The authors conclude that people might be able to reduce their risk of atrial fibrillation (AF) by avoiding certain triggers.

The study is published in JAMA Cardiology and was presented Nov. 14, 2021, at the annual Scientific Sessions of the American Heart Association.

Researchers were surprised to find that although most of the things that participants thought would be related to their AF were not, those in the intervention group still experienced less arrhythmia than the people in a comparison group that was not self-monitoring.

"This suggests that those personalized assessments revealed actionable results," said lead author Gregory Marcus, MD, MAS, professor of Medicine in the Division of Cardiology at UCSF. "Although caffeine was the most commonly selected trigger for testing, we found no evidence of a near-term relationship between caffeine consumption and atrial fibrillation. In contrast, alcohol consumption most consistently exhibited heightened risks of atrial fibrillation."

Atrial fibrillation contributes to more than 150,000 deaths in the United States each year, reports the federal Centers for Disease Control and Prevention, with the death rate on the rise for more than 20 years.

To learn more about what patients felt was especially important to study about the disease, researchers held a brainstorming session in 2014. Patients said researching individual triggers for AF was their top priority, giving rise to the I-STOP-AFib study, which enabled individuals to test any presumed AF trigger. About 450 people participated, more than half of whom (58 percent) were men, and the overwhelming majority of whom were white (92 percent).

Participants in the randomized clinical trial utilized a mobile electrocardiogram recording device along with a phone app to log potential triggers like drinking alcohol and caffeine, sleeping on the left side or not getting enough sleep, eating a large meal, a cold drink, or sticking to a particular diet, engaging in exercise, or anything else they thought was relevant to their AF. Although participants were most likely to select caffeine as a trigger, there was no association with AF. Recent research from UCSF has similarly failed to demonstrate a relationship between caffeine and arrhythmias—on the contrary, investigators found it may have a protective effect.

The new study demonstrated that consumption of alcohol was the only trigger that consistently resulted in significantly more self-reported AF episodes.

The individualized testing method, known as n-of-1, did not validate participant-selected triggers for AF. But trial participants did report fewer AF episodes than those in the control group, and the data suggest that behaviors like avoiding alcohol could lessen the chances of having an AF episode.

"This completely remote, siteless, mobile-app based study will hopefully pave the way for many investigators and patients to conduct similar personalized 'n-of-1' experiments that can provide clinically relevant information specific to the individual," said Marcus.

Source

India’s government appears set to ban private cryptocurrencies.

News of the ban emerged in a Bulletin [PDF] that lists bills to be debated in the winter session of the Lok Sabha, India’s Parliament, which resumes for its winter sittings next week.

The tenth bill on the list is titled “The Cryptocurrency and Regulation of Official Digital Currency Bill, 2021”. While the legislation itself has not been revealed, the Bulletin describes the Bill’s purpose as follows:

To create a facilitative framework for creation of the official digital currency to be issued by the Reserve Bank of India. The Bill also seeks to prohibit all private cryptocurrencies in India; however, it allows for certain exceptions to promote the underlying technology of cryptocurrency and its uses.

In July 2021, the deputy governor of India’s Reserve Bank suggested central bank digital currencies have enormous potential and India can’t afford to be left behind. The Bill suggests that argument has been accepted by India’s government, which has decided to develop the regulations for a CBDC.

The precise meaning of “prohibit all private cryptocurrencies” has not been explained. The Register has encountered opinions suggesting so many Indian citizens have invested in cryptocurrency as an asset that an outright ban would spark a backlash. Bans on using cryptocurrency as a means of exchange have therefore been suggested, a proposal that chimes with the Indian government’s attempts to broaden its tax base.

The last part of the description suggests Indian law will allow use of Blockchain – just not for cryptocurrency.

India is one of many nations that have started work on a CBDC: the UK, Japan, Canada, and Hong Kong have all begun work.

The USA has begun work, too, and on Tuesday took another step towards making crypto mainstream when the nation’s Board of Governors of the Federal Reserve System, Federal Deposit Insurance Corporation, and Office of the Comptroller of the Currency issued a joint statement [PDF] that revealed the agencies have already conducted a series of policy development “sprints”. The three organisations stated that in 2022 they “plan to provide greater clarity on whether certain activities related to crypto-assets conducted by banking organizations are legally permissible, and expectations for safety and soundness, consumer protection, and compliance with existing laws and regulations.”

China, meanwhile, has already issued its Digital Yuan and claims 140 million wallets have been used at least once. The Middle Kingdom has also banned cryptocurrency mining and never authorised its use. ®

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Gopal Rai, Delhi state's environment minister, told journalists that pollution levels in the city had "improved in the last three days" and some of the restrictions would be relaxed.

The authorities had announced a shut down of some coal plants, a ban on entry of non-essential vehicles, construction work restrictions and urged people to stay indoors as some air pollutants reached more than 30 times the World Health Organisation's recommended maximum.

Levels of PM 2.5, the most harmful particulate matter that is responsible for chronic lung and heart disease, were still around 120 micrograms per cubic metre on Wednesday according to monitoring company IQAir - eight times the WHO limit.

Delhi, one of the world's most polluted cities and home to about 20 million people, is covered in a thick blanket of smog every winter after farmers in neighbouring northern states burn crop residue.

"The schools, colleges and institutions can reopen Monday. The government offices where we'd imposed work from home too will reopen and we'll advise officials to use public transport," Rai said.

Restrictions on construction activities in the city had already been eased.

Cleaner electric and compressed natural gas-powered vehicles will also be allowed to re-enter Delhi.

The Commission for Air Quality Management for Delhi last week ordered "anti-smog guns" and water sprinklers to operate at pollution hotspots at least three times a day.

But critics say such measures are cosmetic moves that fail to address the root causes of industrial pollutants, vehicular pollution and crop burn-off coalescing into toxic winter smog.

In a report published last year, Swiss-based IQAir found that 22 of the world's 30 most polluted cities were in India.

Source

"I believe we have a planetary defense program that is worth talking about now."

SpaceX launches NASA’s mission to collide with an asteroid [Update]

A short update on the projected launch date of the $10 billion James Webb Space Telescope came out of NASA on Monday, and it wasn't exactly a heart-warming missive.

The large, space-based telescope's "no earlier than" launch date will slip from December 18 to at least December 22 after an "incident" occurred during processing operations at the launch site in Kourou, French Guiana. That is where the telescope will launch on an Ariane 5 rocket provided by the European Space Agency.

