR1, another protein that binds with type I interferons. They decided to test if this genetic variant might be of West Polynesian origin, through the founder effect, and so analyzed populations across the Pacific, from Taiwan to the eastern part of French Polynesia. “To our great surprise, we found that the allele is indeed Polynesian,” Casanova says. “In western Polynesia in particular it’s a common allele,” meaning it can be found in more than 1 percent of the population. 

Not only that, they discovered that the seven children had suffered adverse reactions to the MMR vaccine, as well as to the yellow fever vaccine—another that contains a live virus—and had also fallen severely ill with viral infection. Four of the seven children died. But the main indicator of carrying the variant, the researchers agreed, was an adverse reaction to the MMR vaccine. Following the release of the paper, Australia’s health authorities issued a warning to health care providers, stating that children of West Polynesian heritage who become very unwell in the weeks following the MMR vaccine may need to be assessed for an immune deficiency.

The biggest surprise, Casanova says, is that even without type I interferons, individuals might still be able to deal with lots of viruses. If it was the case that these proteins were essential in fighting off all viral infections, these IFNAR1 or IFNAR2 mutations wouldn't become so common in remote populations, he argues.

Zanoni takes a slightly different stance. He thinks the remoteness of these populations protected them from being exposed to all the viruses that people on the mainland might have encountered, which allowed the variant to be passed down from generation to generation. “The fact that the frequency of the mutation is so high in this population really suggests that it was negatively selected in the general population in the continent,” he says.

Mogensen has a further theory. “We think that since it was becoming so prevalent, there may have been an advantage of having this mutation,” she says. The idea here is that it may have been protective against other infectious diseases, like tuberculosis—but this remains pure speculation, she says. 

Regardless, there are many people around the world walking down the street without this immune protein, says Casanova. “That is just mind-blowing.”

This Gene Mutation Breaks the Immune System. Why Has It Survived?

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How often should a toothbrush be replaced?

Often, people latch on to one favorite toothbrush and use it until it's completely worn out. But Cotter said you need to replace it more often than you might think.

"The American Dental Association recommends that toothbrushes need to be replaced every three months," she said. "Toothbrushes used longer than three months can become frayed and may damage the gingiva (gums)."

Cotter says the three-month timeline applies to both manual and electric toothbrush heads, but sometimes brushes have to be replaced earlier.

"If the bristles of the toothbrush are fraying or are spreading out, then the brush needs to be replaced," she said. "Some toothbrushes have bristles that change color over time to help patients know when they need replacing."

According to Cotter, toothbrushes and toothbrush heads should also be replaced if someone has been sick. Viruses, including cold, flu and the coronavirus, thrive in a moist environment and can spread through physical contact. While sick, socially distance your toothbrush—don't share a common toothbrush holder with others.

"It is important to store your toothbrush in a vertical, upright position in the open air so that it will dry out between uses," Cotter said. "This helps control bacterial and fungal growth on the bristles."

What is the best toothbrush to use?

"Research has consistently shown that electric toothbrushes clean better than manual toothbrushes," Cotter said. "Most electric toothbrushes have a two-minute timer that beeps or pulses every 30 seconds to alert the user to move to a different quadrant or area of the mouth. Some of the new toothbrushes also have an app that will show the user where they are missing when brushing."

Some individuals prefer a hard-bristled toothbrush to clean teeth, but dental professionals don't typically recommend them. Firm or hard toothbrushes can actually damage the tooth enamel, Cotter says, so it is better to go with a soft bristle toothbrush.

At the end of the day, understanding what toothbrush to use and following proper toothbrush maintenance will help keep those pearly whites healthy.

Source

You've recently had COVID but as we now know, it's possible to be reinfected.

But how sick will you get the second time?

While your symptoms are likely to be less severe, in some cases they can be worse. Here's what we know so far.

After COVID, you don't need to test for 12 weeks

Current guidelines define you as a "cleared case" for 12 weeks after ending COVID isolation. If you develop COVID-like symptoms in that 12 weeks, you don't need to be tested.

The science behind this 12-week timeframe is evolving. The original idea was that if you have recovered from COVID, and you have a healthy immune system, you will have developed immunity against reinfection. And this will protect you for at least 12 weeks.

As case numbers in Australia increase, the reports of reinfections are also on the rise. And it's likely reinfection is occurring sooner than we first thought.

What's happening?

In order for a person to fight off re-infection with any virus, they must have developed a protective immune response.

Two main factors decide whether a person will have a protective immune response:

1.  How long a person's immune memory lasts.
2.  How well that memory recognizes the virus, or a slightly different virus.

Immune memory is made up of many critical parts, which each play a role in the protective army of your immunity. The biggest players in protective immunity memory are your B-cells (which mature to make antibodies) and your T-cells (which destroy virus-infected host cells).

So far, the evidence suggests immune memory for SARS-CoV-2, the virus that causes COVID, lasts for months or even years when it comes to B-cells and the antibodies they produce.

Similarly, current evidence shows the memory T-cells can last over a year.

This means that for a healthy person, immune memory for SARS-CoV-2 appears to last for a year, against reinfection with the exact same virus.

So why the reinfections?

One clear explanation for reinfection is the virus is mutating. SARS-CoV-2 replicates fast and in doing so makes replication errors. We refer to these errors as mutations. Over time, the mutations accumulate and a new sub-variant is born.

Since the start of the pandemic we have seen the parental Wuhan strain mutate to alpha, beta, delta and now omicron.

The current theory is that immunity from one variant may not provide enough protection from another.

Data so far suggest the omicron variant is better at immune escape than its predecessors. This means omicron is "escaping" the immune memory created by SARS-CoV-2 infections from other variants such as delta, beta or alpha.

Emerging data is now showing sub-variants of omicron can also escape immunity from a previous omicron variant. This means a person might be able to get an omicron reinfection.

A small, yet-to-be-peer-reviewed study from Denmark found that in unvaccinated people, reinfection with omicron BA.2 is possible following a primary infection with omicron BA.1. Despite this finding, the study also concluded reinfection rates were low and therefore rare.

With winter approaching and case numbers climbing, we're also seeing the emergence of new sub-variants such as BA.4 and BA.5. Early evidence shows these new sub-variants are even better at escaping immune memory than the parental BA.1 omicron.

What about severity?

For those who get a reinfection, disease severity appears to be milder and less likely to result in hospitalization. This is likely because the immune memory can recognize at least part of the re-infecting virus.

However it's difficult to measure disease severity on a population level. A systemic review of case studies found that while some second infections were milder, this was not so in all cases. Some reinfections resulted in worse outcomes, including death. (During this study period, one of the original strains, B.1, caused most primary infections, with reinfections caused by alpha or beta variants.)

But while omicron appears to be causing more reinfections than other variants, there isn't enough robust data to make firm conclusions about the severity of reinfection with omicron or other variants.

What we know for certain is we need more data from more people to say that reinfection is less severe.

We also know from several studies that being vaccinated does provide protection from reinfection, including in previously infected people who then receive subsequent vaccines.

Another reason to get boosted

A recent study that's yet to be peer-reviewed found immunity from omicron BA.1 variant drops around 7.5 fold with the new omicron BA.4 and BA.5 variants. This means the antibodies you produce from a BA.1 infection, which are able to detect and neutralize the BA.1 virus, are 7.5 times less able to recognize and neutralize BA.4 and BA.5 than BA.1.

This study also found vaccination plus natural exposure to omicron BA.1 gave five times greater protection to omicron BA.4 and BA.5 than the immunity from natural exposure to BA.1 alone.

Data also shows the strongest protective immunity comes from a mix of triple vaccination and natural infection.

A further study found this type of hybrid immunity protects better against both reinfection and hospitalization than natural immunity alone, highlighting the importance of vaccination and vaccine boosters.

So the question remains: if our immune memory lasts for a year, but is too specific to recognize the new variants, will we need a new vaccine every year?

Time will tell.

