Bursts of vigorous activity lasting two minutes at a time and totaling just 15 minutes a week are associated with a reduced risk of death. This is according to new research that was published on October 27 in the European Heart Journal, a journal of the European Society of Cardiology (ESC).[1]

“The results indicate that accumulating vigorous activity in short bouts across the week can help us live longer,” said study author Dr. Matthew N. Ahmadi of the University of Sydney, Australia. “Given that lack of time is the most commonly reported barrier to regular physical activity, accruing small amounts sporadically during the day may be a particularly attractive option for busy people.”

A second study found that for a given amount of physical activity, increasing the intensity was associated with a reduced likelihood of cardiovascular disease. This study was also published on October 27 in the European Heart Journal.[2] “Our study shows that it’s not just the amount of activity, but also the intensity, that is important for cardiovascular health,” said study author Dr. Paddy C. Dempsey of the University of Leicester and University of Cambridge, UK, and the Baker Heart and Diabetes Institute, Melbourne, Australia.

Both studies included adults aged 40 to 69 years from the UK Biobank, a large-scale biomedical database and research resource. Participants wore an activity tracker on their wrists for seven consecutive days. This is an objective way to measure motion and is a particularly good way to gauge sporadic activity of different intensities during the day.

71,893 adults without cardiovascular disease or cancer were enrolled in the first study. Participants had a median age of 62.5 years and 56% were women. The researchers measured the total amount of weekly vigorous activity and the frequency of bouts lasting two minutes or less. Participants were followed for an average of 6.9 years. After excluding events occurring in the first year, the investigators analyzed the associations of volume and frequency of vigorous activity with death (all-cause, cardiovascular disease, and cancer) and incidence of cardiovascular disease and cancer.

The risk of all five adverse outcomes reduced as the volume and frequency of vigorous activity increased, with benefits seen even with small amounts. For example, participants with no vigorous activity had a 4% risk of dying within five years. Risk was halved to 2% with less than 10 minutes of weekly vigorous activity, and fell to 1% with 60 minutes or more.

Compared with just two minutes of vigorous activity per week, 15 minutes was associated with an 18% lower risk of death and a 15% lower likelihood of cardiovascular disease, while 12 minutes was associated with a 17% reduced risk of cancer. Further gains were observed with greater amounts of vigorous activity. For instance, approximately 53 minutes a week was associated with a 36% lower risk of death from any cause.

Regarding frequency, accumulating short bouts (up to two minutes) of vigorous activity on average four times a day was associated with a 27% lower risk of death. But health benefits were observed at even lower frequencies: 10 short bouts a week was associated with 16% and 17% lower risks of cardiovascular disease and cancer, respectively.

The second study included 88,412 adults free of cardiovascular disease. The average age was 62 years and 58% were women. The investigators estimated the volume and intensity of physical activity, then analyzed their associations with incident cardiovascular disease (ischaemic heart disease or cerebrovascular disease). Participants were followed for a median 6.8 years.

The researchers found that both higher amounts and greater intensity were associated with lower rates of incident cardiovascular disease. Increasing the intensity led to greater reductions in cardiovascular disease for the same volume of exercise. For example, the rate of cardiovascular disease was 14% lower when moderate-to-vigorous activity accounted for 20% rather than 10% of activity, the equivalent of converting a 14-minute stroll into a brisk seven-minute walk.

Dr. Dempsey said: “Our results suggest that increasing the total volume of physical activity is not the only way to reduce the likelihood of developing cardiovascular disease. Raising the intensity was also particularly important, while increasing both was optimal. This indicates that boosting the intensity of activities you already do is good for heart health. For example, picking up the pace on your daily walk to the bus stop or completing household chores more quickly.”

Source

Bivalent booster is 4x better against BA.5 in older adults, Pfizer says

Since science keeps on revealing secrets, models keep getting bigger. They integrate discoveries and newly found mechanisms to better reflect the world around us. Many scholars assume that more detailed models produce sharper estimates and better predictions because they are closer to reality. But our new research, published in Science Advances, suggests they may have the opposite effect.

The assumption that "more detail is better" cuts across disciplinary fields. The ramifications are enormous. Universities get more and more powerful computers because they want to run bigger and bigger models, requiring an increasing amount of computing power. Recently, the European Commission invested €8bn euros (£6.9bn) to create a very detailed simulation of the Earth (with humans), dubbed a "digital twin," hoping to better address current social and ecological challenges.

In our latest research, we show that the pursuit of ever more complex models as tools to produce more accurate estimates and predictions may not work. Based on statistical theory and mathematical experiments, we ran hundreds of thousands of models with different configurations and measured how uncertain their estimations are.

We discovered that more complex models tended to produce more uncertain estimates. This is because new parameters and mechanisms are added. A new parameter, say the effect of chewing gum on the spread of a disease, needs to be measured—and is therefore subject to measurement errors and uncertainty. Modelers may also use different equations to describe the same phenomenon mathematically.

Once these new additions and their associated uncertainties are integrated into the model, they pile on top of the uncertainties already there. And uncertainties keep on expanding with every model upgrade, making the model output fuzzier at every step of the way—even if the model itself becomes more faithful to reality.

This affects all models that do not have appropriate validation or training data against which to check the accuracy of their output. This includes global models of climate change, hydrology (water flow), food production and epidemiology alike, as well as all models predicting future impacts.

Fuzzy results

In 2009, engineers created an algorithm called Google Flu Trends for predicting the proportion of flu-related doctor visits across the US. Despite being based on 50 million queries that people had typed into Google, the model wasn't able to predict the 2009 swine flu outbreak. The engineers then made the model, which is no longer operating, even more complex. But it still wasn't all that accurate. Research led by German psychologist Gerd Gigerenzer showed it consistently overestimated doctor visits in 2011–13, in some cases by more than 50%.

Gigerenzer discovered that a much simpler model could produce better results. His model predicted weekly flu rates based only on one teeny piece of data: how many people had seen their GP the previous week.

Another example is global hydrological models, which track how and where water moves and is stored. They started simple in the 1960s based on "evapotranspiration processes" (the amount of water that could evaporate and transpire from a landscape covered in plants) and soon got extended, taking into account domestic, industrial and agricultural water uses at the global scale. The next step for these models is to simulate water demands on Earth for every kilometer each hour.

And yet one wonders if this extra detail will not just make them even more convoluted. We have shown that estimates of the amount of water used in irrigation produced by eight global hydrological models can be calculated with a single parameter only—the extent of the irrigated area.

Ways forward

Why has the fact that more detail can make a model worse been overlooked until now? Many modelers do not submit their models to uncertainty and sensitivity analysis, methods that tell researchers how uncertainties in the model affect the final estimation. Many keep on adding detail without working out which elements in their model are most responsible for the uncertainty in the output.

It is concerning as modelers are interested in developing ever larger models—in fact, entire careers are built on complex models. That's because they are harder to falsify: their complexity intimidates outsiders and complicates understanding what is going on inside the model.

There are remedies, however. We suggest ensuring that models don't keep getting larger and larger for the sake of it. Even if scientists do perform an uncertainty and sensitivity analysis, their estimates risk getting so uncertain that they become useless for science and policymaking. Investing a lot of money in computing just to run models whose estimate is completely fuzzy makes little sense.

Modelers should instead ponder how uncertainty expands with every addition of detail into the model—and find the best trade-off between the level of model detail and uncertainty in the estimation.

To find this trade-off, one can use the concept of "effective dimensions"—a measure of the number of parameters which add uncertainty to the final output, taking into account how these parameters interact with each other—which we define in our paper.