"Technicians were preparing to attach Webb to the launch vehicle adapter, which is used to integrate the observatory with the upper stage of the Ariane 5 rocket," NASA said in a blog post. "A sudden, unplanned release of a clamp band—which secures Webb to the launch vehicle adapter—caused a vibration throughout the observatory."

Let's be honest, words like "incident," "sudden," and "vibration" are not the kinds of expressions one wants to hear about the handling of a delicate and virtually irreplaceable instrument like the Webb telescope. However, NASA, the European Space Agency, and the rocket's operator, Arianespace, have a plan for moving forward.

NASA is leading an anomaly review board to investigate and conduct additional testing to determine with certainty that the incident did not damage any part of the telescope. NASA said it will provide an update when the testing is completed at the end of this week. A senior source at the space agency said this testing is currently running ahead of schedule and that, provided some serious issue is not identified, the December 22 launch date should stick.

Any setbacks now in Webb's progress toward launch feel especially painful because reaching this point has been such a long, long road. NASA's follow-on instrument to the wildly successful Hubble Space Telescope was originally due to launch about a decade ago, with a development cost of $1 billion. Since then, technical problems and delays have bedeviled the complex telescope.

Building Webb has been difficult because its 6.5-meter mirror needs to unfurl itself once it reaches an orbit about 1.5 million kilometers from Earth. This is an exceedingly complex process, and there are more than 300 single points of failure aboard the observatory. NASA has had a difficult time testing them all on Earth in conditions that mimic the temperatures, pressure, and microgravity of deep space.

NASA's science chief, Thomas Zurbuchen, said Monday it was important for NASA to ensure the telescope was healthy before its launch. "I am confident the team will do everything they can to prepare Webb to explore our cosmic past," he wrote on Twitter. "Certainly, this step is worth the wait."

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With a population of 1.3 billion people, Africa is the world’s second most-populous continent, trailing only Asia, and it’s also the world’s poorest. But despite the gap in resources — Africa has much less access to vaccines than places like the Americas and Western Europe — the continent has experienced the second-lowest number of deaths from the virus of any of the World Health Organization’s (WHO) six designated regions.

Nearly 152,000 Africans have died of COVID-19 since the global pandemic began, according to the WHO. The Western Pacific region has seen just 136,267 deaths, but otherwise Africa has had the best pandemic outcome in the world. In the Americas, more than 2.3 million people have died from the virus, and in Europe, the number is nearly 1.5 million.

Scientists acknowledge that sparse reporting systems and poor data collections play some part in the low numbers, according to The Associated Press. But the astronomical gap between the region and the rest of the world is too substantial to simply chalk up to poor record-keeping, they say.
“I think there’s a different cultural approach in Africa, where these countries have approached COVID with a sense of humility because they’ve experienced things like Ebola, polio and malaria,” Devi Sridhar, chair of global public health at the University of Edinburgh, told the AP.

“It’s not always about how much money you have or how sophisticated your hospitals are,” said Christian Happi, director of the African Center of Excellence for Genomics of Infectious Diseases at Redeemer’s University in Nigeria.

One factor may be age. The median age in Africa is around 18 years old, about half that of North America and 24 years younger than Europe. In the United States, the median age is around 38, and COVID-19 is far more threatening to older populations than younger ones. Obesity, another significant risk factor, is also less prominent on the continent than elsewhere: Africa and southeast Asia are the least-obese regions in the world.

What’s most stunning to medical experts is that Africa is doing this with limited access to vaccines. Less than 6% of the population is vaccinated, according to the AP.

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Why it matters: Booster shots provide remarkably strong protection against coronavirus infections, at least for a period of time. But getting the majority of Americans to stick out their arm again would be extremely challenging.

Driving the news: Two governors said this week that they don't consider people who haven't received a booster shot to be fully vaccinated.

•  "We're 11 months into the vaccination program. In my view, if you were vaccinated more than six months ago, you’re not fully vaccinated," Connecticut Gov. Ned Lamont said yesterday.

•  "We are analyzing what we can do to create those incentives — and potentially mandates — for making sure that people are fully vaccinated, which means three vaccines," New Mexico Gov. Michelle Lujan Grisham said Wednesday.

•  The New Mexico state health secretary told the AP that changing the definition of fully vaccinated is being discussed, and that he expects a new public health order to be released in the next few weeks.

•  The U.K. will adjust the definition to include booster shots, Prime Minister Boris Johnson said Monday.

Reality check: Only 17% of U.S. adults have received a booster shot, according to the CDC, although many of those people haven't received their primary series within the last six months and are not yet eligible.

Between the lines: NIAID director Anthony Fauci told Axios earlier this week that changing the definition federally "hasn't been on the table yet," but didn't rule it out in the future.

•  That means a patchwork set of definitions could emerge across the country, at least in the short term.

•  And given the growing number of vaccine mandates in place, formally changing the definition of fully vaccinated could be much more significant than a simple change in rhetoric.

The other side: Changing the definition "would have major implications across many aspects of the pandemic, in some cases making it more difficult to control," said Walid Gellad, a professor of medicine at the University of Pittsburgh.

 "We haven't thought through all the implications to start saying this casually. It's premature," he added.

State of play: The FDA is expected to OK booster shots for all adults at least six months out from their first round of Pfizer or Moderna. The CDC will also begin considering the change today.

•  J&J recipients are already eligible for a booster.

•  Although the federal government currently only recommends booster shots for certain mRNA recipients who are vulnerable to infection or severe disease, many states have plowed ahead and already made all adults eligible six months after their primary round.

The bottom line: Most vaccinated people — particularly younger, healthier ones — are still well protected against severe disease and death with only two doses.

•  But boosters dramatically increase protection against infection, which can help reduce the spread of the virus. They also restore protection against serious infections among vulnerable people.

•  And officials are making the case that merely protecting against hospitalization and death shouldn't be our only goal with vaccines.

•  "I don't know of any other vaccine that we only worry about keeping people out of the hospital," Fauci said at a briefing earlier this week. "I think an important thing is to prevent people from getting symptomatic disease."

Source

Still uncertain of why it misbehaved, controllers are cautiously restoring service.

Hubble update: One camera back, more to come

For many, the Facebook Papers come as no surprise. As a Palestinian digital rights advocate, the recent revelations perfectly describe and validate the archetypal experience of Palestinians and millions of others generating daily content outside the U.S.

For years, activists and civil society organizations have warned of Facebook’s negligence of non-English speaking regions, and its deeply discriminatory content moderation structure which have served to silence globally marginalized voices, not empower them. Yet Facebook, at every ebb and flow, has chosen profit over people.