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The results have been published today in the peer-reviewed journal Investigative Ophthalmology and Visual Science.

Cataract is a clouding of the eye lens that develops over time and affects the quality of vision. It is caused by a disorganization of the proteins in the lens that leads to clumps of protein forming, which scatter light and severely reduce transmission to the retina. Cataracts cause vision loss and blindness for millions of people worldwide.

A team of international scientists, led by Professor Barbara Pierscionek, Deputy Dean (Research and Innovation) in the Faculty of Health, Education, Medicine and Social Care at Anglia Ruskin University (ARU), has been carrying out advanced optical tests on an oxysterol compound that had been proposed as an anti-cataract drug.

In laboratory trials, treatment with the oxysterol compound VP1-001 showed an improvement in refractive index profiles—a key optical parameter that is needed to maintain high focusing capacity—in 61% of lenses. This means that the protein organization of the lens is being restored, resulting in the lens being better able to focus. This was supported by a reduction in lens opacity in 46% of cases.

Professor Pierscionek, who is also a member of the Medical Technology Research Centre at Anglia Ruskin University (ARU), said, "This study has shown the positive effects of a compound that had been proposed as an anti-cataract drug but never before tested on the optics of the lens. It is the first research of this kind in the world.

"It has shown that there is a remarkable difference and improvement in optics between eyes with the same type of cataract that were treated with the compound compared to those that were not.

"Improvements occurred in some types of cataract but not in all, indicating that this may be a treatment for specific cataracts. This suggests distinctions may need to be made between cataract types when developing anti-cataract medications. It is a significant step forward towards treating this extremely common condition with drugs rather than surgery."

Source

Citizen scientists help discover more than 1,000 new asteroids

Scientists have used algae to power a low-energy computer chip for six months.

Researchers from the University of Cambridge sealed a colony of cyanobacteria, commonly known as blue-green algae, inside a metal enclosure the size of an AA battery. The unit was then left on a windowsill, according to New Scientist, where the algae photosynthesized, generating a tiny current of electricity that powered an ARM Cortex-M0+ chip.

The system is only a proof of concept, but its creators hope algae-powered chips could be used in future Internet of Things devices. They say the advantage of using algae over traditional batteries or solar power is that it has a smaller environmental impact and could potentially provide continuous power.

“The growing Internet of Things needs an increasing amount of power, and we think this will have to come from systems that can generate energy, rather than simply store it like batteries,” Professor Christopher Howe, joint senior author of the paper, said in a press statement. “Our photosynthetic device doesn’t run down the way a battery does because it’s continually using light as the energy source.”

The algae-powered ARM chip was used to carry out very basic calculations, during which it consumed a tiny 0.3 microwatts an hour, reports New Scientist. Although the energy usage of normal computers varies based on factors like workload and age, this is a sliver of the electricity needed to run an average PC. If a normal desktop computer consumes, say, 100 watts of power an hour, you would need roughly 333,000,000 algae “batteries” to run it.

The researchers behind the project will obviously need to scale up their solution, but they say the basic attributions of algae power generation are heartening. The algae they used did not need feeding, they say, gathering all its energy needs from natural sunlight, and was able to continue producing power at nighttime based on energy stored during the day.

“We were impressed by how consistently the system worked over a long period of time — we thought it might stop after a few weeks but it just kept going,” Dr. Paolo Bombelli, the first author of the paper, said in a press statement.

Although using algae in this way is definitely unusual, it’s also part of a growing area of research known as “biophotovoltaics.” The aim of the field is to harness the power generated by biological microorganisms that naturally convert light into electricity through photosynthesis.

Although this process is extremely inefficient, with plants absorbing only 0.25 percent of the energy of sunlight (compared to 20 percent absorbed in solar panels), advocates say biophotovoltaic energy systems could be cheap to produce and environmentally friendly. They imagine that, in the future, giant “lily-pads” that float on water could be coated in algae to act as mobile power stations alongside offshore wind farms.

Scientists create algae computer powered by photosynthesis

Inca priests used natural antidepressants for nefarious purposes

How to build a wormhole in just 3 (nearly impossible) steps

The majority of the city’s 25 million residents were mostly confined to their homes or residential compounds in April as part of a sweeping lockdown to stamp out the nation’s worst Covid outbreak since the virus emerged in Wuhan more than two years ago.

Almost all dealerships in the city were closed during the month, the Shanghai Automobile Sales Association said in a statement Monday, when it highlighted the zero sales figure.

In April last year, 26,311 vehicles were sold in the city, according to the association, which represents about 300 companies.

Nationwide, car sales fell the most in two years in April, down almost 36% from a year earlier to 1.06 million units, China Passenger Car Association data released last week showed.

The financial hub is finally on the verge of reaching a goal of three days of zero community transmission of Covid-19, which officials have said is required to start easing the harshest elements of the city’s six-week lockdown. Around 980,000 people remain under the strictest form of lockdown, unable to leave their apartments, while many outside those zones say they’re still confined to residential compounds as authorities seek to meet the zero-spread target.

Passenger throughput at the city’s Pudong International Airport plunged about 99% from a year earlier in April, figures released Monday showed.

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A war of words erupted on Twitter and Facebook between some Muslims and Christians in the country, with each side accusing the other of intolerance and extremism.

Two days after the killing, a peaceful protest in Sokoto turned violent, with demands for the release of the suspected killers of Ms Samuel.

A plethora of fake pictures, videos and posts have been shared by social media users to incite violence and cause further damage and division in the country.

Many of the fake stories are accompanied by comments on why Nigeria should be divided between the predominantly Muslim north and Christian south.

Facebook user Emeka Fans Page posted a video in which he makes many claims, one of which is "Sokoto people done butcher all the whole Christians in their state".

 
His video has been viewed over 670,000 times and shared more than 5,000 times. He also urges his followers to continue sharing the video.

A police statement said two protesters were shot by the police when they tried to occupy the palace of the Sultan of Sokoto, the spiritual leader of Nigeria's Muslims.

There are some genuine videos that show protesters burning tyres on streets, wielding machetes, knives and sticks while running across the streets and chanting Islamic prayers. Another video showed people looting and burning shops in a market. But there is no evidence of killing or butchering as claimed by Emeka Fans Page.

The state government has imposed a 24-hour curfew to regain peace in the state.

Two-year-old video shared

Another video was shared by many users, showing a woman in a torn white dress being beaten by men with sticks and what looks like a thick rope.

Other women wearing hijab can be seen standing and watching as the woman is being abused. She attempts to escape into a house but is pushed out by a group of men.

 
She is heard in Hausa stating: "I won't do it again, forgive me."

The BBC Disinformation unit found the video has been in circulation for at least two years on social media. At first glance, the circumstances surrounding the video are not clear but further investigation indicate the video was shot in Kaduna and the woman was arrested and charged for stealing and selling babies.

However, social media users are currently recirculating it and claiming it is from the recent violence in Sokoto. One user said: "They are killing Christians right now, if you have your relations in Sokoto…"

Non-existent doctor accused of killing Muslims

A screenshot of a Facebook post by a purported Christopher Uche-Ayodeji (Dr Chris) where he "confesses" to allowing many Muslims die while working as a doctor in northern Nigeria has also gone viral.

The screenshot says that "Dr Chris" is a physician at the University Hospitals Birmingham in the UK. He claims he enjoyed "every bit of it" as he was on a revenge mission.

The post said he was avenging the killing of a neighbour in northern Nigeria in 2015. Gimba Kakanda, a social critic with almost 200,000 followers on Twitter sent a tweet to University Hospitals Birmingham reporting Dr Chris.

 
The hospital replied that the individual was unknown to them. But users continued to share the screenshot on social media and went as far as falsely attaching a picture of an unrelated man, claiming it was Christopher Uche-Ayodeji. The picture turned out to be that of a Nigerian writer and journalist Ayodeji Rotinwa who tweeted and pleaded with people to stop using his picture.

On Facebook, the page belonging to Christopher Uche-Ayodeji (Dr Chris) does not exist, and neither does the message in circulation.

