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one of the leading modelers, Gabriela Gomes, suggested the entire area of research was being effectively blackballed out of fear it might encourage a relaxation of pandemic vigilance. “This is the very sad reason for the absence of more optimistic projections on the development of this pandemic in the scientific literature,” she wrote on Twitter. “Our analysis suggests that herd-immunity thresholds are being achieved despite strict social-distancing measures.”

Gomes suggested, herd immunity could happen with as little as one quarter of the population of a community exposed — or perhaps just 20 percent. “We just keep running the models, and it keeps coming back at less than 20 percent,” she told Hamblin. “It’s very striking.” Such findings, if they held up, would be very instructive, as Hamblin writes: “It would mean, for instance, that at 25 percent antibody prevalence, New York City could continue its careful reopening without fear of another major surge in cases.”

But for those hoping that 25 percent represents a true ceiling for pandemic spread in a given community, well, it almost certainly does not, considering that recent serological surveys have shown that perhaps 93 percent of the population of Iquitos, Peru, has contracted the disease; as have more than half of those living in Indian slums; and as many as 68 percent in particular neighborhoods of New York City

overshoot of that scale would seem unlikely if the “true” threshold were as low as 20 or 25 percent.

But, of course, that threshold may not be the same in all places, across all populations, and is surely affected, to some degree, by the social behavior taken to protect against the spread of the disease.

we probably err when we conceive of group immunity in simplistically binary terms. While herd immunity is a technical term referring to a particular threshold at which point the disease can no longer spread, some amount of community protection against that spread begins almost as soon as the first people are exposed, with each case reducing the number of unexposed and vulnerable potential cases in the community by one

you would not expect a disease to spread in a purely exponential way until the point of herd immunity, at which time the spread would suddenly stop. Instead, you would expect that growth to slow as more people in the community were exposed to the disease, with most of them emerging relatively quickly with some immune response. Add to that the effects of even modest, commonplace protections — intuitive social distancing, some amount of mask-wearing — and you could expect to get an infection curve that tapers off well shy of 60 percent exposure.

Looking at the data, we see that transmissions in many severely impacted states began to slow down in July, despite limited interventions. This is especially notable in states like Arizona, Florida, and Texas. While we believe that changes in human behavior and changes in policy (such as mask mandates and closing of bars/nightclubs) certainly contributed to the decrease in transmission, it seems unlikely that these were the primary drivers behind the decrease. We believe that many regions obtained a certain degree of temporary herd immunity after reaching 10-35 percent prevalence under the current conditions. We call this 10-35 percent threshold the effective herd immunity threshold.

Indeed, that is more or less what was recently found by Youyang Gu, to date the best modeler of pandemic spread in the U.S

he cautioned again that he did not mean to imply that the natural herd-immunity level was as low as 10 percent, or even 35 percent. Instead, he suggested it was a plateau determined in part by better collective understanding of the disease and what precautions to take

Gu estimates national prevalence as just below 20 percent (i.e., right in the middle of his range of effective herd immunity), it still counts, I think, as encouraging — even if people in hard-hit communities won’t truly breathe a sigh of relief until vaccines arrive.

If you can get real protection starting at 35 percent, it means that even a mediocre vaccine, administered much more haphazardly to a population with some meaningful share of vaccination skeptics, could still achieve community protection pretty quickly. And that is really significant — making both the total lack of national coordination on rollout and the likely “vaccine wars” much less consequential.

At least 20 percent of the public, and perhaps 50 percent, had some preexisting, cross-protective T-cell response to SARS-CoV-2, according to one much-discussed recent paper. An earlier paper had put the figure at between 40 and 60 percent. And a third had found an even higher prevalence: 81 percent.

The T-cell story is similarly encouraging in its big-picture implications without being necessarily paradigm-changing

These numbers suggest their own heterogeneity — that different populations, with different demographics, would likely exhibit different levels of cross-reactive T-cell immune response

The most optimistic interpretation of the data was given to me by Francois Balloux, a somewhat contrarian disease geneticist and the director of the University College of London’s Genetics Institute

According to him, a cross-reactive T-cell response wouldn’t prevent infection, but would probably mean a faster immune response, a shorter period of infection, and a “massively” reduced risk of severe illness — meaning, he guessed, that somewhere between a third and three-quarters of the population carried into the epidemic significant protection against its scariest outcomes

the distribution of this T-cell response could explain at least some, and perhaps quite a lot, of COVID-19’s age skew when it comes to disease severity and mortality, since the young are the most exposed to other coronaviruses, and the protection tapers as you get older and spend less time in environments, like schools, where these viruses spread so promiscuously.