By calculating a model's effective dimensions after each upgrade, modelers can appraise whether the increase in uncertainty still makes the model suitable for policy—or, in contrast, if it makes the model's output so uncertain as to be useless. This increases transparency and helps scientists design models that better serve science and society.

Some modelers may still argue that the addition of model detail can lead to more accurate estimates. The burden of proof now lies with them.

Journal information: Science Advances

Provided by The Conversation

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Source

“Folks at Twitter past and present are strong and resilient,” Dorsey said on Twitter on Saturday morning. “They will always find a way no matter how difficult the moment. I realize many are angry with me. I own the responsibility for why everyone is in this situation: I grew the company size too quickly. I apologize for that.”

Dorsey, who also stepped down from Twitter’s board five months ago, added that he’s “grateful for, and love, everyone who has ever worked at Twitter. I don’t expect that to be mutual in this moment…or ever…and I understand.”

This is Dorsey’s first public comment since Musk took over the platform last week. In the past, Dorsey said that Musk is the “singular solution I trust.”

Leaked documents from the Elon Musk v. Twitter trial give some insight into how Dorsey was thinking about the future of the social media company. Dorsey texted Musk that he left because Twitter needed to become a new platform – one that isn’t a company.

“I believe it must be an open source protocol, funded by a foundation of sorts that doesn’t own the protocol, only advances it. A bit like what Signal has done. It can’t have an advertising model,” Dorsey texted Musk.

Yesterday, impacted Twitter employees used the hashtag #LoveWhereYouWorked, a riff on the internal hashtag #LoveWhereYouWork, to thank each other, say goodbye and share personal news. As one former employee put it, the new hashtag is a “bittersweet phrase — not because I’m gone, but because it’s gone.”

Despite Dorsey’s departure from his official roles at Twitter, his silence was noticed. Musk, meanwhile, addressed the layoffs on Friday evening.

“Regarding Twitter’s reduction in force, unfortunately there is no choice when the company is losing over [$4 million a day],” Musk tweeted.

“Everyone exited was offered 3 months of severance, which is 50% more than legally required.”

Source

A study recently published in Animal Behavior suggests that bumblebees, when given the chance, like to fool around with toys.

Researchers from Queen Mary University of London conducted an experiment in which they set up a container that allowed bees to travel from their nest to a feeding area. But along the way, the bees could opt to pass through a separate section with a smattering of small wooden balls. Over 18 days, the scientists watched as the bees "went out of their way to roll wooden balls repeatedly, despite no apparent incentive to do so."

The finding suggests that like humans, insects also interact with inanimate objects as a form of play. Also similar to people, younger bees seemed to be more playful than adult bees.

In this experiment from researchers at Queen Mary University of London, bumblebees, especially young ones, appeared to show they liked to cling to wooden balls twice their size and roll them around just for the fun of it.

Samadi Galpayage, Queen Mary University of London YouTube

"This research provides a strong indication that insect minds are far more sophisticated than we might imagine," Lars Chittka, a professor of sensory and behavioral ecology at Queen Mary University of London, who led the study, said in a statement.

Earlier studies have shown that the black and yellow bugs are willing to learn new tricks in exchange for food or other rewards, so in this case Chittka and his team set out to create conditions that would eliminate external variables. They made sure that the bees had acclimated to their new home and that their environment was stress free.

In one experiment, the bees, which were tracked by age and sex, could make their way through an unobstructed path to a feeding area or opt for a detour into a chamber with the wooden balls. Many took the detour. Video shows the chubby insects clinging to balls (about twice the size of the bees) and maneuvering them around. In more comical moments, some bees appeared to do somersaults while holding on. Other times they would walk in reverse, pulling the ball with them — an unnatural movement for bumblebees.

"There are lots of animals who play just for the purposes of enjoyment, but most examples come from young mammals and birds," said Chittka.

The study's first author, Samadi Galpayage, who is a PhD student at Queen Mary University of London, added that it is yet more evidence that insects may be capable of experiencing feelings.

"They may actually experience some kind of positive emotional states, even if rudimentary, like other larger fluffy, or not so fluffy, animals do. This sort of finding has implications to our understanding of sentience and welfare of insects and will, hopefully, encourage us to respect and protect life on Earth ever more," she said in the statement.

Source

The collapse of a bridge in Gujarat that left 135 people dead has prompted concerns over the safety of thousands of other colonial-era structures across India.

The bridge in Morbi was more than a century old when it snapped in two last month while families had gathered on it to enjoy an evening on the river. Many of those standing in the middle of the bridge plunged into the river and drowned, while others died from the impact of falling on to the stones and boulders below.

The Gujarat government, ruled by the Bharatiya Janata party (BJP), had given the contract for repairing the 100-year-old suspension bridge to a local company called Oreva, which makes clocks.

People live and work by Delhi’s Old Iron Bridge, built in 1866, on the Yamuna River. Photograph: Hindustan Times/Getty Images

Now fears are growing for India’s other ageing bridges. The country has about 173,000 bridges and about 36,470 of them were built under the Raj. Almost 6,700 are even older, with some built 140 years ago, according to the most recent information in the Railways Audit Report of 2015.

Many of them are technically “distressed”, meaning they are dilapidated, probably risky, and in need of urgent repair or reinforcement.

The Indian Bridge Management System centre estimates that at least 5,300 bridges are structurally distressed and need attention. One state alone, Uttar Pradesh, had as many as 226 distressed bridges in 2018.

Sahil Mhatre, a member of the Indian Institution of Bridge Engineers, said many distressed and old bridges were “structurally unaudited” and this was a matter of concern because those built by the British were intended for far smaller loads. “The government should be doing structural audits every three to four years, using strain gauge sensors to check the quality of the concrete for cracks or vibrations, to see if they can take the load on them. In modern bridges, sensors are embedded in the structure to sound alerts but India’s old bridges obviously don’t have them,” he said.

The rescue operation after the collapse of the Morbi suspension bridge last week. Photograph: Divyakant Solanki/EPA

In 2018, a parliamentary committee found that India’s railway bridges were a risk to passengers and in dire need of upgrading. It reprimanded the railways for inordinate delays in repairing distressed bridges, which it said resulted in “the possibility of compromising passenger safety”.

Its report also praised old British bridges for their quality: “While certain railway bridges constructed during British rule are in good condition, railway bridges constructed … after independence are of inferior quality and need frequent repair … [The] nexus between railway officials and a few contractors severely affects the quality and life of its construction.”

A bridge over the Yamuna River over in Allahabad. Photograph: Sanjay Kanojia/AFP/Getty Images

However, India’s prime minister, Narendra Modi, has been notoriously critical of Britain’s legacy in India, targeting the English language and branding it a “colonial relic’ that has generated a “slavish mentality”. Abide with Me has been removed from India’s annual republic day celebrations and replaced with a Hindi patriotic song, and the Indian army is considering whether to do away with the English names of some army regiments.

But Modi’s critics have asked if his priorities are misplaced. “Instead of renaming streets and attacking English, the BJP would do better to face the real challenge, namely, to maintain colonial-era bridges that have lasted so long but are now coping with loads they were never intended to handle,” said commentator Parsa Venkateshwar Rao Jr.

One of them is the old Yamuna Bridge in the Indian capital, which was built in 1866, making it one of the oldest in the country. Poor labourers sleep and live under the iron girders.

“The thousands of commuters who use it every day are risking their lives. It was meant for horses, carriages and pack animals. Now it’s got trains and cars on it,” said Atul Bose, who works with slum dwellers in the area.