Another piece of disinformation being shared on social media is of the burning of the residence of the Catholic Bishop of Sokoto Diocese, Reverend Matthew Hassan Kuka during the riots.

A statement released by the Catholic Diocese of Sokoto said the news was false.

"We wish to disclaim that there was an attack of any sort on the residence of Bishop Matthew Hassan Kukah," it said.

The statement also debunked claims that churches had been burnt down. It said protesters had destroyed the windows of the Holy Family Catholic Cathedral on Bello Way and that St Kevin's Catholic Church was attacked and partly burnt.

Source: 

https://www.bbc.com/news/world-africa-61456485

Yet, in a new study published last month in eLife, a group of researchers at the Massachusetts Institute of Technology and Yale University showed that it’s possible to tweak one of these time-honored rules and create a more expansive, entirely new genetic code built around longer codon words. In principle, their discovery points to one of several ways of expanding the genetic code into a more versatile system that synthetic biologists could use to create cells with novel biochemistries that make proteins found nowhere in nature. But the work also showed that an extended genetic code is hampered by its own complexity, becoming less efficient and even surprisingly less capable in some ways—limitations that hint at why life may not have favored longer codons in the first place.

It’s uncertain what these findings mean for how life elsewhere in the universe could be encoded, but it does imply that our own genetic code evolved to be neither too complicated nor too restrictive, but just right—and then ruled life for billions of years thereafter as what Francis Crick called a “frozen accident.” Nature opted for this Goldilocks code, the authors say, because it was simple and sufficient for its purposes, not because other codes were unachievable.

For example, with four-letter (quadruplet) codons, there are 256 unique possibilities, not just 64, which might seem advantageous for life because it would open opportunities to encode vastly more than 20 amino acids and an astronomically more diverse array of proteins. Previous synthetic biology studies, and even some of those rare exceptions in nature, showed that it’s sometimes possible to augment the genetic code with a few quadruplet codons, but until now, no one has ever tackled creating an entirely quadruplet genetic system to see how it compares with the normal triplet-codon one.

“This was a study that asked that question quite genuinely,” said Erika Alden DeBenedictis, the lead author of the new paper, who was a doctoral student at MIT during the project and is currently a postdoc at the University of Washington.

To test a quadruplet-codon genetic code, DeBenedictis and her colleagues had to modify some of life’s most fundamental biochemistry. When a cell makes proteins, snippets of its genetic information first get transcribed into molecules of messenger RNA (mRNA). The organelles called ribosomes then read the codons in these mRNAs and match them up with the complementary “anti-codons” in transfer RNA (tRNA) molecules, each of which carries a uniquely specified amino acid in its tail. The ribosomes link the amino acids into a growing chain that eventually folds into a functional protein. Once their job is complete and the protein is translated, the mRNAs get degraded for recycling and the spent tRNAs get reloaded with amino acids by synthetase enzymes.

The researchers tweaked the tRNAs in Escherichia coli bacteria to have quadruplet anti-codons. After subjecting the genes of the E. coli to various mutations, they tested whether the cells could successfully translate a quadruplet code, and if such a translation would cause toxic effects or fitness defects. They found that all of the modified tRNAs could bind to quadruplet codons, which showed that “there’s nothing biophysically wrong with doing translation with this larger codon size,” DeBenedictis said.

But they also found that the synthetases only recognized nine out of 20 of the quadruplet anticodons, so they couldn’t recharge the rest with new amino acids. Having nine amino acids that can be translated with a quadruplet codon to some degree is “both a lot and a little,” DeBenedictis said. “It’s a lot of amino acids for something that nature doesn’t ever need to work.” But it’s a little because the inability to translate 11 essential amino acids strictly limits the chemical vocabulary that life has to play with.

Moreover, many of the quadruplet code translations were highly inefficient, and some were even detrimental to the cell’s growth. Without a major fitness advantage, it’s very unlikely nature would have selected a more complex code, especially once it had settled on a working code, DeBenedictis said. The authors concluded that the reason why nature didn’t select for a quadruplet code wasn’t because it was unachievable, but rather because the triplet code was simple and sufficient. After all, even if life needed to expand its repertoire of 20 amino acids, there’s still lots of room within the existing 64 codons to do so.

Triplet codons work well on Earth, but it’s not clear if that would be true elsewhere—life in the cosmos might differ significantly in its chemistry or in its coding. The genetic code is “presumably derivative and subservient to the biochemistry of peptides” that are required for life to work, said Drew Endy, an associate professor of bioengineering at Stanford University and president of the BioBricks Foundation, who was not involved in the study. In environments more complex than Earth, life might need to be encoded by quadruplet codons, but in much simpler settings, life might get by with mere doublet codons—that is, of course, if it uses codons at all.

No matter how life is encoded on our planet or on others, the real impact of the paper is that now we know it’s “totally possible to make a quad-code organism,” and the findings suggest it will be straightforward, Endy said. With one study, they’re almost halfway to getting it to work, he added, which is “an infinitely amazing accomplishment.”

Not everyone agrees that creating a full quad-coded life form will be simple. “I don’t think anything they show suggests that it’s going to be easy—but they do show it’s not impossible, and that’s interesting,” said Floyd Romesberg, a synthetic biologist who cofounded the biotech company Synthorx. Getting something that works poorly to work better is a “very, very different game” than trying to do the impossible.

How much effort it will take to make a true quadruplet code work well is an open question, DeBenedictis said. She thinks you would also likely need to reengineer much of the translation machinery to work well with a larger code. She and her team are hoping to bring their work to the next level by adding an extra “tail” to the engineered tRNAs so that they will interact with a set of ribosomes designed to work with them alone. That might improve the efficiency of translation by reducing competition with any triplet-coding aspects of the system.

Overcoming the competition from the triplet code will always be a major challenge, she added, because it already works so well.

Could Life Use a Longer Genetic Code? Maybe, but It’s Unlikely

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A new study has uncovered the sequence of events that precipitated the disaster, providing information that could further our understanding of heat formation on the North American continent.

By reviewing large-scale weather conditions and formations before the heat wave, University of Chicago scientists discovered that a cyclone spawned an "anticyclone," which combined to produce and then trap heat near the surface of the region.

The account may shed light on the likelihood of such extreme heat waves in the future. It also serves as a proof of concept for a comprehensive set of diagnostics developed by UChicago Prof. Noboru Nakamura to lay out the mechanisms behind large-scale atmospheric weather. The scientists hope this approach can help lay out why extreme events happen, and to better understand the odds of future events.

Pressure changes

The heat wave began on June 26, 2021.

Previous record high temperatures shattered one after the other, by huge margins. Streetcar cables melted in Portland, Oregon; pavement buckled across the region. Before it was over, a town in Canadian British Columbia tied Death Valley for the highest temperature ever recorded in North America—121 degrees Fahrenheit.

But the conditions had been set in motion weeks before. Using data collected from satellites and on the ground, UChicago scientists set out to re-create the sequence of events.

They found that in the week prior, a cyclone had formed over the Gulf of Alaska. Cyclones are large, spiral-shaped systems that form around a center of low pressure. (Think of the spiral clouds you see during hurricanes.) When clouds form out of water vapor, the process actually releases heat, which accumulated in the atmosphere.

Then, as the cyclone moved slowly away, it triggered the formation of an anticyclone to the east—a system that rotates slowly around a center of high pressure instead of low. These are known as "blocking" systems because they disrupt the normal eastward movement of weather systems. A blocking anticyclone acts like a blanket, trapping heat in a region.

The result was a warm, stagnant column of air that made it difficult for surface heat to escape to the upper atmosphere as it normally does.

Blocking systems are well known for causing heat waves in the mid-latitudes, explained Emily Neal, a UChicago undergraduate student in environmental science and first author on the paper. "But this was an extraordinarily strong blocking event," said Neal. "Our analysis showed that the warmth of the air column within the blocking system was in the top 0.01% of all events along the same latitude in the past half a century."