Balloux told me he believed it was also possible that the heterogeneous distribution of T-cell protection also explains some amount of the apparent decline in disease severity over time within countries on different pandemic timelines — a phenomenon that is more conventionally attributed to infection spreading more among the young, better treatment, and more effective protection of the most vulnerable (especially the old).

Going back to Youyang Gu’s analysis, what he calls the “implied infection fatality rate” — essentially an estimated ratio based on his modeling of untested cases — has fallen for the country as a whole from about one percent in March to about 0.8 percent in mid-April, 0.6 percent in May, and down to about 0.25 percent today.

even as we have seemed to reach a second peak of coronavirus deaths, the rate of death from COVID-19 infection has continued to decline — total deaths have gone up, but much less than the number of cases

In other words, at the population level, the lethality of the disease in America has fallen by about three-quarters since its peak. This is, despite everything that is genuinely horrible about the pandemic and the American response to it, rather fantastic.

there may be some possible “mortality displacement,” whereby the most severe cases show up first, in the most susceptible people, leaving behind a relatively protected population whose experience overall would be more mild, and that T-cell response may play a significant role in determining that susceptibility.

That, again, is Balloux’s interpretation — the most expansive assessment of the T-cell data offered to me

The most conservative assessment came from Sarah Fortune, the chair of Harvard’s Department of Immunology

Fortune cautioned not to assume that cross-protection was playing a significant role in determining severity of illness in a given patient. Those with such a T-cell response, she told me, would likely see a faster onset of robust response, yes, but that may or may not yield a shorter period of infection and viral shedding

Most of the scientists, doctors, epidemiologists, and immunologists I spoke to fell between those two poles, suggesting the T-cell cross-immunity findings were significant without necessarily being determinative — that they may help explain some of the shape of pandemic spread through particular populations, but only some of the dynamics of that spread.

he told me he believed, in the absence of that data, that T-cell cross-immunity from exposure to previous coronaviruses “might explain different disease severity in different people,” and “could certainly be part of the explanation for the age skew, especially for why the very young fare so well.”

the headline finding was quite clear and explicitly stated: that preexisting T-cell response came primarily via the variety of T-cells called CD4 T-cells, and that this dynamic was consistent with the hypothesis that the mechanism was inherited from previous exposure to a few different “common cold” coronaviruses

“This potential preexisting cross-reactive T-cell immunity to SARS-CoV-2 has broad implications,” the authors wrote, “as it could explain aspects of differential COVID-19 clinical outcomes, influence epidemiological models of herd immunity, or affect the performance of COVID-19 candidate vaccines.”

“This is at present highly speculative,” they cautioned.

big hope for stem cells is that they can be used to replace damaged tissue in everything from spinal cord injuries to Parkinson's disease.

Scientists once thought it was impossible to turn adult tissue back into stem cells, which meant that new stem cells could only be created by harvesting embryos - a practice that raised ethical qualms in some countries and also means that implanted cells might be rejected by the body.

The new stem cells are known as "induced pluripotency stem cells", or iPS cells.

"We would like to be able to find a way of obtaining spare heart or brain cells from skin or blood cells. The important point is that the replacement cells need to be from the same individual, to avoid problems of rejection and hence of the need for immunosuppression."

Thomas Perlmann, Nobel Committee member and professor of Molecular Development Biology at the Karolinska Institute said: "Thanks to these two scientists, we know now that development is not strictly a one-way street."

"You can't take out a large part of the heart or the brain or so to study this, but now you can take a cell from for example the skin of the patient, reprogram it, return it to a pluripotent state, and then grow it in a laboratory," he said.

“This virus has a surface protein that is primed to lock on that receptor and slip its RNA into the cell,”

Once inside, that RNA inserts itself into the cell’s own replication machinery and makes multiple copies of the virus. These burst out of the cell, and the infection spreads. Antibodies generated by the body’s immune system eventually target the virus and in most cases halt its progress.