The thousands of pages of leaked documents now provide incontestable evidence, finally laying to rest one of the biggest claims repeatedly made by Facebook and its leadership since the heyday of the Arab Spring: Safety and freedom of expression are not afforded to all users equally, but are rather dictated by the company’s market interests and bottom line.

As reported by the Wall Street Journal, Facebook has built and maintained a system that favors the most powerful — including politicians, celebrities, and athletes — and exempts them from some or all of its rules under the so-called “cross-check” or “XCheck” program. While VIPs enjoy a preferential status, and with it a lack of accountability, many ordinary users are often erroneously censored and harshly suppressed with little to no explanation of what they did wrong. In a true Orwellian sense, Facebook users are all equal, but some users are more equal than others.

In Arabic — the third most common language on the platform — Facebook’s double standards in content moderation parades the worst of all worlds: Political speech is muzzled due to over-enforcement of policies related to terrorism and incitement to violence, while hate speech and disinformation targeting at-risk users such as women and the LGBTQ+ community are left rampant on the platform.

Arab activists and journalists, many of whom use Facebook to document human rights abuses and war crimes, are routinely censored and booted off the platform — most commonly under the pretext of terrorism.

This is especially pronounced in times of political crisis and violence. Let’s not forget Facebook’s mass censorship of Palestinian voices during the height of Israeli violence and brutality in the months of May and June 2021. Most notably, Facebook deleted content reporting on Israeli forces violently storming into Al-Aqsa Mosque, the third holiest site in Islam, throwing stun grenades and tear gas at worshippers, because company staff mistook “Al-Aqsa” for a terrorist organization.

Such arbitrary mistakes are disturbingly common. Across the region, Facebook’s algorithms incorrectly deleted Arabic content 77% of the time. In one instance, Facebook’s Oversight Board overturned the erroneous removal of a post shared by an Egyptian user on the violence in Israel and Palestine from a verified Al Jazeera page. Not only was the content wrongfully removed for allegedly violating the platform’s Dangerous Individuals and Organisations (DIO) Community Standard, but the user was also disproportionately punished with a read-only account restriction for three days, disabling his ability to livestream content, and prohibiting him from using advertising products on the platform for 30 days.

Digital rights advocates have demanded transparency on these designations. The Oversight Board also recommended Facebook to publish the list, but Facebook refused, citing safety concerns. The Intercept recently revealed the full list, and again, to no one’s surprise, “the DIO policy and blacklist … place far looser prohibitions on commentary about predominately white anti-government militias than on groups and individuals listed as terrorists, who are predominately Middle Eastern, South Asian, and Muslim.”

Now, when it comes to Arabic-language disinformation or hate speech targeting historically oppressed groups or women and gender minorities, Facebook’s overzealous content moderation turns into inaction, again demonstrating that Facebook directs its attention — and resources — to contexts that matter to the company financially or politically.

For LGBTQ+ community in the region, such criteria for action doesn’t hit the mark. They are doxxed, outed, and targeted with smear campaigns on Facebook and Instagram. Yet, Facebook is slow to act, leading, in some cases, to real-world harm. An investigation by Reuters shows, for instance, that despite Facebook’s ban on content promoting gay conversion therapy, much of the Arabic-language conversion content thrives unmoderated on the platform, where practitioners are free to promote their services and post freely to millions of followers through verified accounts.

Similarly, Facebook knew of the human-trafficking networks using the platform as a modern slavery market to buy and sell domestic workers in the Gulf, yet chose to remain idle after it shut down a few pages. According to the Wall Street Journal, Facebook only took action after Apple threatened to remove Facebook’s products from the App Store, following a BBC investigation into these onlive slave markets.

As one Egyptian LGBTQ+ activist puts it, “This is very dangerous content to us — but to Facebook, it doesn’t seem to be a priority.” Indeed, Facebook spent more than 3.2 million hours searching, labeling or removing “false or misleading” content in 2020, but only 13% of those hours were spent working on content outside the U.S. Facebook employed only 766 content moderators in 2020 to manually moderate content posted by its 220 million users in the Arabic-speaking world.

Relying on automation makes matters worse. While engineers have cast doubt over AI’s ability to catch and remove hate speech in English, it’s utterly disastrous in other world languages. According to an internal memo from 2020, Facebook does not have enough content or data “to train and maintain the Arabic classifier currently.” In Afghanistan, where hate speech is reportedly one of the top “abuse categories,” Facebook took action against just 0.23% of the estimated hate speech posts in the country.

Can any of this be fixed? There are no silver bullet solutions to content moderation issues at scale. But for a start, Facebook should admit to the problem. Creating a new “Meta” world does not absolve the company from its responsibilities if its content moderation system continues to wreak havoc on the rest of the world.

Facebook must dedicate sufficient financial and human resources for the 90% of users who live outside of the U.S. A first step would be to hire staff that understand and experience the world beyond Menlo Park, speak the local languages of the content they moderate, and understand local and regional nuances.

The platform needs to work with communities on the ground and co-design policies with them, and most importantly, for once, be fully transparent. Facebook’s profit margins cannot come at the cost of our rights and our lives.

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The megacity of nearly 11 million people near the border with India was once the ancient capital of the Mughal Empire and remains Pakistan's cultural epicentre.

But now it regularly ranks among the worst cities in the world for air pollution—a mixture of low-grade diesel fumes, smoke from seasonal crop burn off, and colder winter temperatures coalescing into stagnant clouds.

Syed Hasnain is visibly exhausted as he waits on his four-year-old son who has been admitted at the city's Mayo Hospital.

"He was coughing and not able to breathe properly and had a high temperature. We thought maybe it is coronavirus so we brought him to the hospital. But the doctors told us he has developed pneumonia because of the smog," Hasnain tells AFP.

"It's very worrisome," he admits. "I knew that the smog can be bad for health—but I didn't know it would be so bad that my son would be hospitalised."

Teachers also worry for the children.

"The pollution is a problem even inside class. We see children with red eyes and irritation, others continually cough," Nadia Sarwar, a government school teacher, tells AFP.

Once the capital of the ancient Mughal empire, Lahore is now shrouded in pollution each winter as air quality in Pakistan worsens.

One child, who has asthma, has had to stay home for several days because he kept suffering attacks, she says.

Across the border, Delhi has closed schools until the end of the month because of its pollution woes.

But Sarwar says it would be difficult to do the same in Lahore.

The children have already missed so much thanks to the coronavirus pandemic, and to shut schools down now would be making them "pay for a problem they didn't create."