The scientists also hope their research can help fill in gaps in our understanding of how and why heat waves form. They noted that most studies on heat waves have examined events on the European subcontinent, which has its own unique geography and meteorology that may not apply elsewhere.

For example, Neal said, soil moisture is thought to be a major player in European heat waves. "But we don't think this was at play here," she said.

"Particularly in British Columbia, where much of this is taking place, it's a very dry environment. So that means we may be looking at a different mechanism than what is in the common literature."

On 24 June, a heavy band of clouds associated with an extratropical cyclone is seen over the Eastern Pacific and Gulf of Alaska. Heat released in these clouds ended up in the cloud-free region over Western North America on 29 June, where a blocking anticyclone formed and caused the extreme heat. Credit: NOAA GOES17 weather satellite

A better way to project the future

The detective work is also the first real-world test for a framework developed by Prof. Nakamura to lay out the mechanisms behind large-scale atmospheric weather events.

Typically, when scientists run climate simulations, they run their model forward in time for tens and hundreds of years and collect statistics on the frequency and intensity of weather events. Then they change one variable, such as the carbon dioxide level, and rerun the simulation and see how the statistics change. When scientists use this method to predict the average surface temperature and rainfall in the future, most of the models tend to agree. But when they try to predict the frequency of extreme weather events, the models don't converge.

"If you ask these models to predict the frequency and intensity of future extreme events, such as blocking anticyclones, the answers tend to be all over the map," Nakamura said.

"This is due to the fundamental nature of atmospheric dynamics affecting statistics in a complex way," he explained. "Statistics are useful for cataloging and describing the sequence of events, but it's much harder to be sure about causation when you're only using that approach."

Instead, he said, "To really nail causation, you need dynamical theory so that you can understand why it's happening."

To that end, Nakamura and his group have spent the past decade working out fluid dynamics and hydrology behind large-scale atmospheric events, and creating a rigorous framework that explains how mid-latitude weather systems work.

This groundwork allowed them to identify the heat released by the upstream cyclone as the main driver of the unusually strong Pacific Northwest heat wave.

Nakamura said the framework can complement the statistical approach: "This tool can help us understand when models do not converge, why, and what things need to be fixed."

This is especially important as we try to understand how climate change will affect the world. Scientists worry that we are approaching—or have already approached—a tipping point in the alteration of the Earth's atmosphere, after which extreme events become much more likely. Other scientific studies have estimated that the magnitude of the Pacific Northwest heat wave was "virtually impossible" without climate change.

"There is increased urgency and interest in understanding the prospects for future heat waves," said Nakamura. "We're looking forward to begin using this framework to dissect data in a meaningful way, to actually see the important processes and driving forces behind events.

"Since the heating mechanism identified in this work involves condensation of water vapor into clouds, the intensity of atmospheric blocking and heat waves will likely increase in the future as the warming climate allows more water vapor to be present in the atmosphere," he said.

The other author on the paper, published in Geophysical Research Letters, was Clare S.Y. Huang, PhD.

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Switch to Moderna booster after Pfizer shots better against omicron in 60+

With the rise of new variants, the symptoms of COVID have also evolved. Initially, the NHS regarded a fever, cough, and loss or change in sense of smell or taste as the main symptoms which could indicate COVID infection. Now, recently updated NHS guidance suggests also looking out for symptoms including a sore throat, blocked or runny nose, and a headache.

But what about some of the more obscure signs and symptoms? From skin lesions to hearing loss, emerging data is increasingly showing us that COVID symptoms can go beyond what you might expect from a regular cold or a flu.

1. Skin lesions

COVID-related skin complaints are not uncommon. In fact, a U.K. study published in 2021 found that one in five patients only exhibited a rash and no other symptom.

COVID can affect the skin in a variety of ways. Some people may experience a widespread maculopapular rash (flat or raised areas of discolored skin), while others might present with hives (raised areas of itchy skin).

"COVID toes," meanwhile, describes red, swollen or blistering skin lesions on the toes. This symptom is more commonly seen in adolescents or young adults with mild or no symptoms.

Most COVID skin lesions tend to go away after a few days, or in some instances a few weeks, without the need for any specialized treatment. If the skin is very itchy or painful though, you can consult a GP or dermatologist, who may recommend treatment such as a cream.

2. COVID nails

During an infection, including that of SARS-CoV-2 (the virus which causes COVID-19), our bodies naturally try to express that they're under an unusual amount of stress. They can do this in a variety of weird and wonderful ways, including through our nails. "COVID nails" encompasses changes such as:

•  Beau's lines—horizontal indentations that occur at the base of the fingernails or toenails when there's a temporary interruption in nail growth due to a physical stress on the body

•  Mees' lines—horizontal white lines that appear on the nails, thought to be caused by the abnormal production of proteins in the nail bed

•  a red half-moon pattern which develops at the base of the fingernails (the mechanism underlying this change is unclear).

The data on how many people experience COVID nails is limited, but it's been estimated it could be up to 1–2% of COVID patients.

COVID nails tend to appear in the days or weeks following COVID infection as the nails grow. Although they might be painful initially, the vast majority tend to return to normal over a few weeks.

Notably, while these changes may be indicative of COVID, they can also be caused by different things. For example, Beau's lines can be secondary to chemotherapy or another infection.

3. Hair loss

Hair loss is perhaps an understated symptom of COVID-19, usually occurring one month or more after the acute infection. In one study of almost 6,000 people who had previously had COVID, hair loss was the most common post-COVID symptom, reported by 48% of participants. It was especially prevalent among people who had severe COVID and white women.

It is thought that this results from the hair "sensing" the stress in the body, leading to excess shedding. Indeed, hair loss can also be triggered by other stressful events, such as childbirth. The good news is that with time the hair grows back to normal.

4. Hearing loss and tinnitus

As with other viral infections, such as the flu and measles, COVID has been found to affect the cells in the inner ear, with hearing loss or tinnitus (a constant ringing sensation in the ear) sometimes following infection.

In a review study that included 560 participants, hearing loss occurred in 3.1% of patients with COVID, while tinnitus occurred in 4.5%.

In one study of 30 people who had been diagnosed with COVID, and 30 who hadn't—none with pre-existing hearing problems—the researchers found that COVID was associated with damage to the inner ear which led to hearing impairment at higher frequencies. While for the vast majority of patients this resolves on its own, cases of permanent hearing loss linked to COVID have been reported.

Why all these symptoms?

We don't understand exactly what causes these symptoms, but we know the most important part is played by a process called inflammation. Inflammation is our body's natural defense mechanism against pathogens; SARS-CoV-2 in this case. It involves the production of "cytokines"—proteins which are important in controlling the activity of immune cells.

Excessive production of these proteins, as a part of the inflammation triggered by COVID infection, can cause sensory deficits, which potentially explain why some people are presenting with hearing loss and tinnitus. It can also disrupt the capillary networks, very tiny blood vessels which provide blood to organs including the ears, skin and nails.

The symptoms we've described here are not exclusive to COVID infection. That said, if you notice any of these symptoms, it would be appropriate to consider a COVID test, especially if you're in an area where COVID is circulating.

You can also contact your GP, particularly if the symptoms are getting worse or causing you significant discomfort. At the same time, you can be reassured that most of these symptoms are likely to improve with time.

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Based on scientific data, a main reason for the increasing health risk in young people is obesity: while primary hypertension is found in 1.4% of normal-weight adolescents and 7.1% of overweight adolescents, the percentage rises to 25% in obese adolescents. "Increased waist circumference presenting the abdominal fat in particular, is associated with high blood pressure and early onset of cardiovascular diseases," reports Susanne Greber-Platzer, Head of the Department of Pediatrics and Adolescent Medicine at MedUni Vienna.