Jatin L Singh, founder of the Rail Enthusiasts’ Society, marvelled at how far-sighted British-era engineers were in designing bridges in such a way that they allowed for additional capacity to be added later.

“The former Jubilee Bridge over the River Hooghly in Calcutta, built to mark Queen Victoria’s 50th anniversary, opened in 1885. It had one track for trains but the engineers created capacity for two tracks in case it was needed in future, which of course it was,” said Singh. After 131 years, the bridge was decommissioned in 2016.

Source

Terry Horgan, a 27-year-old who had Duchenne muscular dystrophy, died last month, according to Cure Rare Disease, a Connecticut-based nonprofit founded by his brother, Rich, to try and save him from the fatal condition.

Although little is known about how he died, his death occurred during one of the first studies to test a gene editing treatment built for one person. It’s raising questions about the overall prospect of such therapies, which have buoyed hopes among many families facing rare and devastating diseases.

“This whole notion that we can do designer genetic therapies is, I would say, uncertain,” said Arthur Caplan, a medical ethicist at New York University who is not involved in the study. “We are out on the far edge of experimentation.”

The early-stage safety study was sponsored by the nonprofit, led by Dr. Brenda Wong at the University of Massachusetts Chan Medical School and approved by the Food and Drug Administration. The hope was to use a gene-editing tool called CRISPR to treat Horgan’s particular form of Duchenne muscular dystrophy. The rare, genetic muscle-wasting disease is caused by a mutation in the gene needed to produce a protein called dystrophin. Most people with Duchenne die from lung or heart issues caused by it.

At this point, it’s unclear whether Horgan received the treatment and whether CRISPR, other aspects of the study or the disease itself contributed to his death. Deaths are not unheard of in clinical trials, which test experimental treatments and sometimes involve very sick people.

But trials involving CRISPR are relatively new. And Fyodor Urnov, a CRISPR expert at the Innovative Genomics Institute at University of California, Berkeley, said any death during a gene therapy trial is an opportunity for the field to have a reckoning.

“Step one is to grieve for the passing of a brave human soul who agreed to be basically a participant in an experiment on a human being,” Urnov said. “But then, to the extent that we can, we must learn as much as we can to carve out a path forward.”

< Watch the video at the Source page. >

A statement from Cure Rare Disease said multiple teams across the country are looking into the details of the trial and its outcome, and the company intends to share findings with the scientific community.

“It will probably be 3-4 months to come up with a full conclusion,” said spokesman Scott Bauman. “At this stage of the game, saying anything is pure speculation.”

The company, which is also working on 18 other therapeutics, said in its statement that the teams’ work is essential not only to shed light on the study’s outcome but also “on the challenges of gene therapy broadly.” Meanwhile, it said, “we will continue to work with our researchers, collaborators, and partners to develop therapies for the neuromuscular diseases in our pipeline.”

Bauman said the company has filed a report on death the with the FDA as required. The FDA declined to release or confirm the report.

Sarah Willey, spokeswoman for Chan Medical School, said scientists there provided data to the company for the report. She later emailed to say no one there would comment further; out of respect for the family’s wishes, all information would come from Cure Rare Disease. Monkol Lek, a Yale genetics expert who has been collaborating on the effort, did not respond to a request for comment. Yale spokeswoman Bess Connolly asked a reporter for context on the story but didn’t respond to a follow-up email or phone call.

A crucial question is whether CRISPR played a part in Horgan’s death.

The chemical tool can be used to “edit” genes by making cuts or substitutions in DNA. The tool has transformed genetic research and sparked the development of dozens of experimental therapies. The inventors of the tool won a Nobel Prize in 2020.

In this case, scientists used a modified form of CRISPR to increase the activity of a gene. The CRISPR therapeutic is inserted directly into the body and delivered to cells with a virus.

But CRISPR is not perfect.

“We know that CRISPR can miss its target. We know that CRISPR can be partially effective. And we also know that there may be issues with … viral vectors” that deliver the therapy into the body, Caplan said. “Red flags are flying here. We’ve got to make sure that they get addressed very, very quickly.”

Safety issues have arisen in gene therapy studies before. Late last year, Pfizer reported the death of a patient in its early-stage trial for a different Duchenne muscular dystrophy gene therapy. And in a major earlier setback for the gene therapy field, 18-year-old Jesse Gelsinger died in 1999 during a study that involved placing healthy genes into his liver to combat a rare metabolic disease. Scientists later learned that his immune system overreacted to the virus used to deliver the therapy. Many recent studies, including the Cure Rare Disease trial, use a different virus that’s considered safer.

Another difference? The recent trial involved just one person — a type of trial Caplan is skeptical about.

Horgan’s recent death, he said, “may make us think whether we really do like studies that are just on one person, and do we want to say: ‘No, ethically, you’ve got to at least have a trial where you line up 5, 10, 20 people (and) you learn from the data.’ ”

A ‘MEDICAL PIONEER’

On the company’s web site, Horgan was described as a “medical pioneer” who “will be remembered as a hero.”

In 2020, the Montour Falls, New York resident blogged that he was diagnosed with Duchenne at age 3. As a kid, he said, he loved computers — once building his own — and would play catch in the driveway with his family when he could still walk. Later in his life, he used a motorized wheelchair. He studied information science at Cornell University and went on to work at the school in the information science department.

“As I grew up and began to understand what it meant to have DMD, my fears about this disease began to grow as it began to manifest,” Horgan wrote. “There weren’t many, or any, trials available to me through the years” — until this one brought the prospect of a customized drug.

Horgan was enrolled in the study on Aug. 31. The plan was to suppress his immune system to prep his body for a one-time, gene-editing therapy delivered by IV at UMass medical school, followed by monitoring in the hospital. The company explained that the therapy is designed to increase the level of an alternate form of the dystrophin protein using CRISPR, with the goal of stabilizing or potentially reversing the progression of symptoms.

Urnov, scientific director for technology and translation at the Berkeley genomics institute, said no other trial targeted this disease using this kind of virus to deliver this particular payload with its modified form of CRISPR.

Some other gene therapy trials – such as those targeting the blood disorders sickle cell disease and beta thalassemia – involve removing stem cells from someone’s blood, using CRISPR in the lab, then putting the altered cells back into the person. The first time CRISPR was used to edit genes within the body was to address a blindness-causing mutation.

Given the “exceptional distinctness” of the Cure Rare Disease approach, Urnov said he doesn’t think Horgan’s death will have a major impact on things like using gene therapy to fix blood diseases. But he said pinpointing the exact cause will help inform scientists throughout the field.

“History teaches us that in the case of such fatalities – which have been rare – that a deep dive into what happened was critical for the field to move forward.”

Source

“We’re really at a point that may be a crossroads here. As we’re entering into the cooler months, we are starting to see the emergence of sublineage variants of omicron,” White House advisor Dr. Anthony Fauci said on the Conversations on Health Care radio show yesterday.

In fact, across the country, the long-dominant BA.5 variant no longer holds that distinction. It is being pushed out by a rogue’s gallery of new strains including BQ1.1, BQ1, BA4.6 and BF.7, the combined proportions of which are now larger than BA.5 for the first time in months.

Variant proportions over time, courtesy CDC

For the past month, LA County has been noting signals that the local case rate may no longer be declining. The steady drop observed since July appeared to plateau in mid-October — and now indicators look to be headed upward.

This week, L.A. County is reporting a nearly 10% increase in the 7-day-average number of cases from one week ago. Today, L.A. County Public Health reported 7 additional deaths and 1,447 new positive cases. That number of new cases, while certainly an undercount, is the highest single day tally in weeks.