“A Covid-19 infection is generally mild, and that really is the secret of the virus’s success,” adds Ball. “Many people don’t even notice they have got an infection and so go around their work, homes and supermarkets infecting others.”

the virus can cause severe problems. This happens when it moves down the respiratory tract and infects the lungs, which are even richer in cells with Ace-2 receptors. Many of these cells are destroyed, and lungs become congested with bits of broken cell. In these cases, patients will require treatment in intensive care.

Even worse, in some cases, a person’s immune system goes into overdrive, attracting cells to the lungs in order to attack the virus, resulting in inflammation

This process can run out of control, more immune cells pour in, and the inflammation gets worse. This is known as a cytokine storm.

Just why cytokine storms occur in some patients but not in the vast majority is unclear

Doctors examining patients recovering from a Covid-19 infection are finding fairly high levels of neutralising antibodies in their blood. These antibodies are made by the immune system, and they coat an invading virus at specific points, blocking its ability to break into cells.

Instead, most virologists believe that immunity against Covid-19 will last only a year or two. “That is in line with other coronaviruses that infect humans,

“It is clear that immune responses are being mounted against Covid-19 in infected people,” says virologist Mike Skinner of Imperial College London. “And the antibodies created by that response will provide protection against future infections – but we should note that it is unlikely this protection will be for life.”

“That means that even if most people do eventually become exposed to the virus, it is still likely to become endemic – which means we would see seasonal peaks of infection of this disease. We will have reached a steady state with regard to Covid-19.”

Skinner is doubtful. “We have got to consider this pandemic from the virus’s position,” he says. “It is spreading round the world very nicely. It is doing OK. Change brings it no benefit.”

In the end, it will be the development and roll-out of an effective vaccine that will free us from the threat of Covid-19,

the journal Nature reported that 78 vaccine projects had been launched round the globe – with a further 37 in development.

vaccines require large-scale safety and efficacy studies. Thousands of people would receive either the vaccine itself or a placebo to determine if the former were effective at preventing infection from the virus which they would have encountered naturally. That, inevitably, is a lengthy process.

some scientists have proposed a way to speed up the process – by deliberately exposing volunteers to the virus to determine a vaccine’s efficacy.

Volunteers would have to be young and healthy, he stresses: “Their health would also be closely monitored, and they would have access to intensive care and any available medicines.”

The result could be a vaccine that would save millions of lives by being ready for use in a much shorter time than one that went through standard phase three trials.

phase-three trials are still some way off, so we have time to consider the idea carefully.”

In the new study, researchers, including chemist Shankar Balasubramanian, of the University of Cambridge and Cambridge Research Institute, crafted antibody proteins specifically for this type of DNA. The proteins were marked with a fluorescent chemical, so when they hooked up to areas in the human genome packed with G-quadruplexes, they lit up.

Next, they incubated the antibodies with human cells in the lab, finding these structures tended to occur in genes of cells that were rapidly dividing, a telltale feature of cancer cells. They also found a spike in quadruplexes during the s-phase of the cell cycle, or the phase when DNA replicates just before the cell divides.

the researchers think the four-stranded DNA could be a target for personalized medicine in the future

"What makes me personally very happy about this work is that it again demonstrates that mechanisms first described in ciliated protozoa hold also true for other organisms up to human, demonstrating the strength of this model organism," wrote Lipps wrote.

The two reports together establish the feasibility of trying to grow replacement human organs in animals, though such a goal is still far off.

Creating chimeras, especially those with human cells, may prove controversial, given the possibility that test animals could be humanized in undesirable ways. One would be if human cells should be incorporated into a pig’s brain, endowing it with human qualities. Almost no one wants a talking pig.

The ban is still in place, and it’s unclear whether the Trump administration would continue to consider lifting the moratorium or whether new objections would be raised to using public funds for this line of research.

But no one knows exactly what sequence of chemicals is required for the generation of each different tissue or organ. This may be why glassware experiments with stem cells have not yet lived up to their full promise.