"I feel bad for them," she said. "In the summers it is too hot here for outdoor activities. And in the winters there is pollution and dengue now. What can a child do? Where can he go?"

'Nobody cares'

Adults are also struggling. Rana Bibi, a 39-year-old mother of three who works as a cleaner, uses her dupatta (shawl) as a face mask while waiting for a rickshaw to take her home.

Residents in Pakistan's Lahore complain of pollution which hurts their eyes and throats, gets in their clothes, hair and skin.

"The smoke hurts my eyes and throat. That's why I have covered my face this way. First they made us do it for corona(virus), but now I am doing it myself," she says.

"When I reach home I am always smelling of smoke; my clothes, my hair, and my hands are dirty. But what can one do? I can't sit at home. I got used to it."

Some of the homes she cleans "have these machines that clean the air. I don't know. That's what they tell me. But there is smoke everywhere here."

In recent years residents have built homemade air purifiers and filed lawsuits against government officials in desperate bids to clean the air.

But authorities have been slow to act, blaming the smog on India or claiming the figures are exaggerated.

"Every year we read in the news that Lahore is the most polluted city or that it had the worst smog in the world. Nothing happens. Nobody cares," says Saira Aslam, who works in the HR department of a tech company.

Pakistani officials say smog in Lahore has drifted over from India, or that the air quality figures are exaggerated.

The 27-year-old is angry: "The government got away with it last year because we were all sitting at home anyway due to the lockdown. But they can't keep acting like nothing is wrong," she says.

"I have elderly people at home who are literally at risk because of the smog. It's a health hazard and needs to be treated like one."

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First-of-its-kind reactor to be built in Wyoming with heavy Dept. of Energy backing.

Bill Gates’ nuclear power company selects a site for its first reactor

Aspirin is a pain reliever and blood thinner, often used to reduce the chance for blood clots. This has consistently been shown as beneficial for those who have a history of heart disease or have already had a heart attack, stroke or blockages in other blood vessels. However, blood thinners can also increase your risk of bleeding and may not be as helpful for those without heart disease, or those who are not entirely aware of their family history and individual risk factors.

Adults aged 60 or older taking aspirin daily are at an increased risk for bleeding, according to the U.S. Preventative Services Task Force, and in those without a history of a prior heart attack, stroke or other blockages, this risk of bleeding may outweigh the benefit from taking a daily aspirin. There may be a small benefit of taking aspirin for younger patients (those in their 40s and 50s), especially if their bleeding risk is low, but the supporting evidence is less clear as age increases.

It is essential to talk with your health care provider about taking or stopping a daily aspirin. It is important to know your family history and other medical conditions so that your health care provider can make a proper and educated recommendation specifically for you.

The U.S. Preventative Services Task Force recommendation change does not apply to patients who are taking (or have been recommended to take) a low-dose aspirin daily after a heart attack or stroke. Others who may be recommended to take daily aspirin include those who:

•  Have high blood pressure.
•  Have high cholesterol.
•  Have diabetes.
•  Have other conditions that might increase their chances of having a heart attack or stroke.

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One of the most common infections worldwide, UTIs are not normally serious or life threatening but in rare cases can progress into sepsis, also known as septicaemia.

In older people the risk of developing severe UTIs often overlaps with conditions that require anticoagulant treatment.

Researchers found that in zebrafish, the commonly prescribed anticoagulant medications—specifically aspirin and warfarin—increased UTI severity.

"We commonly use zebrafish in medical research to better understand diseases in order to find cures," said Dr. Stefan Oehlers, Head of the Centenary Institute's Immune-Vascular Interactions Laboratory and study senior author.

"Zebrafish share 70 percent of the same genes as people and 84 percent of human genes known to be associated with human diseases have a zebrafish counterpart. This makes them perfect for study."

Dr. Oehlers said that UTI-associated sepsis is most often caused by uropathogenic Escherichia coli (UPEC), a bacterium that first infects the urinary system.

"We used the zebrafish to model the sepsis phase of UPEC infection," said Dr. Oehlers.

"Using this model we demonstrated that commonly used anticoagulant medicines reduced zebrafish survival and increased UPEC bacteria burden."

The researchers believe that the administration of the anticoagulant medications prevented natural clotting that would have helped to contain bacteria in the blood.

The research was published in the journal Microbiological Research.

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A new gene expression study reveals broad cellular diversity as well as possibly ancient connections between the nervous, immune, and digestive systems.

 

When the first sponge genomes were sequenced in the early 2000s, researchers were surprised to find that sponges not only have roughly as many genes as humans and other complex creatures but also have many of the same genes. Sponges are among the earliest branching lineages on the evolutionary tree of animal life; their simple bodies don’t even have a pattern of symmetry or a set number of parts. The presence of those genes implied that the genetic information for functions like muscle contraction and the differentiation of neurons was much more ancient than muscles or nervous systems themselves.

 

But what were those genes doing in an animal without neurons or muscles? Researchers could only make educated guesses and investigate expression patterns on a painstaking gene-by-gene basis.

 

Today, however, a new study taking advantage of rapid advances in genomic technologies has illuminated where about 26,000 genes are expressed in the freshwater sponge Spongilla. This atlas of gene expression reveals the genetic configuration of cell types throughout the sponge’s body, including some cell types never described before. It offers important hints about how cell types evolved in the first place, and it may help to settle a long, thorny debate about whether neurons evolved just once or many times. The study appears in the latest issue of Science.

 

This ambitious paper “leapfrogs” over previous work, according to Scott Nichols, who studies sponge evolution at the University of Denver. “What is extraordinary about it is that really fascinating hypotheses have emerged from this data set,” he said. “But I would emphasize strongly that they need to be experimentally tested.”

 

The most exciting hypothesis concerns cells inside the sponge’s digestive chambers. The chambers are lined with distinctive cells called choanocytes, which have a collar of fingerlike protrusions (microvilli) and a flagellum. The choanocytes beat their flagella to regulate the flow of water through the digestive chamber, all the while feeding on small particles and debris the water carries. The digestive chambers also contain mobile “neuroid” cells that were described years ago, although their identity and function were mysterious.

 

Using high-throughput single-cell RNA sequencing technology, Detlev Arendt’s team at the European Molecular Biology Laboratory in Heidelberg discovered that choanocytes express genes that in neurons produce the postsynaptic “scaffolding” involved in receiving and responding to neurotransmitters. They also discovered that the mobile neuroid cells express a suite of genes that are typically active in the presynaptic bulb of a neuron. This led the researchers to hypothesize that the neuroid cells might be talking to the choanocytes and that the neuroid cells’ job might be to patrol the microbial environment in the digestive chamber and regulate the choanocytes’ feeding behaviors accordingly.