The 7-day average test positivity rate has risen more than 25% in the past week, to 5% today. That’s quite a jump in a number that is averaged over the course of a week to smooth out data hiccups.

Los Angeles County Department of Public Health

 While Omicron BA.5 continues to be the dominant subvariant, each week it is accounting for a smaller proportion of samples in L.A. As of the week ending Oct. 15, it accounted for about 72% of sequenced specimens.  BF.7, a descendant of BA.5, makes up the second largest proportion of cases sequenced at 7.8%.

Recently, county officials added two additional descendant strains of BA.5 to weekly variant reporting: BQ.1 and BQ.1.1. Each of these sublineages account for 3.4% of sequenced specimens for the week ending October 15. There are reports that BQ.1 and BQ.1.1 have some growth advantages over some of the other sublineages, and they may begin to increase here as well.

Over the past seven days, the average number of daily Covid-positive patients in L.A. County hospitals increased slightly to 403. The week before, the average daily Covid-positive patients per day was 389.

Deaths, which typically lag hospitalizations by several weeks, have decreased slightly and they are at an average of 8 deaths reported each day this past week.

“With recent unusually high levels of flu and other respiratory diseases, there are signs the county could be headed toward a Covid surge this fall and winter,” said County Director of Public Health Barbara Ferrer.

Source

In addition to DUI charges, Joseph Yanta, MD, 38, is also facing charges of homicide by vehicle while driving under the influence, involuntary manslaughter, and reckless driving, court records filed earlier this week confirmed.

In the lead-up to the crash, Yanta was driving over 120 mph in a 35-mph zone when he lost control around a bend and crashed the vehicle, data from his Tesla showed.

According to CBS Pittsburgh, Rockacy's family told police that the two physicians had participated in a golf outing and later visited a local pizzeria prior to the accident. While there, Yanta is alleged to have consumed six drinks over a 2.5-hour period, the outlet reported, citing a criminal complaint filed in the case.

Within 2 hours of the accident, police said that Yanta had a 0.172% blood alcohol content, more than double the legal limit. While Yanta was using a seat belt at the time of the crash, Rockacy was not.

An obituary for Rockacy noted that he was "a loving husband, father, brother, son, uncle, and friend."

Rockacy worked at UPMC Mercy, the center's main hospital facility, in Pittsburgh. "He was a dedicated doctor who spent his time treating patients and educating residents," the obituary read. "He was also a devoted father who unconditionally loved his children. He enjoyed golfing with his son, taking his daughter horseback riding, and spending time with family and friends."

UPMC did not respond to MedPage Today's request for comment regarding the charges against Yanta. Legal counsel for Yanta was not immediately clear.

The Pittsburgh Post-Gazette reported earlier this week that a spokesman for UPMC told the outlet that Yanta is not currently seeing patients and has no clinical duties assigned to him at this time.

Source

The logic of getting up and heading to another room comes from considering stimulus control (we learn to behave in a certain way in the presence of a certain stimulus). We want to pair sleep (rather than being awake) with the bedroom environment. Only return to the bedroom when you are ready to sleep.

Although people will differ in terms of what they want to do while up at night, some might be keen to try out relaxation techniques. Breathing exercises come in different forms, but one technique is to breathe in through your nose for the count of four (feeling your tummy fill with air) and then breathe out through your mouth for the count of four (stop immediately if you feel faint).

Mindfulness, which involves being in the moment, without judgment, can also help to reduce stress and support sleep, and some people enjoy taking part in guided meditations.

Mental imagery can also be helpful, and in a study by the eminent psychologist Dr Allison Harvey from the University of California, Berkeley, it was found that the participants of a study who were asked to remember a relaxing scene in detail (and considering how it impacted their different senses) fell asleep more quickly than those who were not asked to do this. One explanation is that the relaxing scene filled up ‘cognitive space’ that could not then be used to engage in stressful or distressing thoughts which could interfere with sleep.

Source

Rocket Report: SLS boosters may expire in December; Blue Origin delivers the BE-4s

University of California, Los Angeles (UCLA) researchers used a molecule present in green tea to uncover more molecules that may break up protein tangles in the brain, which are known to cause Alzheimer’s disease and other disorders.

Tau fibers, which are lengthy, multilayered filaments that create tangles and attack neurons, are known to be broken up by the green tea molecule EGCG.

UCLA biochemists detail how EGCG breaks tau fibers layer by layer in a paper that was recently published in the journal Nature Communications. They also describe how they found other compounds that are likely to function in the same manner and might be better potential candidates for drugs than EGCG, which has difficulty penetrating the brain. The discovery offers up new possibilities for treating Alzheimer’s, Parkinson’s, and other neurodegenerative diseases by developing drugs that target the structure of tau fibers and other amyloid fibrils.

Thousands of J-shaped layers of tau molecules joined together form the type of amyloid fibrils known as tangles, which were originally identified in the post-mortem brain of a dementia patient by Alois Alzheimer a century ago. As these fibers grow and spread throughout the brain, they kill neurons and cause brain atrophy. Many researchers believe that the removal or destruction of tau fibers can slow the progression of dementia.

“If we could break up these fibers we may be able to stop the death of neurons,” said David Eisenberg, UCLA professor of chemistry and biochemistry whose lab led the new research. “Industry has generally failed at doing this because they mainly used large antibodies that have difficulty getting into the brain. For a couple of decades, scientists have known there’s a molecule in green tea called EGCG that can break up amyloid fibers, and that’s where our work departs from the rest.”

EGCG has been studied extensively but has never worked as a drug for Alzheimer’s because its ability to dismantle tau fibers works best in water, and it doesn’t enter cells or the brain easily. Also, as soon as EGCG enters the bloodstream it binds to many proteins besides tau fibers, weakening its efficacy.

To investigate the mechanisms through which EGCG breaks up tau fibers, the researchers extracted tau tangles from the brains of people who died from Alzheimer’s and incubated them for varying amounts of time with EGCG. Within three hours, half the fibers were gone and those that remained were partially degraded. After 24 hours, all the fibers had disappeared.

Fibrils in the middle stage of EGCG-induced degradation were flash-frozen, and images of these frozen samples showed how EGCG snapped the fibrils into apparently harmless pieces.

“The EGCG molecules bind to each layer of the fibers, but the molecules want to be closer together. As they move together the fiber snaps,” Eisenberg said.

Kevin Murray, who was a UCLA doctoral student at the time and is now in the neurology department at Brown University, identified specific locations, called pharmacophores, on the tau fiber to which EGCG molecules are attached. Then he ran computer simulations on a library of 60,000 brain and nervous system-friendly small molecules with the potential to bind to the same sites. He found several hundred molecules that were 25 atoms or less in size, all with the potential to bind even better to the tau fiber pharmacophores. Experiments with the top candidate molecules identified from the computational screening identified about a half dozen that broke up the tau fibers.

“Using the super-computing resources available at UCLA, we are able to screen vast libraries of drugs virtually before any wet-lab experiments are required,” Murray said.

A few of these top compounds, most notably molecules called CNS-11 and CNS-17, also stopped the fibers from spreading from cell to cell. The authors think these molecules are candidates for drugs that could be developed to treat Alzheimer’s disease.

“For cancer and many metabolic diseases knowing the structure of the disease-causing protein has led to effective drugs that halt the disease-causing action,” Eisenberg said. “But it’s only recently that scientists learned the structures of tau tangles.

We’ve now identified small molecules that break up these fibers. The bottom line is, we’ve put Alzheimer’s disease and amyloid diseases in general on the same basis as cancer, namely, that structure can be used to find drugs.”