Concern about human cells’ incorporation into a lower animal’s brain is not without basis. Dr. Steven Goldman of the University of Rochester Medical Center found in 2013 that mice injected with a special type of human brain cell had enhanced learning abilities.

because the mutation is specific to the tumor — and can serve as a sort of beacon to properly designed immune cells — it might actually be this cancer's Achilles' heel.

treatment involves taking patients' T cells, then inserting a new gene that allows the cells to recognize the mutant protein.

the cells can be reinfused and begin their task of zeroing in on and eliminating cells with the mutation.

"It's taking an antibody, which is typically a kind of molecule that's circulating around in the blood," said Maus. "And it's fusing it to proteins that will cross the membrane and that then will signal to T cells to replicate and kill."

Whatever else, it is sure to unnerve most of us.

Scientists, for example, should never create a Sheef that feels pain.

Scientists began grappling with the ethics of lab-raised embryos more than four decades ago.

In 1979, a federal advisory board recommended that the cutoff should be 14 days.

The embryonic cells develop into three types, called germ layers. Each of those germ layers goes on to produce all the body’s tissues and organs.

This triggered communication by the cells, and they organized themselves into the arrangement found in an early mouse embryo.

Even if ethicists do manage to agree on certain limits, Paul S. Knoepfler, a stem cell biologist at the University of California, Davis, wondered how easy it would be for scientists to know if they had crossed them.

Spotting a primitive streak is easy. Determining whether a collection of neurons connected to other tissues in a dish can feel pain is not.

Associate Professor Ruth Empson of Otago's Department of Physiology says these innovations are powerful new techniques that will greatly advance worldwide efforts to understand how different parts of the brain connect and communicate during behaviour

Dr. Krogan and his colleagues set about finding proteins in our cells that the coronavirus uses to grow. Normally, such a project might take two years. But the working group, which includes 22 laboratories, completed it in a few weeks.

In 2011, Dr. Krogan and his colleagues developed a way to find all the human proteins that viruses use to manipulate our cells — a “map,” as Dr. Krogan calls it. They created their first map for H.I.V.

That virus has 18 genes, each of which encodes a protein. The scientists eventually found that H.I.V. interacts, in one way or another, with 435 proteins in a human cell.

In February, the research group synthesized genes from the coronavirus and injected them into cells. They uncovered over 400 human proteins that the virus seems to rely on.

The flulike symptoms observed in infected people are the result of the coronavirus attacking cells in the respiratory tract.

The new map shows that the virus’s proteins travel throughout the human cell, engaging even with proteins that do not seem to have anything to do with making new viruses.

Kevan Shokat, a chemist at U.C.S.F., is poring through 20,000 drugs approved by the Food and Drug Administration for signs that they may interact with the proteins on the map created by Dr. Krogan’s lab.

If promising drugs are found, investigators plan to try them in an animal infected with the coronavirus — perhaps ferrets, because they’re known to get SARS, an illness closely related to Covid-19.

Even if some of these drugs are effective treatments, scientists will still need to make sure they are safe for treating Covid-19. It may turn out, for example, that the dose needed to clear the virus from the body might also lead to dangerous side effects.

In past studies on animals, remdesivir blocked a number of viruses. The drug works by preventing viruses from building new genes.

In February, a team of researchers found that remdesivir could eliminate the coronavirus from infected cells. Since then, five clinical trials have begun to see if the drug will be safe and effective against Covid-19 in people.

Other researchers have taken startling new approaches. On Saturday, Stanford University researchers reported using the gene-editing technology Crispr to destroy coronavirus genes in infected cells.

During this time, the BrainEx system not only preserved brain cell structure and reduced cell death, but also restored some cellular activity.

For example, although scientists are a long way from being able to restore brain function in people with severe brain injuries, if some restoration of brain activity is possible, "then we would have to change our definition of brain death," Singhal told Live Science.

The work also could stimulate research on ways to promote brain recovery after loss of blood flow to the brain, such as during a heart attack.

Yehoash Raphael of the University of Michigan, who didn't participate in the work, said it's possible the stem cell transplants worked by stimulating the gerbils' own few remaining nerve cells, rather than creating new ones. But either way, "this is a big step forward in use of stem cells for treating deafness," he said.

"If you could clear senescent cells, you perhaps could treat age-related diseases as a group rather than individually," said Jan van Deursen, senior author of the paper and a professor in the departments of biochemistry and pediatric and adolescent medicine at Mayo.