 

When Jacob Musser, the postdoctoral fellow in Arendt’s lab who led the project, stained the sponge to look at where exactly the pre- and postsynaptic genes were being expressed, he saw that the neuroid cells expressing presynaptic genes were indeed near the choanocytes expressing postsynaptic genes. In fact, the neuroid cells reached out pseudopod arms that seemed to touch the choanocytes.

 

“This was obviously really tantalizing,” Musser said. “But you can’t really tell what is going on.”

 

To get a more detailed picture of what the cells were doing, Musser and the team used focused ion beam electron microscopy at the X-ray synchrotron facility in Hamburg to get very high-resolution 3D images of the cells, which could distinguish cellular features as small as 15 nanometers, roughly the size of many folded proteins. They saw that projections from the neuroid cells enveloped the choanocytes’ microvilli collar and flagellum and that the neuroid cells held vesicles like those in the presynaptic bulb of a neuron. They suspect the vesicles are probably releasing glutamate, a neurotransmitter.

 

But tempting as it is to imagine these sponges as having primitive synapses, the researchers never observed direct, stable contacts between the neuroid cells and choanocytes. The connections between the cells instead seem to be transient. Furthermore, the DNA of sponges lacks genes for some of the key ion channels needed to create an action potential—the sharp electrical signal that stimulates the release of neurotransmitters in neurons.

 

Nevertheless, because sponges have always been thought to lack anything even resembling a nervous system, the suggestion that they have cellular mechanisms with a deep evolutionary relationship to neurons “is an exciting path forward to connect sponge biology to neural cell biology, to understand where neuronal signaling came from at all in animals,” Nichols said.

The origin of neurons and nervous systems—and in particular, the question of whether neurons arose once or multiple times—is one of the most contentious topics in the field of evolutionary developmental biology, according to Maria Antonietta Tosches, who studies the evolution of cell types in vertebrates at Columbia University and previously trained in Arendt’s lab. The findings from this new study seem to bear on that mystery because the researchers found presynaptic gene sets expressed in neuroid cells and postsynaptic genes expressed in choanocytes. (Both sets of genes were active in other cell types as well.) That fact suggests that the genetic modules responsible for both the sending and receiving ends of cell-cell communication systems were deployed in various types of ancestral animal cells. Neurons could therefore have evolved repeatedly and independently through different applications of these gene modules, Tosches said.

 

In fact, many multifunctional cells in sponges express modules of genes usually associated with specialized cells in more complex animals like vertebrates. For example, sponge neuroid cells not only express some of the presynaptic machinery of neurons, but also express immune genes. (It’s possible that if neuroid cells monitor the microbial content of the digestive chambers for sponges, these immune genes assist in that role.) Sponges also have cells called pinacocytes that contract in unison like muscle cells to squeeze the animal and expunge waste or unwanted debris; pinacocytes have some sensory machinery that responds to nitric oxide, a vasodilator.

 

“Nitric oxide is what relaxes our smooth muscle in our blood vessels, so when our blood vessels expand, that’s nitric oxide causing that relaxation,” Musser said. “And we’ve actually shown through experiments in the paper that nitric oxide is also regulating contractions in this sponge.” Like glutamate, nitric oxide might have been part of an early signaling mechanism to coordinate primitive behaviors in the sponge, he suggests.

 

“Our data are very consistent with this notion that a large number of important functional pieces of machinery existed early in animal evolution,” Musser said. “And a lot of early animal evolution was about starting to subdivide this out to different cells. But likely these very first cell types were very multifunctional, and they had to do multiple things.” The earliest animal cells, like their close relatives the protozoans, probably had to be cellular Swiss Army knives. As multicellular animals evolved, their cells may have taken on different roles, a division of labor that may have led to more specialized cell types. But different lineages of animals may have divvied things up differently and to different degrees.

 

If the mixing and matching of genetic modules was a crucial theme of early animal evolution, then comparing the arrangement and expression of those modules in different species could tell us about their history—and about possible limitations on how haphazardly they can be shuffled. One researcher looking for those answers is Arnau Sebé-Pedrós, who studies cell type evolution at the Center for Genomic Regulation in Barcelona and who published the first atlases of cell types in sponges, placozoans and comb jellies in 2018.

 

Sebé-Pedrós thinks that the spatial configuration of the genes along the chromosomes could be revelatory because genes located together can share regulatory machinery. “I’m absolutely shocked by the degree of conservation of the gene orders in animal genomes,” he said. He suspects that the need to co-regulate sets of functionally related genes keeps them in the same chromosomal neighborhood.

 

Scientists are still in the early days of learning how cell types evolve and relate to one another. But as important as it is to clarify the muddy origins of animal evolution, sponge cell atlases are also making a major contribution by revealing the possibilities in animal cell biology. “It is not just important for us to understand the very origin of animals,” Sebé-Pedrós said, “but also to understand things that may be radically different from anything else that we know about other animals.”

Sponge Genes Hint at the Origins of Neurons and Other Cells

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Cut a panther worm into thirds and each section will grow a new body. Researchers injected some with a fluorescent protein to study how.

 

In 1961, Osamu Shimomura and Frank Johnson isolated a protein from jellyfish that glow green under UV light. Corals, too, can fluoresce in a wide range of hues, thanks to similar proteins. Now scientists at Harvard University have genetically modified the three-banded panther worm to enable the creature to emit a similar green glow, according to a new paper published in the journal Developmental Cell. Their hope is to uncover the secrets to regeneration.

 

Most animals exhibit some form of regeneration: regrowing hair, for instance, or knitting a fractured bone back together. But some creatures are capable of particularly amazing regenerative feats, and studying the mechanisms by which they accomplish these could have important implications for human aging. If a salamander loses a leg, the limb will grow back, for example, while some geckos can detach their tails as a distraction to evade predators and then regrow them later. The zebra fish can regrow a lost or damaged fin, as well as repairing a damaged heart, retina, pancreas, brain, or spinal cord. Cut a planarian flatworm, a jellyfish, or a sea anemone in half, and it will regenerate its entire body.

 

And then there is the three-banded panther worm (Hofstenia miamia), a tiny creature that looks a bit like a plump grain of rice, so named because of its trademark trio of cream-colored stripes across its body. If a panther worm is cut into three parts, each part will generate into a fully formed worm within eight weeks or so. These worms are found primarily in the Caribbean, Bahamas, and Bermuda, as well as Japan, and they are voracious predators, not above taking a few bites out of their fellow panther worms if they're hungry enough and can't find other prey. They also offer a promising new model for studying the mechanics of regeneration.