CNS-11 is not a drug yet but the authors call it a lead.

“By studying variations of this, which we are doing, we may go from this lead into something that would be a really good drug,” Eisenberg said.

Source

A growing body of research shows that exercise can enhance brain function and delay, or even prevent, the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Although the underlying mechanisms still remain unclear, recent research indicates that exercise-induced activation of peripheral systems such as muscle, gut, liver, and adipose tissue may affect neural plasticity. A special issue of the journal Brain Plasticity presents new research and insights on neural plasticity and the role of peripheral factors in cognitive health.

“At least a dozen peripheral factors have been identified that affect neurotrophin levels, adult neurogenesis, inflammation, synaptic plasticity, and memory function,” explained co-Guest Editor and journal Editor-in-Chief Henriette van Praag, PhD, Charles E. Schmidt College of Medicine and Brain Institute, Florida Atlantic University.

Cathepsin B (CTSB), a myokine, and brain-derived neurotrophic factor (BNDF) have been found to possess robust neuroprotective effects. In a new study presented in the special issue, investigators examined whether increasing aerobic exercise intensity would increase the amount of CTSB and BDNF circulating in the blood. Sixteen young healthy subjects were selected as participants and completed treadmill-based aerobic exercise at maximum capacity and then at 40%, 60%, and 80% of capacity.

After each bout of exercise, blood samples were taken to measure circulating CTSB and BDNF, and CTSB protein, BDNF protein, and mRNA expression were measured in skeletal tissue. Scientists discovered that high-intensity exercise elevates circulating CTSB in young adults immediately after exercise, and that skeletal muscle tissue expresses both message and protein of CTSB and BDNF.

“CTSB and BDNF are promising therapeutic targets that may delay the onset and progression of cognitive impairments,” said lead investigator Jacob M. Haus, PhD, School of Kinesiology, University of Michigan. “Future studies are needed to elucidate the mechanisms regulating their release, processing, and fiber-type specific role in skeletal muscle tissue.”

The special issue of Brain Plasticity also shares new research that CTSB may play a role in cognitive control by modulating processing speed, and that both moderate-intensity and high-intensity interval exercise increase serum BDNF levels and working memory performance in young adult females.

Five review articles cover interorgan crosstalk between muscle, liver, adipose tissue, the gut microbiome, and the brain. While it is well known that exercise protects the central nervous system, it has only recently been found to depend on the endocrine capacity of skeletal muscle. In their review, co-authors Mamta Rai, PhD, and Fabio Demontis, PhD, both of the Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, highlight the impact of myokines, metabolites, and other unconventional factors that mediate effects of muscle-brain and muscle-retina communication on neurogenesis, neurotransmitter synthesis, proteostasis, mood, sleep, cognitive function and feeding behavior following exercise.

They also raise the possibility that detrimental myokines resulting from inactivity and muscle disease states could become a novel focus for therapeutic intervention. “We propose that tailoring muscle-to-central nervous system signaling by modulating myokines and myometabolites may combat age-related neurodegeneration and brain diseases that are influenced by system signals,” they said.

Men and women exhibit differences in their biological responses to physical activities and also in their vulnerabilities to the onset, progression, and outcomes of neurodegenerative disease. A review by co-authors Constanza J. Cortes, PhD, University of Alabama at Birmingham, and Zurine De Miguel, PhD, California State University, discusses emerging research on the sex-specific differences in immune system response to exercise as a potential mechanism by which physical activity affects the brain.

“Individual findings suggest that the immune response to exercise might be increased in females, but additional studies are needed,” Dr. Cortes and Dr. De Miguel observed. “Cross-disciplinary research integrating neuroscience, exercise physiology, and geroscience is needed to explain sex differences in cognitive aging and age-related neurodegenerative disease, and to develop novel therapeutic targets.”

Research on cross-talk between the brain and adipose tissue, particularly on a hormone that can cross the BBB and has been shown to improve neuronal function in animal models of Alzheimer’s disease; accumulating evidence that neurogenesis can be regulated by the gut microbiome; and research on effects of exercise and diet on hippocampal BDNF signaling, which suggest approaches to the treatment of neurodegenerative conditions are also reviewed.

“The research collected in this issue corroborates the importance of exercise for memory function,” said co-Guest Editor Christiane D. Wrann, PhD, DVM, Massachusetts General Hospital and Harvard Medical School. “We are pleased to share this exciting special issue. In the coming years likely many more systemic molecules relevant to the brain will be discovered and may provide a basis for novel therapeutic approaches to neurodegenerative diseases.”

Source

NASA will accept feedback until December 1 on the draft request for proposals for the LTV Services (LTVS) contract, which is now ready for industry to review. The draft outlines NASA’s expectation for use of the LTV on the lunar surface in the 2028 timeframe. After taking industry feedback into account, NASA plans to issue a final request for proposals by early 2023.

Lara Kearney is the manager of the Extravehicular Activity (EVA) and Human Surface Mobility (HSM) Program at NASA’s Johnson Space Center in Houston. “This draft is one of the first important steps in this exciting project that will allow astronauts to explore farther on the Moon than ever before,” says Kearney. “Gaining industry feedback is crucial as we move forward in issuing a final request for proposal.”

Artist’s depiction of a lunar terrain vehicle on the surface of the Moon. Credit: NASA

 

Debuting during the Apollo missions, this iconic style of unpressurized, human-class rover is a cornerstone in NASA’s plans to develop a long-term presence on the lunar surface. While those human-driven vehicles expanded lunar exploration capabilities significantly, the new Artemis LTV will feature multiple upgrades and advanced technology.

Because Artemis missions will be targeting the lunar South Pole area, the new LTV must be able to withstand and operate in cold and unique lighting conditions. The Artemis LTV is also expected to be able to cover a range of hundreds of miles per year, enabling access to diverse locations that will facilitate science discoveries, resource prospecting, and exploration. It will also be capable of remote operation and will be available for other commercial uses when not carrying out NASA research and operations.

By contracting services from industry partners, NASA is able to leverage commercial innovation and provide the best value to U.S. taxpayers while achieving its human spaceflight and exploration goals. The contract will support continued science and long-term human exploration at the Moon under Artemis, which will land the first woman and first person of color on the lunar surface.

Learn more about this new approach to lunar surface exploration and NASA’s plans to contract for LTV services at: https://www.nasa.gov/jsc/procurement/ltv

Source

What makes something hilarious has baffled philosophers and scientists since at least the time of inquiring minds like Plato. The Greeks believed that feeling superior at others’ expense was the source of humor. Sigmund Freud, a German psychologist, thought humor was a means to let off pent-up energy. In order to make people laugh, US comedian Robin Williams tapped his anger at the absurd.

No one appears to be able to agree on the answer to the question, “What’s so funny?” So picture attempting to train a robot to laugh. But by creating an AI that gets its signals from a shared laughing system, a team of researchers at Kyoto University in Japan is trying to do that. The researchers describe their novel technique for creating a funny bone for the Japanese robot ‘Erica’ in the journal Frontiers in Robotics and AI.

It’s not like robots are incapable of understanding or even laughing in response to a lousy dad joke. Instead, the difficulty is in developing the subtleties of human humor for an AI system to enhance ordinary conversations between robots and humans.

An example of a conversation between the researchers and Erica. Credit: Inoue et al

 

“We think that one of the important functions of conversational AI is empathy,” explained lead author Dr. Koji Inoue, an assistant professor at Kyoto University in the Department of Intelligence Science and Technology within the Graduate School of Informatics. “Conversation is, of course, multimodal, not just responding correctly. So we decided that one way a robot can empathize with users is to share their laughter, which you cannot do with a text-based chatbot.”