When cells become senescent, they produce harmful compounds such as those that cause inflammation. Chronic tissue inflammation with aging is thought to underlie dementia, atherosclerosis and diabetes, among other ills,

Because senescence is believed to have developed as a defense against cancer, in which cells divide uncontrollably, simply halting the process could be dangerous. But scientists have wondered for decades if the damage inflicted by senescent cells could be stopped if they were removed from the body altogether, or if the harmful substances they produced were neutralized.

This kind of modeling is already in use to study individual cellular processes like metabolism. But Dr. Covert said: “Where I think our work is different is that we explicitly include all of the genes and every known gene function. There’s no one else out there who has been able to include more than a handful of functions or more than, say, one-third of the genes.”

The simulation, which runs on a cluster of 128 computers, models the complete life span of the cell at the molecular level, charting the interactions of 28 categories of molecules — including DNA, RNA, proteins and small molecules known as metabolites, which are generated by cell processes.

They called the simulation an important advance in the new field of computational biology, which has recently yielded such achievements as the creation of a synthetic life form — an entire bacterial genome created by a team led by the genome pioneer J. Craig Venter. The scientists used it to take over an existing cell.

A decade ago, scientists developed simulations of metabolism that are now being used to study a wide array of cells, including bacteria, yeast and photosynthetic organisms. Other models exist for processes like protein synthesis.

“Right now, running a simulation for a single cell to divide only one time takes around 10 hours and generates half a gigabyte of data,” Dr. Covert wrote. “I find this fact completely fascinating, because I don’t know that anyone has ever asked how much data a living thing truly holds. We often think of the DNA as the storage medium, but clearly there is more to it than that.”

scientists chose an approach called object-oriented programming, which parallels the design of modern software systems. Software designers organize their programs in modules, which communicate with one another by passing data and instructions back and forth.

“The major modeling insight we had a few years ago was to break up the functionality of the cell into subgroups, which we could model individually, each with its own mathematics, and then to integrate these submodels together into a whole,”

“Usually by four to six weeks, there’s not much left,” said Deepta Bhattacharya, an immunologist at the University of Arizona. But germinal centers stimulated by the mRNA vaccines are “still going, months into it, and not a lot of decline in most people.”

The broader the range and the longer these cells have to practice, the more likely they are to be able to thwart variants of the virus that may emerge.

“Everyone always focuses on the virus evolving — this is showing that the B cells are doing the same thing,” said Marion Pepper, an immunologist at the University of Washington in Seattle. “And it’s going to be protective against ongoing evolution of the virus, which is really encouraging.”

Dr. Ellebedy’s team found that 15 weeks after the first dose of vaccine, the germinal center was still highly active in all 14 of the participants, and that the number of memory cells that recognized the coronavirus had not declined.

“The fact that the reactions continued for almost four months after vaccination — that’s a very, very good sign,” Dr. Ellebedy said. Germinal centers typically peak one to two weeks after immunization, and then wane.

After an infection or a vaccination, a specialized structure called the germinal center forms in lymph nodes. This structure is an elite school of sorts for B cells — a boot camp where they become increasingly sophisticated and learn to recognize a diverse set of viral genetic sequences.

The results suggest that a vast majority of vaccinated people will be protected over the long term — at least, against the existing coronavirus variants

But older adults, people with weak immune systems and those who take drugs that suppress immunity may need boosters; people who survived Covid-19 and were later immunized may never need them at all.

In the absence of variants that sidestep immunity, in theory immunity could last a lifetime, experts said. But the virus is clearly evolving.

“Anything that would actually require a booster would be variant-based, not based on waning of immunity,” Dr. Bhattacharya said. “I just don’t see that happening.”

The good news: A booster vaccine will probably have the same effect as prior infection in immunized people, Dr. Ellebedy said. “If you give them another chance to engage, they will have a massive response,” he said, referring to memory B cells.

Dr. Ellebedy said the results also suggested that these signs of persistent immune reaction might be caused by mRNA vaccines alone, as opposed to those made by more traditional means, like Johnson & Johnson’s

But that is an unfair comparison, because the Johnson & Johnson vaccine is given as a single dose, Dr. Iwasaki said: “If the J & J had a booster, maybe it will induce this same kind of response.”