Anxiety, pressure and stress

Lack of exercise, in turn, leads to a threefold increase in the risk of hypertension. Chronic exposure to anxiety, pressure and stress is also increasing in children and adolescents, with significant effects on their health and blood pressure. Additionally sugary drinks and salty foods are directly affecting the blood pressure. Rapid growing during puberty, especially in boys, often leads to pathological blood pressure values. Prematurity, low birth weight and genetic predisposition may also play a role.

Factors such as age, gender and height must be taken into account when measuring hypertension in children under 15 years of age. For adolescents aged 16 and older, a blood pressure above 140/90 is considered as hypertensive after three independent measurements, the same as in adults. Like adults, children and adolescents do not notice high blood pressure, therefore early diagnosis is challenging. General symptoms like headache, dizziness or nose bleeding can occur, but are not necessarily present. Hypertensive crises, markedly elevated systolic blood pressure values, can lead to confusion and seizures and even unconsciousness, presenting life threatening situations.

High risk for early onset of cardiovascular diseases

Long-term high blood pressure leads to left ventricular hypertrophy and endothelial damage of the arterial vessels including coronary arteries, consequently increasing the risk for premature myocardial infarction or stroke, even in young adulthood. "To prevent the risk of early cardiovascular damage, a screening from the age of three years would be necessary," says Susanne Greber-Platzer, emphasizing the importance of measuring blood pressure in children and adolescents at least every two years. Therefore, a healthy lifestyle should be forced and additional medication to lower the blood pressure can be indicated in childhood to prevent early cardiovascular damage.

If hypertension is caused by other diseases (secondary hypertension), it is necessary to treat the primary disease appropriately and enabling blood pressure reduction. For example, Diabetes mellitus type I causes high blood pressure in about 15%, which frequently manifests in childhood or adolescence.

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Global change and human actions are driving rapid changes to tidal wetlands—tidal marshes, mangroves and tidal flats—worldwide. However, ecosystem restoration and natural processes are playing a part in reducing total losses.

But efforts to estimate their current and future status at the global scale remain highly unclear due to uncertainty about how tidal wetlands respond to drivers of change.

In a new study, researchers have developed a machine-learning analysis of vast archives of historical satellite images to detect the extent, timing and type of change across the world's tidal wetlands between 1999 and 2019.

They found that globally, 13,700 square kilometers of tidal wetlands were lost, offset by gains of 9,700 square kilometers, leading to a net loss of 4,000 square kilometers over the two-decade period.

The study is published today in the journal Science.

"We found 27% of losses and gains were associated with direct human activities, such as conversion to agriculture and restoration of lost wetlands," said Dr. Nicholas Murray, Senior Lecturer and head of James Cook University's Global Ecology Lab, who led the study.

All other changes were attributed to indirect drivers such as human impacts to river catchments, extensive development in the coastal zone, coastal subsidence, natural coastal processes and climate change.

About three-quarters of the net global tidal wetland decrease happened in Asia, with almost 70% of that total concentrated in Indonesia, China and Myanmar.

"Asia is the global center of tidal wetland loss from direct human activities. These activities had a lesser role in the losses of tidal wetlands in Europe, Africa, the Americas and Oceania, where coastal wetland dynamics were driven by indirect factors such as wetland migration, coastal modifications and catchment change," said Murray.

The scientists found that almost three-quarters of tidal wetland loss globally has been offset by the establishment of new tidal wetlands in areas where they formerly did not occur—with notable expansion in the Ganges and Amazon deltas.

Most new areas of tidal wetlands were the result of indirect drivers, highlighting the prominent role that broad-scale coastal processes have in maintaining tidal wetland extent and facilitating natural regeneration.

"This result indicates that we need to allow for the movement and migration of coastal wetlands to account for rapid global change," said Murray.
He added: "Global-scale monitoring is now essential if we are going to manage changes in coastal environments effectively."

More than 1 billion people now live in low-elevation coastal areas globally.

Tidal wetlands are of immense importance to humanity, providing benefits such as carbon storage and sequestration, coastal protection, and fisheries enhancement.

"Protecting our coastal wetlands is critical to supporting coastal communities and the wider health of the planet. These areas are the last refuge for many plants and animals," said Dr. Thomas Worthington, Senior Research Associate in the University of Cambridge's Department of Zoology and co-author of the study.

He added: "This data can help identify coastal areas most impacted—and therefore in need of protection, or areas where we can prioritize restoration."

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Her 10-time achievement, reported by her brother and confirmed by a Nepalese official, makes her the first woman to do so.

The Nepalese single mother was born in a cave, had no formal education and worked as a janitor.

She last made the 8,848.86m (29,031.69ft) ascent in 2018.

"I felt like I'd reached my dream when I reached Everest's summit for the first time," she told the BBC ahead of Thursday's climb.

"I thought to myself, 'No more just being a housewife!'

"I felt like I'd changed Sherpa culture, the status of Sherpa women and Nepali women. I enjoyed being outside of my home and I wanted to share that feeling with all women."

Lhakpa was chosen by the BBC as one its 100 most inspirational and influential women for 2016.

News of her 10th summit was broken by her brother Mingma Gelu Sherpa, who said she had reached the top at 06:15 (00:30 GMT). Nepali tourism official Bhishma Kumar Bhattarai confirmed the report for Reuters news agency.

Speaking from base camp earlier, her youngest daughter Shiny, 15, told the BBC she was excited and keenly watching her mother's progress.
"I look up to my mum," she said. "She has achieved so much even though she had nothing."

Lhakpa Sherpa packs her bags before starting a trek (file photo)

However, Lhakpa's hard work and achievements have yet to translate into wealth and recognition.

She began life in a village more than 4,000m (13,000ft) above sea level in the Makalu region of eastern Nepal. She is a member of the Sherpa ethnic group, descended from nomadic Tibetans, who are used to living in hostile high altitudes.

"I was born in a cave," she said, breaking into laughter. "I don't even know my date of birth. My passport says I am 48."

"I remember having to walk for hours, sometimes carrying my brothers to school, only to be turned away when I got there. At the time, girls were not allowed to go to school."

Agriculture was the mainstay for her village, which had no electricity. What it did have was a certain magical neighbour.

"I grew up right next to Everest," she recalled. "I could see it from my home. Everest continues to inspire and excite me."

Since the first conquest of the mountain in 1953, more and more people have tried to scale the peak every year. Those who do so inevitably hire Sherpa guides and porters. But some Sherpas, like Lhakpa, set out to become mountaineers in their own right.

It was not an easy transition. Lhakpa's parents didn't back her.

"My mum said I would never get married," she told the BBC. "She warned me that I would become too masculine and undesirable. The villagers told me that it's a man's job and I would die if I tried it."

She brushed aside those concerns and made it to Everest's highest ridge in 2000. In 2003, she became the first woman to scale Everest three times - and more records followed.

During her 2003 climb, she was joined by her brother and sister, becoming the first three siblings simultaneously on an 8,000-metre-high mountain. The Guinness Book of World Records recognised the feat.

After reaching the summit, Lhakpa (centre) says she usually thinks of her children Sunny (far left) and Shiny (far right)

She then married US-based Romanian-born climber George Dijmarescu, and scaled the peak with him five times.

After getting married she moved to the US, but the relationship ended in acrimonious divorce in 2015.

Lhakpa now lives in the US state of Connecticut with their two daughters. She also has a son from a previous relationship.

During her initial expeditions she used to plant the Nepali flag at the summit. This time, she was carrying the US flag.

But her achievements failed to attract media attention and sponsors. For many years she was living unrecognised, and working for minimum wage.
"My jobs included taking care of the elderly, house cleaning and dish washing," she said.

Lhakpa is known as Everest Queen, but in reality she often struggled to pay for essentials

"I didn't make much money. I couldn't afford to buy clothes or pay for haircuts. I just had to focus on taking care of my children and then hope I had enough to return to Everest."

But she maintained a passion for climbing. She went up twice as a guide, and on some occasions friends and family helped support her trips.

Mountaineering was "not very rewarding compared with the risks involved", she said, but she believes it helped her escape what otherwise would have been a mundane life in the village.