A funny thing happened

In the shared-laughter model, a human initially laughs and the AI system responds with laughter as an empathetic response. This approach required designing three subsystems – one to detect laughter, a second to decide whether to laugh and a third to choose the type of appropriate laughter.

The scientists gathered training data by annotating more than 80 dialogues from speed dating, a social scenario where large groups of people mingle, or interact, with each other one-on-one for a brief period of time. In this case, the matchmaking marathon involved students from Kyoto University and Erica, teleoperated by several amateur actresses.

“Our biggest challenge in this work was identifying the actual cases of shared laughter, which isn’t easy, because as you know, most laughter is actually not shared at all,” Inoue said. “We had to carefully categorize exactly which laughs we could use for our analysis and not just assume that any laugh can be responded to.”

The type of laughter is also important, because in some cases a polite chuckle may be more appropriate than a loud snort of laughter. The experiment was limited to social versus mirthful laughs.

The robot gets it

The team eventually tested Erica’s new sense of humor by creating four short two- to three-minute dialogues between a person and Erica with her new shared-laughter system. In the first scenario, she only uttered social laughter, followed only by mirthful laughs in the second and third exchanges, with both types of laughter combined in the last dialogue. The team also created two other sets of similar dialogues as baseline models. In the first one, Erica never laughs. In the second, Erica utters a social laugh every time she detects a human laugh without using the other two subsystems to filter the context and response.

The researchers crowdsourced more than 130 people in total to listen to each scenario within the three different conditions – shared-laughter system, no laughter, all laughter – and evaluated the interactions based on empathy, naturalness, human-likeness, and understanding. The shared-laughter system performed better than either baseline.

“The most significant result of this paper is that we have shown how we can combine all three of these tasks into one robot. We believe that this type of combined system is necessary for proper laughing behavior, not simply just detecting a laugh and responding to it,” Inoue said.

Like old friends

There are still plenty of other laughing styles to model and train Erica on before she is ready to hit the stand-up circuit. “There are many other laughing functions and types which need to be considered, and this is not an easy task. We haven’t even attempted to model unshared laughs even though they are the most common,” Inoue noted.

Of course, laughter is just one aspect of having a natural human-like conversation with a robot.

“Robots should actually have a distinct character, and we think that they can show this through their conversational behaviors, such as laughing, eye gaze, gestures, and speaking style,” Inoue added. “We do not think this is an easy problem at all, and it may well take more than 10 to 20 years before we can finally have a casual chat with a robot like we would with a friend.”

Source

In this image, the focus is on the dark, dusty heart of the nebula, where a star cluster resides, mostly hidden from view. Nearby (but not visible in this image) is the bright star Alnitak, the easternmost star in the Belt of Orion. Radiation from Alnitak ionizes the Flame Nebula’s hydrogen gas. As the gas begins to cool from its higher-energy state to a lower-energy state, it emits energy in the form of light, causing the visible glow behind the swirled wisps of dust.

Researchers have used Hubble to measure the mass of stars in the cluster as they search for brown dwarfs, a type of dim object that’s too hot and massive to be classified as a planet but also too small and cool to shine like a star.

The Flame Nebula, also called NGC 2024, is part of the Orion Molecular Cloud Complex and is found near the Horsehead Nebula. Credit: NASA, ESA, and N. Da Rio (University of Virginia), ESO, DSS2, and D. De Martin; Processing: Gladys Kober (NASA/Catholic University of America)

 

The Orion molecular cloud complex (or, simply, the Orion complex) is a star-forming region with stellar ages ranging up to 12 Myr. Two enormous molecular clouds are a part of it, dubbed Orion A and Orion B. The stars currently forming within the complex are located within these two clouds.

The Orion complex is one of the most active regions of nearby stellar formation visible in the night sky and is home to both protoplanetary discs and very young stars. Much of it shines brightly in infrared wavelengths due to the heat-intensive processes involved in stellar formation. However, the complex contains dark nebulae, emission nebulae, reflection nebulae, and H II regions.

Source

A multinational team headed by University College London scientists has discovered a new mechanism that slows down and maybe even prevents the normal aging of immune cells, one of the nine “hallmarks of aging.”

The discovery in-vitro (cells) and validated in mice was “unexpected,” according to the researchers, who believe harnessing the mechanism might extend the life of the immune system, enabling people to live healthier and longer lives, and would also have therapeutic use for diseases such as cancer and dementia. Their findings were recently published in the journal Nature Cell Biology.

Explaining the study, lead author, Dr. Alessio Lanna, Honorary Professor at UCL Division of Medicine, said: “Immune cells are on constant high-alert, always ready to fight pathogens. To be effective they also must persist for decades in the body – but the strategies employed to execute this life-long protection are largely unknown.

“In this research, we sought to find out what mechanisms exist to confer longevity to immune system cells, known as T cells, at the initiation of the immune response against an antigen – a foreign substance recognized by the immune-surveillance mechanisms of defense of the body.”

Why the immune system ages

Each chromosome has a protective cap called a telomere, which is a particular DNA sequence that is repeated thousands of times. The sequence has two functions: first, it shields the coding regions of the chromosomes from damage, and second, it serves as an aging clock that regulates the number of replications (also known as divisions) that a cell can make.

T cells (a type of white blood or immune cell), like other cells, have telomeres that shorten with each cell division (telomere attrition). When telomeres reach a critical length, the cell stops dividing and enters senescence, which is the process of being disposed of by the immune system or persisting in an altered, dysfunctional condition.

With the immune system no longer functioning effectively, this leads to the onset of chronic infections, cancerous disease, and death. Telomere attrition has been described as one of the “hallmarks of aging”.

Study findings

In the study, in vitro, researchers initiated an immune response of T-lymphocytes against a microbe (foreign infection). Unexpectedly, they observed a telomere transfer reaction between two types of white blood cells, in ‘extracellular vesicles’ (small particles that facilitate intercellular communication). An antigen-presenting cell (APC), consisting either of B cells, dendritic cells, or macrophages, functioned as a ‘telomere donor’, to the T lymphocyte – the telomere recipient cell. Upon transfer of the telomeres, the recipient T cell became long-lived and possessed memory and stem cell attributes, enabling the T cell to protect a host against lethal infection in the long term.

The telomere transfer reaction extended certain telomeres about 30 times more than the extension exerted by telomerase. Telomerase is the single DNA synthesizing enzyme that is devoted to telomere maintenance in stem cells, cells of the immune systems, and found in fetal tissue, reproductive cells, and sperm. However, it does not provide this function in other cells, leading to telomere attrition. Even in immune cells where the enzyme is naturally active, continuous immune reactions cause progressive telomerase inactivation leading to telomere shortening, when cells stop dividing, and replicative senescence occurs.

Professor Lanna added: “The telomere transfer reaction between immune cells adds to the Nobel-prize-winning discovery of telomerase and shows that cells are capable of exchanging telomeres as a way to regulate chromosome length before telomerase action begins. It is possible that aging may be slowed down or cured simply by transferring telomeres.”

Utilizing the new mechanism

On discovering the new ‘anti-aging’ mechanism, the same research team established that telomere extracellular vesicles can be purified from the blood, and, when added to T cells, present anti-aging activities in immune systems from both humans and mice.

The researchers discovered (in human cells and mice) that the purified extracellular vesicle preparations may be administered alone or in combination with a vaccine and this extended durative immune protection that, in principle, may avoid the need for revaccination.

Alternatively, the ‘telomere donor’ transfer reaction can be boosted directly in cells. While much more research is needed, the scientists say this illustrates the possibilities of new forms of prophylactic (preventative) therapies for immune senescence and age.