"The science tells [us] when [we're] on the phone while driving, it is a high-risk activity -- very, very risky,"

Even hands-free phones appear to contribute to unsafe driving

These sorts of injuries, known as repetitive strain injuries or a repetitive motion disorders, are sometimes minor. But they can also lead to serious medical problems.

Our reliance on our cell phones may actually be "training" some of us to believe it is vibrating when it is not. In the case of cell phones, people are rewarded when they pick up their calls and read their incoming text messages, which causes them to pick up their cell phones more and more frequently.

The sores and blisters that some experience from too much texting and typing have earned monikers such as "BlackBerry thumb." And while the sore thumbs may seem like a new phenomenon, medical experts say there is a rational explanation for this modern-day nuisance.

What they found was that when children were on the cell phones, their attention to traffic -- the number of times a participant looked right or left -- went down 20 percent. The risk of getting hit by a car, or the number of close calls, went up 43 percent

According to statistics from the U.S. Centers for Disease Control and Prevention (http://www.cdc.gov/healthyyouth/noise/index.htm), about 12.5 percent of children and adolescents 6 and 19 years old and 17 percent of adults between 20 and 69 years of age have suffered permanent damage to their hearing from excessive exposure to noise. In total, this accounts for more than 30 million people.

Sounds louder than 85 decibels can damage hearing. Normal conversation is about 60 decibels, and stereo headphones out of our MP3-enabled devices often reach 100 decibels.

it’s unclear whether infectious virus can persist in blood or stool

the infection can spread through the mucous membranes, from the nose down to the rectum.

while the virus appears to zero in on the lungs, it may also be able to infect cells in the gastrointestinal system, experts say. This may be why some patients have symptoms like diarrhea or indigestion

“The virus will actually land on organs like the heart, the kidney, the liver, and may cause some direct damage to those organs,

some patients in China recovered but got sick again, apparently because they had damaged and vulnerable lung tissue that was subsequently attacked by bacteria in their body.

As the body’s immune system shifts into high gear to battle the infection, the resulting inflammation may cause those organs to malfunction, he said.

About 80 percent of people infected with the new coronavirus have relatively mild symptoms. But about 20 percent of people become more seriously ill and in about 2 percent of patients in China, which has had the most cases, the disease has been fatal.

the effects appear to depend on how robust or weakened a person’s immune system is. Older people or those with underlying health issues, like diabetes or another chronic illness, are more likely to develop severe symptoms

the course a patient’s coronavirus will take is not yet fully understood.

Some patients can remain stable for over a week and then suddenly develop pneumonia, Dr. Diaz said. Some patients seem to recover but then develop symptoms again.

more than half of 121 patients in China had normal CT scans early in their disease.

Coronavirus particles have spiked proteins sticking out from their surfaces, and these spikes hook onto cell membranes, allowing the virus’s genetic material to enter the human cell.

That genetic material proceeds to “hijack the metabolism of the cell and say, in effect, ‘Don’t do your usual job. Your job now is to help me multiply and make the virus,’

As copies of the virus multiply, they burst out and infect neighboring cells. The symptoms often start in the back of the throat with a sore throat and a dry cough.

The virus then “crawls progressively down the bronchial tubes,”

That can damage the alveoli or lung sacs and they have to work harder to carry out their function of supplying oxygen to the blood

The swelling and the impaired flow of oxygen can cause those areas in the lungs to fill with fluid, pus and dead cells. Pneumonia, an infection in the lung, can occur

Some people have so much trouble breathing they need to be put on a ventilator

In the late 1900s, researchers discovered that mitochondria were free-living bacteria at some point in the past. Somehow they were drawn inside another cell, providing new fuel for their host. In 2015, Thijs Ettema of Uppsala University in Sweden and his colleagues discovered fragments of DNA in sediments retrieved from the Arctic Ocean. The fragments contained genes from a species of archaea that seemed to be closely related to eukaryotes.Dr. Ettema and his colleagues named them Asgard archaea. (Asgard is the home of the Norse gods.) DNA from these mystery microbes turned up in a river in North Carolina, hot springs in New Zealand and other places around the world.