 

Coauthor Mansi Srivastava, an evolutionary biologist at Harvard University, has been studying the three-banded panther worm since 2010, when she was a postdoc scholar in Peter Reddien's lab at MIT's Whitehead Institute. They collected 120 or so of the worms in Bermuda and brought them back to Cambridge. The worms did not immediately adapt to laboratory life: Srivastava and Reddien had to figure out the correct salinity levels for their water and find an acceptable food source. The worms didn't care for the liver Reddien had been feeding his planarian flatworms, and a few resorted to cannibalism to survive. Eventually, the researchers figured out that the panther worms loved brine shrimp (aka sea monkeys), and the creatures finally began to thrive and breed.

 

A report in 1960 had claimed that the worms could regrow their severed heads, but there was little scientific follow-up. Reddien and Srivastava's early experiments proved that the panther worms could not only regrow their heads, they could regenerate pretty much any body part, just like the planarian flatworms—even though the two are only distantly related. Srivastava now runs her own laboratory at Harvard studying regeneration in panther worms.

 

In 2019, Srivastava and her lab released the full genome sequence of the panther worm, as well as their identification of a number of "DNA switches" that appear to control the genes for whole-body regeneration. Specifically, they pinpointed a section of noncoding DNA that controls whether a kind of "master control gene" for regeneration, known as early growth response (EGR), is activated. EGR can, in turn, switch other genes involved in various processes on or off. If EGR isn't activated, regeneration in the worms can't occur.

 

EGR is also present in other species, including humans—and yet humans cannot regenerate their entire bodies. According to Srivastava, the process likely works very differently in humans than in the panther worms. "If EGR is the power switch, we think the wiring is different," she told The Harvard Gazette at the time. "What EGR is talking to in human cells may be different." Discovering more about how the genome interacts on a larger scale, rather than just at the level of individual switches, will be key to future breakthroughs. In other words, it's not just which genes are present, but how they are wired or networked together that enables full-body regeneration.

 

For this latest study, Srivastava and her colleagues figured out how to breed transgenic panther worms by introducing a gene that encodes a fluorescent protein. There are various kinds of fluorescent proteins, the most famous of which is green fluorescent protein (GFP).

GFP contains a special chromophore that absorbs and emits light. Shining UV or blue light on the chromophore causes it to absorb the energy, become excited, and then emit the excess energy as green light. GFP has since become a standard tagging tool for researchers all over the globe, enabling them to study biological processes previously invisible to the naked eye at the cellular level.

 

Srivastava and her team injected DNA modified to express a fluorescent protein into just-fertilized panther worm embryos, which were then incorporated into the genomes of other cells as they divided, again and again, until the embryos became full-grown worms. The adult worm's muscle cells glow green under UV light, and that fluorescent ability will be passed down to the worm's offspring. "We don't know how any one of these cells actually behave in the animal during regeneration," said Srivastava. "Having the transgenic worms will allow us to watch the cells in the context of the animal as it regenerates."

 

Thus far, this window into the inner workings of the panther worms as they regenerate has yielded structural insight into how the creatures' muscle fibers connect to each other, as well as to other cells. Srivastava et al. reported that extensions on the muscle cells interlock in columns to create a tight-knit grid, akin to a skeleton. The next step is to determine whether the muscles only serve a structural purpose or are involved in storing or communicating information about the regeneration process.

 

This article originally appeared on Ars Technica. 

Glowing Worms Could Shed Light On the Secrets of Regeneration

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Reconstructing past temperatures from marine sediments dating back to the peak of the last ice age, the study reinforces – once again – humans have caused a shift in Earth's climate never before detected in the geological record.

"This reconstruction suggests that current temperatures are unprecedented in 24,000 years, and also suggests that the speed of human-caused global warming is faster than anything we've seen in that same time," says Jessica Tierney, a paleoclimatologist at the University of Arizona and co-author of the study.

The findings underscore the latest report from the UN's Intergovernmental Panel on Climate Change (IPCC), released in August, which concluded that burning fossil fuels has heated the planet at a rate unprecedented in the past 2,000 years, such that human influence on Earth's climate is simply "unequivocal".

"The fact that we're today so far out of bounds of what we might consider normal is cause for alarm," adds lead author of the new paper, climate scientist Matthew Osman, also of the University of Arizona.

In this new study, Tierney, Osman and colleagues analyzed a staggering 539 paleoclimate records, dating back at least 4,000 years each and together spanning the past 24,000 years – from the peak of the last ice age (aka the Last Glacial Maximum) when vast ice sheets covered most of the Northern Hemisphere, to today.

Global temperatures for the last 24,000 years. #climate #paleoclimate #NSFfunded @UA_Climate @uazgeosciences @uarizona pic.twitter.com/agrTDUQGLg

— Jessica Tierney (@leafwax) November 10, 2021

Looking at geochemical signatures in marine sediments, sampled from coastlines and seafloors around the globe, the researchers inferred historical temperatures and used this so-called proxy data to update climate model simulations that are becoming increasingly sophisticated but still depend on data inputs.

Past attempts to reconstruct global temperatures over millennia have either focused on very narrow time windows, to hone in regional variability, or studied temperature changes averaged out over the globe, to get a big picture view of how Earth's climate has changed over time.

"The benefit of this [new] hybrid approach is that the proxy data bring the model closer to reality, and the model fills in gaps where no data are available," Shaun Marcott of the University of Wisconsin-Madison and Jeremy Shakun of Boston College, explain in a commentary about the study.

In graphs charting global temperature, the likes of which we've seen before, sharp temperature increases in the last 150 years are a sudden departure from earlier, gradual warming, the study shows.

The results "imply modern warming is extraordinary compared with that of the past 10,000 years," Marcott and Shakun add.

lobal average surface temperature since the last ice age (Osman et al.)

What's more, mapping global temperature changes around the world in 200-year intervals as ice sheets retreated and greenhouse gases soared provided a more "complete view of climate change" on Earth over the past 24,000 years, the study authors write.

There should be no surprise their analysis found that rising levels of greenhouse gases and the retreat of vast ice sheets are the two main drivers of climate change since the last ice age, but their maps of global temperature change do add something new. 

"With them, it's possible for anyone to explore how temperatures have changed across Earth, on a very personal level," Osman says. As you can see below, the darker the shade of blue, the colder the temperature compared to today.

Maps of global surface temperatures over 24,000 years (Osman et al. 2021).