Professor Lanna concluded: “Telomere biology has been studied for more than 40 years. For decades, a single enzyme, telomerase, has been credited as the sole mechanism responsible for telomere elongation and maintenance in cells. Our results illuminate how a different mechanism that does not require telomerase to extend telomeres and act when telomerase is still inactive in the cell.”

Source

Mozilla has announced the successor to the Mozilla Builders incubator: Mozilla Ventures.

Mozilla defined the project in a post as an investment fund for early-stage internet startups that Mozilla feels align with the Mozilla Manifesto. The fund will officially open next year, but has already made some preliminary investments.

The news came from Mozilla executive director Mark Surman, and the new fund will be run by Mohamed Nanabhay, previously senior advisor at the Media Development Investment Fund. The new fund succeeds 2020's Mozilla Builders program, which apparently "invested in 80+ people, projects, and technologies reshaping the internet."

The initial pot of $35 million will go towards "seed to series A startups… whose products or technologies advance… values… like privacy, inclusion, transparency, and human dignity."

Some backing has already been given to three new companies: Block Party, heylogin, and Secure AI Labs.

The investments will be guided by partner company Lucid Capitalism. Even so, like any investment fund, this is essentially a gamble. As for the companies it has backed so far, heylogin offers a passwordless authentication tool, a sort of password manager without a master password, while SAIL offers a tool to pool and query clinical results from medical trials in multiple hospitals while preserving patient confidentiality.

Of the three, given the scale of the layoffs happening at Twitter, Block Party's tools to block harassment on Twitter could have the strongest prospects right now. Unless, that is, the platform implodes.

This isn't a move we expected from Mozilla, but then again, the organization does have a track record of unexpected maneuvers. A fine example is this rather bemusing Mozilla email submitted by reader Adam Kean:

Venture capital isn't the only unexpected move from Mozilla of late

This message was followed closely by another, containing an apology for spamming "a couple hundred thousand friends." Or possibly former friends, we suspect.

Mozilla apologizes for spamming, er, a couple hundred thousand friends

The text, apparently, came from the Sagan Ipsum generator – the server for which, note, doesn't use HTTPS, so you might get a security warning. Adam did.

Could have been worse, we suppose: Mozilla could have emailed billions and billions.

Source

A new nationwide study published in the Journal of Affective Disorders estimated that in Canada, 34.7% percent of the population, or just over one out of three Canadians, experienced severe loneliness in the second wave of COVID-19 infections, in January 2021. Moreover, this estimate of Canadian loneliness was substantially higher than statistics (14%–27%) reported elsewhere in the world during the pandemic.

"This concerning magnitude implies that during the pandemic lockdown, severe loneliness was ubiquitous in Canada," says the sole author, Dr. Lamson Lin Shen, an assistant professor in City University of Hong Kong's Department of Social and Behavioral Sciences, who conducting the research while finishing his Ph.D. degree at the University of Toronto's Factor-Inwentash Faculty of Social Work.

"This is probably due to the disruption in daily social activities, which normally help people cope with stress, as well as the intense social isolation caused by the lockdown measures implemented in many provinces of Canada."

Based on the population-representative data from the Canadian Perspective Survey Series, collected from 25 to 31 January 2021 (during the larger second wave of the pandemic in Canada), the study adopted a machine-learning approach, Classification and Regression Tree (CART) modeling, to discover population patterns of loneliness symptoms measured by the standardized UCLA 3-item loneliness scale among 3,772 participants.

The CART algorithm found that migrants who experienced pandemic-triggered job insecurity, such as business closures, layoffs or absence from work due to COVID-19 diagnosis, were the among the groups most at risk of severe loneliness.

"It is not surprising that immigrants were particularly vulnerable to isolation and loneliness in pre-pandemic times, because they were in a new environment, where they may have faced a variety of post-migration stressors, such as language obstacles, limited social networks, and a diminished sense of community belonging," says Dr. Lin. "What struck me the most is that my study discovered the double jeopardy of immigrant status and an unstable job situation during the COVID period."

According Dr. Lin's findings, individuals who experienced job instability during the pandemic had double the odds of experiencing severe loneliness compared to people who were securely employed, after controlling for confounding variables, including sociodemographic factors. Among those experiencing insecure employment, the prevalence of loneliness was substantially higher among immigrant population than among Canadian-born residents (86.2 % vs. 48.7 %).

"The COVID-19 pandemic indeed amplified immigrants' susceptibility to loneliness," says Dr. Lin. "This may be due to the fact that many migrants to Canada are over-represented in low-paid, low-skilled, unstable jobs, such as retail positions, cleaners, or cashiers, that require extensive interaction with the public, so they are at greater occupational risk of COVID-19 infection and consequential employment insecurity."

In addition, Dr. Lin's research identified several at-risk groups of loneliness that are consistent in ordinary times, including youth and adolescents, women, people with a low educational background, people living alone, people with a limited social circle (less than three persons), binge drinkers, and past-month cannabis users.

His study also demonstrated that, compared to Canadians who did not experience loneliness, severely lonely individuals in Canada were 1.7 times more likely to seek treatment from mental health professionals, 1.5 times more likely to seek informal support for mental health concerns, and 1.8 times more likely to have unmet mental health needs.

"My findings further shed light on the importance of building an equitable mental health care system in the pandemic response and recovery in Canada and other immigrant-receiving countries of the world," said Dr. Lin.

"Primary care providers and mental health clinicians should assess loneliness symptoms in their routine patient examinations. At the community level, social care organizations should develop early prevention and intervention programs targeting high-risk groups with a greater burden of loneliness, especially for immigrant and marginalized populations."

Source

Deepak Ram said that he was playing in his backyard when the snake attacked him. "The snake got wrapped around my hand and bit me," he told local media. "I was in great pain. As the reptile didn't budge when I tried to shake it off, I bit it hard twice."

The bizarre incident took place in Jashpur District in the state of Chhattisgarh, known locally as Naglok—or realm of serpents—because of the abundance of snakes in the area.

Over 60 of the nearly 300 snake species that live in India are venomous. Between 2000 and 2019, the World Health Organization estimates, snakebites killed over 1.2 million people in India, more than in any other nation.

"The Indian spectacled cobra—Naja naja—is one of the leading causes of snakebite morbidity and fatality in South Asia," Timothy Jackson, a toxicologist from the Australian Venom Research Unit at the University of Melbourne, told Newsweek.

"Cobra venoms are diverse, but the most prevalent and perhaps most clinically important toxins are neurotoxins and cytotoxins," he continued.

"That is, toxins which interfere with the nervous system—for example by preventing cell signaling—and toxins which destroy cells. As a result, the consequence of cobra envenoming most likely to result in death is neurotoxicity—paralysis.

"Cobra venoms may also cause horrendous tissue damage due to the presence of cytotoxins," the toxicologist said.

Source

The case is Cornet v. Twitter Inc., 22-cv-06857, US District Court, Northern District of California.

The layoffs come just about a week after businessman Elon Musk took over the social media platform and sacked CEO Parag Agrawal, CFO Ned Segal, and head of legal policy Vijaya Gadde. These are a part of Musk's moves to streamline the company's operations and make Twitter more profitable.

The Worker Adjustment and Retraining Notification (WARN) Act protects workers, their families, and communities by requiring most employers with 100 or more employees to notify their staff at least 60 calendar days in advance before plant closings and mass layoffs.

As such, the complaint filed by attorney Shannon Liss-Riordan asks the court to order Twitter to obey the WARN Act and restrict the company from forcing employees to sign documents that could waive their right to participate in litigation.