Financially, things began to change after she learned to speak English well. She gave interviews, and spoke at events.

She got a sponsor for her ninth scale of the summit. But this time, her 10th, she raised the money through crowdfunding.

Lhakpa says she felt as though she had changed Sherpa culture by reaching the summit of Mount Everest

Lhakpa always starts her trek with a customary prayer. Safety is her biggest priority.

More than 300 people have died while trying to scale Mount Everest, so Lhakpa and her team have to pass bodies preserved by ice.

"The mountain decides the weather," she said. "During bad weather I would just wait. We can't wrestle a mountain."

"Past 8,000m, I feel like a zombie," she said. "You can't eat and everything is frozen. You have to climb at night so that you can descend from the summit in the daylight. It's scary."

Climbers get very little time at the top. For Lhakpa, it is only five to 10 minutes - just enough time to take pictures and reflect on all the people who support her climbs.

She has no plans to retire after this season. She wants to scale K2, the world's second-highest peak. She is also thinking of climbing Everest in the future with her son and daughters, because "mountain climbing is my passion and this is what I want to do."

"I've had a challenging life," she added. "Mountains made me happy and relaxed. I will never give up. I want young women not to give up."

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In the western state of Gujarat – where the temperature has hovered above 40C for weeks now and is set to touch 46C in several pockets – rescuers are coming across birds that have fallen from the sky every day.

The impact of the excrutiating heat on animals has been neglected so far, even as humans suffering from heatstrokes and dehydration are being treated in hospitals where separate wards for heatwave-related conditions are being set up in several areas of the state.

In this picture taken on 3 May 2022, Shervin Everett (not pictured), a hospital curator, feeds an Indian Flying Fox bat at Jivdaya Charitable Trust in Ahmedabad (Getty Images)

Conditions have deteriorated significantly for animals because this year’s heat is “one of the worst in recent times,” according to rescuers working in an animal hospital managed by nonprofit Jivdaya Charitable Trust in Gujarat.

“We have seen a 10 per cent increase in the number of birds that need rescuing,” Manoj Bhavsar, who works closely with the trust and has been rescuing birds for more than a decade, told the Reuters news agency.

Activists have been picking up these birds and taking them to the trust-run hospital to provide immediate care, including injecting water into their mouths using syringes and feeding birds multi-vitamin tablets.

A vet provides medicine to an eagle in Ahmedabad (Reuters via Amit Dave)

Extreme hot spells, or heatwaves, began much earlier in India and Pakistan this year, with the first spell recorded as early as March.

Heatwaves in the subcontinent are usually reported either in May, or in some instances, in April.

While the change in the pattern of heatwaves becoming stronger and longer stems from several reasons, the underlying cause for this extreme weather event is climate change.

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Zoom in for our first look at the black hole at the center of our Milky Way, courtesy of the Event Horizon Telescope collaboration.

Feast your eyes on the first image of the black hole at the center of our Milky Way

In a paper recently published in Neuron, researchers from the group of Professor Botond Roska at the University of Basel and the Institute of Molecular and Clinical Ophthalmology (IOB) reveal how different cell types in cortex change their activity during general anesthesia, helping to understand how unconsciousness may be induced.

You are lying on the operating table. The doctor tells you to count to 5, and places an anesthetic mask on your face. By the count of 4, you've lost consciousness. You will not wake up until after the surgery. What happened in your brain during this time?

One would probably assume that your brain has been silent. Especially your cortex, the brain area thought to be the seat of conscious processing. However, for close to 100 years, it has been known that some cells in the cortex are active and that cortex alternates between periods of high and low activity during general anesthesia.

Using EEG electrodes attached to the scalp is one of the few tools available to measure this activity, but electrodes don't allow one to identify the cells underlying this activity. Therefore, the question has remained: which cells contribute to the rhythmic activity in the cortex, and how might that contribute to the loss of consciousness during general anesthesia.

On the trail of unconsciousness

Cortex is composed of different cell types, each with different functions. Different general anesthetics act on different receptors, located on different types of neurons, distributed throughout the brain. Yet, all general anesthetics lead to the loss of consciousness, so "we were interested in finding if there is a common neuronal mechanism across different anesthetics," says Dr. Martin Munz, one of the three first authors of the study.

< Watch the video at the source page. >

In this Neuron publication, the researchers used modern genetic tools, in combination with mouse lines labeling individual cortical cell types to address this question. They found that in contrast to what had previously been suspected, only one specific cell type within cortex, layer 5 pyramidal neurons, showed an increase in activity when the animal was exposed to different anesthetics.

"Each anesthetic induces a rhythm of activity in layer 5 pyramidal neurons. Interestingly, these rhythms differed between anesthetics. Some were slower, and some were faster. However, what was common across all anesthetics was that they all induced an alignment of activity. That is, when they were active, all layer 5 pyramidal neurons were active at the same time," says Dr. Arjun Bharioke from the same research group and also a first author of the study. "We called this 'neuronal synchrony'".

Layer 5 pyramidal neurons serve as a major output center for the cerebral cortex and also connect different cortical areas to each other. Thus, they communicate both between different cortical areas, as well as from the cortex to other areas of the brain. Therefore, a synchronization of activity across layer 5 pyramidal neurons restricts the information that the cortex can output.

Like a crowd at a soccer match

"It seems that instead of each neuron sending different pieces of information, during anesthesia all layer 5 pyramidal neurons send the same piece of information," says Arjun Bharioke, "One could think of this as when people in a crowd transition from talking to each other, for example before a soccer or basketball game, to when they are cheering for their team, during the game. Before the game starts, there are many independent conversations. In contrast, during the game, all the spectators are cheering on their team. Thus, there is only one piece of information being transmitted across the crowd."

Prior work has proposed that loss of consciousness occurs through the disconnection of cortex from the rest of the brain. The results of the IOB team suggest a mechanism by which this may occur—by the transition to lowered information output from cortex, during anesthesia.

Alexandra Brignall, the third first author and a veterinarian by trade says: "Anesthetics are very powerful, as anyone who has been in a surgery can attest to. But they are also not always easy to use. During a surgery, one has to continuously monitor the depth of the anesthetic to ensure that the patient is not too deep or too shallow. The more we know how anesthetics work and what they do in the brain, the better. Maybe this will help researchers develop new drugs to more specifically target the cells in the brain associated with unconsciousness."

"Our findings are highly relevant for medicine, since anesthesia is one of the most frequently performed medical procedures. Understanding the neuronal mechanism of anesthesia could lead to better anesthetic drugs and improved surgical outcomes," says Botond Roska, corresponding author and director of the IOB Molecular Research Center.

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Prior research has suggested that parts of the Martian surface were covered with water up until approximately 3 billion years ago. The time since the water dried up on Mars is known as the Amazonia period. In this new effort, data from the Chinese rover Zhurong has shown the researchers evidence that water on Mars might have persisted longer than has been thought.

Rover Zhurong has been traveling around in an impact crater on the Mars surface for approximately one year. During that time, it has used its two spectrometers to analyze rocks. It also takes pictures of the rocks using its microimaging camera. The rover also blasts them with a laser to create smoke that can be analyzed. The researchers compared the signatures they found in the rocks on Mars with rocks on Earth, finding that some of the rocks are hydrated minerals, which are minerals containing water. They also found instances of layers of duricrust, the formation of which they note would have required a large amount of water either rising from below the surface or from a large quantity of melting ice.

A look at the landing area and the heat shield. Credit: China National Space Administration (CNSA)

The researchers suggest that water must have persisted on Mars longer than has been thought to account for the hydrated minerals on its surface—perhaps much longer. They also suggest that the existence of such rocks on the surface hints at the possibility of ground ice. If that is the case, future astronauts could use it for a wide variety of purposes.

The findings back up evidence from other research efforts that have suggested Mars not only had water on its surface in more recent times, but that it also flowed, creating sculpted rock features.