"For me, being able to visualize the 24,000-year evolution of temperatures at the exact location I'm sitting today, or where I grew up, really helped ingrain a sense of just how severe climate change is today," Osman says.

Alas, Pacific Islanders who are already feeling the impacts of climate change need no such maps to understand what's at stake or how their homelands are changing.

There are also some technical limitations of the study worth noting. Just one climate model was used, which is not ideal, and no terrestrial data were included, only marine records – with very few data sourced from the central Pacific, Indian, and Southern oceans at that.

Nevertheless, the new study bolsters previous estimates of global temperature change produced from smaller amounts of data – the patterns of global heating through time, across the globe and in both hemispheres, are all very much alike, Marcott and Shakun write.

The team are now looking to apply their approach to ancient climates that were warmer than today, Tierney says, "because these times are essentially windows into our future as greenhouse gas emissions rise."

But as climate scientists keep stressing, the future climate is not a done deal. Every fraction of a degree of heating matters in our efforts to cut carbon emissions and avert the worst impacts of climate change.

"The climate we experience in the future depends on our decisions now," climatologist Valérie Masson-Delmotte told Nature in August upon delivering the sixth IPCC report. 

There's no time to waste.

The study was published in Nature.

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Blood pressure drugs could prevent millions of people worldwide from developing type 2 diabetes, a large study suggests.

Lowering high blood pressure is an effective way to slash the risk of the disease in the future, according to the research published in the Lancet.

Doctors already prescribe cheap blood pressure drugs to reduce the chances of a life-threatening heart attack or stroke. However, until now, the question of whether these drugs could also help fend off the threat of type 2 diabetes had been unanswered.

Now researchers have found the protective effects of the drugs are much wider than previously thought. The study shows they may directly reduce someone’s risk of type 2 diabetes, a condition that an estimated 13.6 million people in the UK are at high risk of developing.

In the largest study of its kind, researchers at the universities of Oxford and Bristol followed more than 145,000 people from 19 global randomised clinical trials for an average of about five years.

They found that a 5 mmHg reduction in systolic blood pressure – easy to achieve via blood pressure drugs or lifestyle changes – reduced the risk of type 2 diabetes by 11%.

Researchers also investigated the effects of five major types of blood pressure drugs from 22 clinical trials compared with a placebo. They found angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) had the strongest protective effect, both reducing someone’s relative risk of developing diabetes by 16%.

Other types of blood pressure-lowering drugs were not protective. Calcium channel blockers had no effect on type 2 diabetes risk, while beta blockers and thiazide diuretics actually increased the risk despite their known beneficial effects in preventing heart attacks and strokes.

Currently, health experts say being a healthy weight and adopting a healthy lifestyle is the best way to reduce the risk of type 2 diabetes.

Researchers say existing drugs – particularly ACE inhibitors and ARBs – should now be considered for some patients who are at higher risk of the disease.

Prof Kazem Rahimi, lead researcher of the study at the University of Oxford and a consultant cardiologist, said: “Our research provides clear evidence that giving ACE inhibitors or ARBs, which are widely available and affordable worldwide, to patients at high risk could curb the growing burden of type 2 diabetes.”

The research was funded by the British Heart Foundation (BHF), the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre and the Oxford Martin School.

Prof Sir Nilesh Samani, the BHF medical director, said: “Diabetes and high blood pressure are two important and growing problems which increase a person’s chance of developing an array of other serious health complications, including heart attacks and strokes. This research shows that the two are inter-connected and that lowering blood pressure could be a powerful way to reduce the risk of developing diabetes.

“It also shows that different commonly used drugs for lowering blood pressure have very different effects on risk of diabetes. Doctors should therefore consider the patient’s risk of developing diabetes when they are choosing an anti-hypertensive drug to lower their blood pressure.”

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In the agreement, Boeing accepted responsibility for Ethiopian Airways flight 302 losing control shortly after takeoff from Addis Ababa Bole International Airport. The plane nose-dived into a barren patch of land about 40 miles (65 kilometers) from Addis Ababa. There were no survivors.

At the time, it was the second crash to involve a Boeing 737-Max aircraft in six months. After the Ethiopian crash, U.S. authorities grounded the 737-Max until Boeing could fix the plane's faulty software.

In court documents filed Wednesday in federal court in Chicago, where Boeing is based, the company admitted that its software was to blame for ET 302's loss of control and destruction, and that the 737-Max was in an "unsafe condition" to fly. Boeing's 737-Max were recertified to start flying again earlier this year.

The agreement does not involve monetary compensation to the families as of Wednesday, according to court records, but it does allow victims' families to pursue individual claims in U.S. courts instead of their home country. The crash killed people of 35 nationalities.

It allows Boeing to consolidate its 737-Max legal issues to the U.S. while allowing victims' families to access the U.S. legal system, which is more equipped to handle such cases.

"This is a significant milestone for the families in their pursuit of justice against Boeing, as it will ensure they are all treated equitably and eligible to recover full damages under Illinois law while creating a pathway for them to proceed to a final resolution, whether through settlements or trial," said Robert Clifford, Steven Marks and Justin Green, the lead attorneys representing the victims, in a statement.

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Official adjudicator Carlos Tapia presented the award for the most hotspots—21,500—in a single free urban Wi-Fi network to Mexico City Mayor Claudia Sheinbaum.

The access points are spread across the sprawling city of some nine million people, particularly in public transport, although at times the network can become saturated.

When schools closed for more than a year during the Covid-19 pandemic, some students turned to the service to take part in online classes.

Sheinbaum said that the aim was to make internet access a right for all, in particular disadvantaged families with no connection at home.

Source

In short, nothing good—and just one bad night can trigger a cascade of scary side effects.
Outside

Scientists have a firm grasp on the purpose of certain automatic physical functions, like blinking, breathing, or digestion. When it comes to sleep, however, researchers still aren’t clear on why exactly your body needs to shut off every night. Details aside, one thing’s for sure: When you don’t sleep, your body revolts.

The effects of acute sleep deprivation—which is more akin to pulling an all-nighter than to getting just a few hours of sleep every night for weeks at a time (that’s chronic sleep deprivation)—generally kick in after 16 to 18 hours of being awake and get progressively worse with each proceeding hour. Your mind, heart, endocrine system, and immune system are all affected, malfunctioning in ways both subtle and severe.

The consequences of chronic sleep deprivation are far worse than one sleepless night. But the decision to pull an all-nighter just once can leave some serious damage in its wake.