"We filed this lawsuit tonight in an attempt the [sic] make sure that employees are aware that they should not sign away their rights and that they have an avenue for pursuing their rights," says Liss-Riordan.

Back in June, Liss-Riordan also represented workers of Musk's electric car company Tesla when the organization laid off 10% of its workforce. The lawsuit seeked pay and benefits for the 60-day notification period. Musk called the lawsuit "trivial" and "pre-emptive".

“We will now see if he is going to continue to thumb his nose at the laws of this country that protect employees,” Liss-Riordan said of Musk. “It appears that he’s repeating the same playbook of what he did at Tesla.”

Twitter has not yet commented on the issue.

Source: Bloomberg (paywall)

Source

•     Some Twitter staff say they are already being locked out of email and Slack accounts as mass sackings at the company begin

•     All staff are set to receive an email with the subject "Your Role at Twitter" by 09:00 Pacific time on Friday (16:00 GMT)

•     New owner Elon Musk is expected to reduce the platform's workforce of 8,000 by as much as half

•     An internal email said the cuts were designed to put Twitter on a "healthy path" - the platform struggles to make a profit

•     A class action lawsuit has already been filed against the company over the mass job cuts and the amount of notice given

•     Tesla and SpaceX owner Musk bought the social media platform in a $44bn (£39.3bn) deal last week after a protracted process

•     He has already removed the entire board and is now the sole executive

Source

In 1936, English mathematician Alan Turing imagined an autonomous machine capable of carrying out any precisely coded algorithm. The hypothetical machine would read a strip of tape dotted with symbols that, when interpreted sequentially, would instruct the machine to act. It might transcribe, translate, or compute—turning code into a message, or a math problem into an answer. The Turing machine was a prophetic vision of modern computers. While your laptop doesn’t rely on tape to run programs, the philosophy behind it is the same. “That laid the foundation for modern computing,” says Leigh.

Leigh now believes that tiny molecular versions of the Turing machine could assemble what we struggle to build in the organic realm, like new drugs and plastics with traits so enhanced and precise that they’re out of reach for current tools. And he’s confident that he can do it. “It's absolutely clear that it's possible,” he says, “because there already is this working example called biology.” Nature has given every life-form its version of the Turing machine: ribosomes, cellular structures that slide down sequences of mRNA to churn out proteins one amino acid at a time. No life on earth can function without them.

A molecular machine would work like a ribosome, in that instructions would be encoded on one molecule, and another one would interpret them, or read them out. Or, you can think of it a bit like a tape recorder, in that information is encoded on one molecule that serves as a track, and is read by a second molecule that serves as the reader “head” that plays it back.

A fully working machine doesn’t exist yet. Researchers like Leigh are building it piece by piece. His team designed a ring-like “ratchet” molecule in 2007 that was powered by light and could move forward along a molecular track. But that wasn’t what Leigh really wanted: Biological systems are powered by chemical fuels, not light.

So five years ago, they discovered how to nudge these ratchet molecules along using trichloroacetic acid as a chemical fuel. The machines are in a liquid, and the team pulsed the acid into it. The surrounding liquid's pH changes as the acid decomposes, triggering the track molecule to usher the head molecule forward one step—and never backward. Think of it like an escalator, or a zip tie: The sawtoothed shape of the track restricts motion to only one direction.

Now, in a study recently published in Nature, Leigh’s team combined these innovations to demonstrate that a molecule-sized machine can read as it moves. They encoded blocks of information on one molecule (the tape) and designed another to slide down its length (the head). As the head moved along the tape, it would contort into a predictable shape each time it scanned a specific block of information. That allowed the team to interpret the information on the tape based on the changes to the shape of the head—to essentially read its code.

Leigh’s team designed the molecular tape for this study to be more ambitious than the binary bits we’re used to in computing, which can be either a 0 or a 1. Instead, each block of information on the tape is written in three-way, or ternary, code, taking the values -1, 0, or +1.

The reason they could opt for a more information-dense bit is because of the physics of the reading head. When the head sticks to a -1, it contorts in a predictable way. When it sticks to a section deemed +1, it contorts the opposite way. For 0, no contortion.

Then, if you shine light at the molecular machine while it reads, each of the three contortions will twist that light in a unique way. The scientists were able to follow along with how the head was changing its shape by reading this light. They used a process called circular dichroism spectroscopy to determine the shape of the ratchet as it inched down the tape.

Final result: They showed that the head reacts to what it reads. In other words, they found that you can use the fundamental processes of physics and chemistry to relay information at the molecular level. "This is the first proof of principle, showing that you can effectively do it," says Jean-François Lutz, a polymer chemist with France’s National Center for Scientific Research who was not involved in the research. “It has been conceptualized, but never really achieved.” 

“The way the molecular machines have been designed is really intricate, and really nice,” says Lee Cronin, a chemist at the University of Glasgow who was not involved in the study. (Cronin’s team has pioneered a different type of chemical computer, called the Chemputer, which reliably automates chemical reactions.) “If you could digitally control assembly at the molecular level, and make every single strand bespoke, then you can make amazing materials,” he continues. “But we're a little bit far away from that. And I'm anxious not to over-promise that.”

Lutz, too, is careful not to overpromise. He points out that the “read” function is slow and the information that can be read is minimal. It’s also not yet possible to “write” information using a molecular computer, which is what would be required to actually fabricate new drugs or plastics.

Leigh isn’t worried about speed. In the current experiment, it took several hours to move between blocks of information. He thinks it will ultimately go faster, because in nature, “ribosomes can read about 20 digits a second.” And to him, the minimalism of the information is also the point. It’s about packing information into as small a space as possible—perhaps for computing, data storage, or manufacturing—and retrieving it autonomously. He calls it “the ultimate miniaturization of technology.”

That said, he does have ideas for growth. He imagines one day being able to use 5- or 7-way code, which would embed even more information into each block of tape.

The next step forward will be getting his molecular machines to write. In the current paper, Leigh’s team proposes that the shape-shifting reader molecules may be able to catalyze different chemical reactions depending on their shape. (Read a +1, create molecule A. Read a 0, create molecule B.) You can imagine a vat full of such molecular readers, all programmed to print the same molecules, functioning as a sort of factory—perhaps to churn out super-polymers that cells could never make. “As synthetic scientists, we've got the whole of the periodic table of elements that we can use,” says Leigh. “It’s breaking free of ways that biology is restricted.”

Leigh is especially tempted to manufacture new plastics this way. Plastics like polystyrene, polymethacrylate, and polypropylene are polymers, long chains of the same repeating unit, or monomer. Their physical properties are useful to us. But who knows what kind of super-materials could arise from mixing and matching monomers intentionally?

Combining building blocks is a powerful concept in biology. For example, all the proteins in the world are based on some combination of only 20 amino acids. “Take spider silk—that's a protein, and it's five times tougher than steel,” says Leigh. “If you take exactly the same 20 amino acids but assemble them in a different sequence, you'll get myosin, which is the constituency of muscle and can generate a force, or you can make antibodies.”

Lutz cautions that lofty ambitions for molecular machines are nothing new. “Dreaming in chemistry is always quite easy—making it happen is different,” he says.

Still, incremental advances like Leigh’s are getting chemistry a little closer. “If they can scale it, it will be amazing,” says Cronin. “But they're a very long way from a Turing machine.”

The Sci-Fi Dream of a ‘Molecular Computer’ Is Getting More Real

(May require free registration to view)

Toxic cleanup technique can get more rare earth metals out of ores