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"Doctors perform approximately 1 million surgical knee replacements each year," he said. "Of course, a proportion of these people need surgery. However, I've always felt that a lot of patients with OA are getting knee replacements much sooner in life than needed."

Dr. Jayabalan is the physician-scientist director of the Nancy W. Knowles Strength + Endurance Lab at Shirley Ryan AbilityLab and assistant professor of physical medicine and rehabilitation at Northwestern University Feinberg School of Medicine.

The question—how to help patients with knee OA feel better without surgery—has prompted two research studies he leads at Shirley Ryan AbilityLab.

One is a new test to identify OA earlier. And the other is the novel use of equipment to help patients with OA get the full benefits of exercise without pain.

Identifying knee OA earlier

Staying active is the best way for a patient to keep OA from getting worse. Yet, one of the biggest challenges of current knee OA treatment practices is that diagnosis typically happens only after a patient is in such severe pain that activity is difficult.

"Right now, I can diagnose patients with knee OA using an X-ray and send them for physical therapy, pain management and maybe injections," Dr. Jayabalan said. "However, by that point, the OA is already far down the line. I don't have anything to prescribe that will prevent its progression."

To help doctors diagnose knee OA much earlier, Dr. Jayabalan and his lab team are developing a new protocol that he describes as a "cartilage stress test."

"We have the patient exercise to put stress on the joints, and then we measure the body's responses to that stress by looking at blood- or synovial-based biomarkers," he said.

The design of the cartilage stress test relies on two novel aspects to measure the metabolic state of joints. First, it uses a real-time approach. Dr. Jayabalan's team takes blood during periodic intervals using an IV line while the patient is walking on the treadmill, instead of relying on blood taken pre- and post-evaluation.

Second, the test uses a special treadmill that provides a mediolateral tilt of up to 10 degrees. This angle creates individualized stress loads on each joint.
This new protocol could lead to individualized treatment plans for patients at risk of early OA—for example after anterior cruciate ligament (ACL) reconstruction—while they are still relatively healthy, years before their joints start hurting. Ideally, early intervention will delay or even eliminate the need for joint replacements.

"We generally tell patients to walk 30 minutes a day, five times per week," he said. "My goal is to identify an optimal prescription for each patient that would prevent disease progression. With early diagnosis, we could prescribe an individualized, preventive exercise program."

Taking the load off

For patients with joint pain caused by advanced knee OA, an exercise prescription consisting of even the simplest tasks, such as walking for 30 minutes, can present an overwhelming challenge. Dr. Jayabalan's lab is pursuing a hopeful alternative—use of an anti-gravity treadmill that allows knee OA patients to walk longer without increasing joint pain, while still reaping the full cardiac benefits.

Anti-gravity treadmills are increasingly more common in physical therapy regimens for patients recovering from ACL and other knee injuries. These devices enclose the patient's lower body in a vacuum, and allow the therapist to vary the body-weight load that patients feel as they walk or run on the treadmill.

In a pilot study, Dr. Jayabalan's team observed 30 patients with knee OA over the course of two 30-minute sessions. In one session, research subjects attempted to walk for 30 minutes on a treadmill at their full body weight. In the second, they attempted the same goal on an anti-gravity treadmill, set to reduce their body weight by 50 percent. Study results were overwhelmingly positive.

"We've had subjects who felt they could not walk 15 minutes on a flat surface—but when they were walking on the anti-gravity treadmill, and we reduced their body weight, they were able to walk the full 30 minutes," he said. "The reduced body weight enabled them to walk longer due to significantly less joint pain, and they got the full cardiovascular benefit of 30-minutes' exercise. Additionally, their biomarker responses indicated significantly less stress placed on their cartilage and improved gait parameters."

Clearly, anti-gravity treadmills are showing promise for these patients, but they are expensive. The good news, Dr. Jayabalan said, is that there is a much simpler, more affordable and readily available way to reduce load on arthritic joints—aquatic therapy.

"A pool can un-weight the patient, too," he said. "Buoyancy affords significant biological and biomechanical benefits that potentially could allow someone with knee OA to walk without joint pain for longer."

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The WHO says excess mortality is calculated as the "difference between the number of deaths that have occurred and the number that would be expected in the absence of the pandemic based on data from earlier years." It includes deaths associated with COVID-19 directly or indirectly—as a result of the pandemic's impact on health systems and society.

According to the report, there were 14.91 million additional deaths in the first two years of the pandemic, over and above the 60 million people who die globally each year. The WHO estimated India's excess mortality at 4.74 million—830,000 in 2020 and the rest in 2021.

But the Indian government rejected the WHO report as based on "statistically unsound and scientifically questionable methodology of data collection for making excess mortality projections in case of India."

"India's basic objection has not been with the results but rather the methodology adopted for the same," says one of a series of official notes issued before and after the 5 May WHO report release.

A rebuttal on the same day accused the WHO of ignoring official data for 2020, published 3 May by India's central registration system, according to which the "increase in number of deaths over previous years" was 474,806. India claims to have achieved 99.9 percent death registration by 2020.

"Owing to its large area, diversity and a population of 1.3 billion which witnessed variable severity of the pandemic both across space and time, India consistently objected to the use of one size fits all, approach and model, which may be applicable to smaller countries but cannot be applicable to India," the 5 May release said.

So what is the truth?

"No matter how you look at it, if the crude death rate on an average is one per thousand per month, anything above that average over a period of two years can be safely taken as death due to the differentiator—in this case the only known differentiator during the 2020–2021 period was the COVID-19 pandemic," Satya N. Mohanty, a former career bureaucrat and currently adjunct professor of economics at the Jamia Milia Islamia University in New Delhi, told SciDev.Net.

India's health system was already overburdened when the pandemic struck, said Mohanty. Warnings by a Parliamentary standing committee report in November 2020 on the management of the pandemic had dwelt on the gross inadequacy of hospital beds and oxygen supplies.

The Parliamentary committee's report was ignored and India's leaders were confident enough to allow the holding of the Kumbh Mela, the world's biggest religious gathering at Haridwar that attracted millions of pilgrims during March and April 2021. That so-called "super-spreader" event triggered a devastating second wave, marked by severe shortages of hospital beds, oxygen supplies and medicines.

Worst of all there was an epidemic within the pandemic of mucormycosis, or black fungus, which attacked many of those who did manage to get treatment for COVID-19 infection. This was attributed to the inappropriate use of steroids which can lower immunity and open the way for opportunistic infections.

Earlier assessments, such as one published in March by The Lancet, indicated the difficulty of obtaining accurate data in India. However, by using figures gleaned from the civil registration system in 12 of India's 28 states, The Lancet arrived at the figure of four million deaths for the two pandemic years—fairly close to the WHO figures.

The Lancet said its estimation had accounted for "under-registration of mortality by the civil registration system at the state level," which seemed at odds with the Indian government's claim of 99.9 percent levels of death registration in 2020.

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In a new paper published in the journal Communications Biology, University of Florida researchers showed that plants can successfully sprout and grow in lunar soil. Their study also investigated how plants respond biologically to the Moon's soil, also known as lunar regolith, which is radically different from soil found on Earth.

This work is a first step toward one day growing plants for food and oxygen on the Moon or during space missions. More immediately, this research comes as the Artemis Program plans to return humans to the Moon.

"Artemis will require a better understanding of how to grow plants in space," said Rob Ferl, one of the study's authors and a distinguished professor of horticultural sciences in the UF Institute of Food and Agricultural Sciences (UF/IFAS).

Even in the early days of lunar exploration, plants played an important role, said Anna-Lisa Paul, also one of the study's authors and a research professor of horticultural sciences in UF/IFAS.

"Plants helped establish that the soil samples brought back from the moon did not harbor pathogens or other unknown components that would harm terrestrial life, but those plants were only dusted with the lunar regolith and were never actually grown in it," Paul said.