Masaru K. Nobu, a microbiologist at the National Institute of Advanced Industrial Science and Technology in Tsukuba, Japan, and his colleagues managed to grow these organisms in a lab. The effort took more than a decade.The microbes, which are adapted to life in the cold seafloor, have a slow-motion existence. Prometheoarchaeum can take as long as 25 days to divide. By contrast, E. coli divides once every 20 minutes.

In the lab, the researchers mimicked the conditions in the seafloor by putting the sediment in a chamber without any oxygen. They pumped in methane and extracted deadly waste gases that might kill the resident microbes.The mud contained many kinds of microbes. But by 2015, the researchers had isolated an intriguing new species of archaea. And when Dr. Ettema and colleagues announced the discovery of Asgard archaea DNA, the Japanese researchers were shocked. Their new, living microbe belonged to that group.The researchers then undertook more painstaking research to understand the new species and link it to the evolution of eukaryotes.The researchers named the microbe Prometheoarchaeum syntrophicum, in honor of Prometheus, the Greek god who gave humans fire — after fashioning them from clay.

This finding suggests that the proteins that eukaryotes used to build complex cells started out doing other things, and only later were assigned new jobs.Dr. Nobu and his colleagues are now trying to figure out what those original jobs were. It’s possible, he said, that Prometheoarchaeum creates its tentacles with genes later used by eukaryotes to build cellular skeletons.

Before the discovery of Prometheoarchaeum, some researchers suspected that the ancestors of eukaryotes lived as predators, swallowing up smaller microbes. They might have engulfed the first mitochondria this way.

Instead of hunting prey, Prometheoarchaeum seems to make its living by slurping up fragments of proteins floating by. Its partners feed on its waste. They, in turn, provide Prometheoarchaeum with vitamins and other essential compounds.

Because cells are connected in a network, brain activity produces a synchronised pulse of electrical activity, which is called a “brain wave”.

Brainwaves are detected using a technique known as electroencephalography (EEG),

The pattern of activity is then recorded and interpreted using computer software.

The electrical nature of the brain allows not only for sending of signals, but also for the receiving of electrical pulses

A TMS device creates a magnetic field over the scalp, which then causes an electrical current in the brain.

The connection was reinforced by giving both rats a reward when the receiver rat performed the task correctly.

By combining EEG and TMS, scientists have transmitted the thought of moving a hand from one person to a separate individual, who actually moved their hand.

including EEG, the Internet and TMS – the team of researchers was able to transmit a thought all the way from India to France.

Words were first coded into binary notation

Now that these BBI technologies are becoming a reality, they have a huge potential to impact the way we interact with other humans. And maybe even the way we communicate with animals through direct transmission of thought.

Such technologies have obvious ethical and legal implications, however. So it is important to note that the success of BBIs depends upon the conscious coupling of the subjects.

Maybe not, according to an admonitory new study of the molecular effects of high-intensity interval training

suggesting that the benefits of extremely vigorous exercise may depend on just how much we do.

for example, that intense bursts of exercise increase the number of mitochondria in our muscle cells, and more mitochondria are thought to contribute to better cellular and metabolic health.

HIIT also may have unexpected downsides. In a study I wrote about in January, people who worked out with HIIT routines three times a week for six weeks did not improve their blood pressure or body fat as much as people who exercised far more moderately five times a week.

by being sedentary for four days each week, the intense exercisers in the study may have undermined the otherwise potent effects of their HIIT sessions.

These volunteers visited the researchers’ lab for tests of their current fitness and metabolic health, including blood-sugar levels over the course of a day.

Then they compared how people’s bodies had changed week over week.

At first, the findings were encouraging. By the end of week two, the riders were pedaling harder and appeared to be getting fitter, with better daily blood-sugar control and more total mitochondria in their muscle cells.

But something began to go wrong during week three. The volunteers’ ability to generate power while cycling flattened, and their subsequent muscle biopsies showed sputtering mitochondria, each of which was now producing only about 60 percent as much energy as during the previous week. The riders’ blood-sugar control also slipped, with se

The researchers are not sure precisely what changes within their volunteers’ bodies and muscles precipitated the negative results in week three.

Even so, the findings strongly suggest that anyone interested in high-intensity interval training start small, Mr. Flockhart says. Train a few times a week and on the remaining days, maybe take a walk.