Anna-Lisa Paul tries moistening the lunar soils with a pipette. The scientists found that the soils repelled water (were hydrophobic), causing the water to bead-up on the surface. Active stirring of the material with water was required to break the hydrophobicity and uniformly wet the soil. Once moistened, the lunar soils could be wetted by capillary action for plant culture. Credit: UF/IFAS , Tyler Jones

Paul and Ferl are internationally recognized experts in the study of plants in space. Through the UF Space Plants Lab, they have sent experiments on space shuttles, to the International Space Station and on suborbital flights.

"For future, longer space missions, we may use the Moon as a hub or launching pad. It makes sense that we would want to use the soil that's already there to grow plants," Ferl said. "So, what happens when you grow plants in lunar soil, something that is totally outside of a plant's evolutionary experience? What would plants do in a lunar greenhouse? Could we have lunar farmers?"

To begin to answer these questions, Ferl and Paul designed a deceptively simple experiment: plant seeds in lunar soil, add water, nutrients and light, and record the results.

The complication: The scientists only had 12 grams—just a few teaspoons—of lunar soil with which to do this experiment. On loan from NASA, this soil was collected during the Apollo 11, 12 and 17 missions to the Moon. Paul and Ferl applied three times over the course of 11 years for a chance to work with the lunar regolith.

The small amount of soil, not to mention its incalculable historical and scientific significance, meant that Paul and Ferl had to design a small scale, carefully choreographed experiment. To grow their tiny lunar garden, the researchers used thimble-sized wells in plastic plates normally used to culture cells. Each well functioned as a pot. Once they filled each "pot" with approximately a gram of lunar soil, the scientists moistened the soil with a nutrient solution and added a few seeds from the Arabidopsis plant.

Arabidopsis is widely used in the plant sciences because its genetic code has been fully mapped. Growing Arabidopsis in the lunar soil allowed the researchers more insight into how the soil affected the plants, down to the level of gene expression.

Rob Ferl, left, and Anna-Lisa Paul looking at the plates filled part with lunar soil and part with control soils, now under LED growing lights. At the time, the scientists did not know if the seeds would even germinate in lunar soil. Credit: UF/IFAS, Tyler Jones

As points of comparison, the researchers also planted Arabidopsis in JSC-1A, a terrestrial substance that mimics real lunar soil, as well as simulated Martian soils and terrestrial soils from extreme environments. The plants grown in these non-lunar soils were the experiment's control group.

Before the experiment, the researchers weren't sure if the seeds planted in the lunar soils would sprout. But nearly all of them did.

"We were amazed. We did not predict that," Paul said. "That told us that the lunar soils didn't interrupt the hormones and signals involved in plant germination."

However, as time went on, the researchers observed differences between the plants grown in lunar soil and the control group. For example, some of the plants grown in the lunar soils were smaller, grew more slowly or were more varied in size than their counterparts.

These were all physical signs that the plants were working to cope with the chemical and structural make-up of the Moon's soil, Paul explained. This was further confirmed when the researchers analyzed the plants' gene expression patterns.

"At the genetic level, the plants were pulling out the tools typically used to cope with stressors, such as salt and metals or oxidative stress, so we can infer that the plants perceive the lunar soil environment as stressful," Paul said. "Ultimately, we would like to use the gene expression data to help address how we can ameliorate the stress responses to the level where plants—particularly crops—are able to grow in lunar soil with very little impact to their health."

Anna-Lisa Paul, left, and Rob Ferl, working with lunar soils in their lab. Credit: UF/IFAS, Tyler Jones

How plants respond to lunar soil may be linked to where the soil was collected, said Ferl and Paul, who collaborated on the study with Stephen Elardo, an assistant professor of geology at UF.

For instance, the researchers found that the plants with the most signs of stress were those grown in what lunar geologists call mature lunar soil. These mature soils are those exposed to more cosmic wind, which alters their makeup. On the other hand, plants grown in comparatively less mature soils fared better.

Growing plants in lunar soils may also change the soils themselves, Elardo said.

"The Moon is a very, very dry place. How will minerals in the lunar soil respond to having a plant grown in them, with the added water and nutrients? Will adding water make the mineralogy more hospitable to plants?" Elardo said.

Follow up studies will build on these questions and more. For now, the scientists are celebrating having taken the first steps toward growing plants on the Moon.

"We wanted to do this experiment because, for years, we were asking this question: Would plants grow in lunar soil," Ferl said. "The answer, it turns out, is yes."

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The sinkhole is 630 feet (192 meters) deep, according to the Xinhua news agency, deep enough to just swallow St. Louis' Gateway Arch.

A team of speleologists and spelunkers rappelled into the sinkhole on Friday (May 6), discovering that there are three cave entrances in the chasm, as well as ancient trees 131 feet (40 meters) tall, stretching their branches toward the sunlight that filters through the sinkhole entrance.

"This is cool news," said George Veni, the executive director of the National Cave and Karst Research Institute (NCKRI) in the US, and an international expert on caves.

Veni was not involved in the exploration of the cave, but the organization that was, the Institute of Karst Geology of the China Geological Survey, is NCKRI's sister institute.

A site for sinkholes

The discovery is no surprise, Veni told Live Science, because southern China is home to karst topography, a landscape prone to dramatic sinkholes and otherworldly caves.

Karst landscapes are formed primarily by the dissolution of bedrock, Veni said. Rainwater, which is slightly acidic, picks up carbon dioxide as it runs through the soil, becoming more acidic. It then trickles, rushes and flows through cracks in the bedrock, slowly widening them into tunnels and voids.

Typical karst sinkhole in Chongqing, China. (Eastimages/Getty Images)

Over time, if a cave chamber gets large enough, the ceiling can gradually collapse, opening up huge sinkholes.

"Because of local differences in geology, climate and other factors, the way karst appears at the surface can be dramatically different," he said.

"So in China you have this incredibly visually spectacular karst with enormous sinkholes and giant cave entrances and so forth. In other parts of the world you walk out on the karst and you really don't notice anything. Sinkholes might be quite subdued, only a meter or two in diameter. Cave entrances might be very small, so you have to squeeze your way into them."

In fact, 25 percent of the United States is karst or pseudokarst, which features caves carved by factors other than dissolution, such as volcanics or wind, Veni said. About 20 percent of the world's landmass is made of one of these two cave-rich landscapes.

The new discovery took place in the Guangxi Zhuang Autonomous Region, near Ping'e village in the county of Leye, according to Xinhua. Guangxi is known for its fabulous karst formations, which range from sinkholes to rock pillars to natural bridges and have earned the region UNESCO world heritage site designation.

Why sinkholes matter

The sinkhole's interior is 1,004 feet (306 meters) long and 492 feet (150 meters) wide, Zhang Yuanhai, a senior engineer with the Institute of Karst Geology, told Xinhua.

The Mandarin word for such enormous sinkholes is "tiankeng", or "heavenly pit", and the bottom of the sinkhole did indeed seem like another world.

Chen Lixin, who led the cave expedition team, told Xinhua that the dense undergrowth on the sinkhole floor was as high as a person's shoulders. Karst caves and sinkholes can provide an oasis for life, Veni said.

"I wouldn't be surprised to know that there are species found in these caves that have never been reported or described by science until now," Lixin said. 

In one West Texas cave, Veni said, tropical ferns grow abundantly; the spores of the ferns were apparently carried to the sheltered spot by bats that migrate to South and Central America.

Not only do sinkholes and caves offer refuge for life, they are also a conduit to aquifers, or deep stores of underground water. Karst aquifers provide the sole or primary water source for 700 million people worldwide, Veni said. But they're easily accessed and drained – or polluted. 

"Karst aquifers are the only types of aquifers that you can pollute with solid waste," Veni said. "I've pulled car batteries and car bodies and barrels of God-knows-what and bottles of God-knows-what out of the active cave stream." 

The new discovery brings the number of sinkholes in Leye County to 30, according to Xinhua. The same researchers have previously discovered dozens of sinkholes in Northwest China's Shaanxi province and a cluster of interconnected sinkholes in Guangxi, China Daily reported. 

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