Mind

When it comes to the effects of acute sleep deprivation, “It’s really all about the brain,” says Steven Feinsilver, director of sleep medicine at Lenox Hill Hospital and a leading sleep researcher. The first signal that your body is overtired will be a sluggish mind. Your reaction time will begin lagging around hour 18; after a full night without sleep, it will nearly triple—which, for context, is about the same as being legally drunk. Your ability to form memories will start deteriorating, and after a while, your capacity to create any new memories at all will shut off entirely.

“It’s almost as though without sleep, the memory inbox of the brain shuts down,” Matthew Walker, a UC-Berkeley professor and author of Why We Sleep, told Business Insider. “So those new incoming informational emails are just bounced.”

From hour 18 onward, your decision-making and math-processing abilities and your spatial awareness slowly deteriorate.

Stay up longer than 24 hours and your brain, now in panic mode, will soon take over and force sleep upon you. “You’re basically going to have microsleeps,” Feinsilver says. Though you will appear to be awake—walking, talking, eyes open—your brain will quite literally put itself to sleep for ten to 20 seconds at a time.

During these microsleeps, you can’t process what you’re seeing around you. “We say during sleep you are cortically blind—your brain does not process visual information,” Feinsilver says. “Your brain goes on on autopilot. So, if you’re driving, you might realize that you missed your exit and don’t remember the last ten minutes. And that’s really scary stuff, because it means you’ve been asleep for moments when you really should be awake.”

Stay up for longer than 35 hours, as Walker and a team of scientists from Berkeley and Harvard had research subjects do in a 2007 study, and your emotional mind will start behaving irrationally. When you’re up for that long, the emotion-emitting amygdala becomes 60 percent more reactive to negative stimuli or experience, while also limiting communication with the part of the brain that regulates emotion and contextualizes experiences. In other words, you’re more reactive and judgmental to the people and events around you, and your brain loses its natural ability to run things through a filter or any internal voice of reason.

If you’re up past 48 hours, hallucinations are common, as Feinsilver experienced firsthand years ago as a medical student. It was October, just before Halloween, and while he was suffering from both acute and weeks of chronic sleep deprivation, a nearby pumpkin started talking to him. “I realized, okay, it’s time to go home,” Feinsilver says.

Stay up for longer than 48 hours and you’re looking at behavior that mimics psychosis—incoherent rambling, disconnection from reality, prone to outbursts. Push yourself longer than a few days without sleep, and the effects can be lethal. The exact ways in which sleep deprivation can cause you to die aren’t entirely understood, but researchers believe it has to do with your mind losing its ability to control life-giving processes and the total disruption of your system that results.

So, why exactly does the brain malfunction in such a profound way without sleep? Researchers aren’t exactly sure, but their best guess has to do with something they’ve dubbed “substance S.”

“The brain is a very active metabolic area. When it works full-time, it generates toxic products,” Feinsilver says. “It’s like when you work out: Your muscles build up lactate, and eventually you can’t do anything more because it hurts, and it’s time to let them relax. Your brain is kind of on all the time while you’re awake, and sleep is designed to be a time to get rid of the toxic products that build up.” Substance S—which scientists think might be adenosine, a byproduct of metabolism that builds up in the blood—might be the toxic metabolite that accumulates in the brain throughout the day, and the need to flush it could be the reason your brain demands sleep every night.

At this point, though, the daily buildup of this metabolite and whether the brain is responsible for purging it during sleep is still only a theory “It’s just a good way of explaining why people might need sleep—it’s the most efficient way to purge a toxic product,” Feinsilver says.

Mechanism aside, we know that “wakefulness is essentially low-level brain damage,” Walker said in an interview with Business Insider.
Heart

Your blood pressure rises over the course of the day, usually due to the physical and emotional stressors you inevitably encounter. Every night while you sleep, your blood pressure (as well as your heart rate) drops back down. Sleep, in other words, is a natural blood pressure medication. Without that daily reboot, it steadily rises, and your risk of heart attack, stroke, and even long-term heart disease skyrockets.

If you’re awake for longer than 18 hours, your heart doesn’t get its daily respite, and that can have lethal consequences. In fact, research has found that on the Monday after spring daylight saving time, when we lose an hour of sleep, there’s a 25 percent increase in heart attacks. Conversely, in the fall, when we gain an extra hour, there is a 21 percent reduction in heart attacks. While scientists aren’t exactly sure why this is happening, it is clear that sleep—or lack thereof—has an immediate effect on your heart.

Endocrine System

Sleep is vital for hormone production, and if you’re up for more than 18 hours, your testosterone will slowly deplete, affecting energy levels.

The good news: Studies have shown that a subsequent night of good sleep can work to return testosterone levels to normal.

Where you get into real trouble, hormonally speaking, is after days, weeks, or months of bad sleep—when you dig yourself into a hole that your body can’t get out of. Studies have shown that just one week of sleep deprivation—less than five hours per night—dropped young male’s testosterone levels by a whopping 10 to 15 percent. For comparison, a healthy individual’s testosterone will naturally decline by 1 to 2 percent per year. In other words, as far as your hormonal system is concerned, a week of bad sleep will age you a decade.

Immune System

As you stay awake for longer than 18 hours, your body starts to build up pro-inflammatory proteins like IL-6, a blood marker associated with chronic health conditions and heart disease. Your number of immune cells begins to decline as well, as your body is deprived of its opportunity to make more.

Fight sleep even longer and your body will have a harder time producing natural killer cells, which fight cancer and virus-infected cells in your body. In fact, researchers have found that just one night of poor sleep reduces the amount by over 70 percent. Not sleeping will profoundly and immediately increase your risk for cancer, which is part of the reason that, in 2007, the World Health Organization deemed nighttime shift work a probable carcinogen.

Performance

If the body malfunctions, it’s safe to assume that your performance takes a hit as well, right? Yes, but the effect is more mental than physical. According to Shona Halson, senior recovery physiologist at the Australian Institute of Sport who specializes in sleep, “During exercise, you don’t see many changes in the physiological systems.” Instead, she says, “What we tend to see are changes in perception of effort. Everything feels harder, so you’ll do worse on a performance test, not because of physiological changes, but because your perception of effort has changed.”

And that’s a fact worth broadcasting, says Halson, because everyone has felt that panic after only managing a few hours of sleep before a big race. You’ll certainly feel tired, and your brain might be a little foggy, but you can still extract your fitness potential. “It’s important to tell athletes that if you get one bad night of sleep, the 20 years of training you have previously done doesn’t go away,” Halson says. “Your fatigability may have gone up a little bit after one bad night, but if it’s an important event, adrenaline usually kicks in.”

That’s not to say you shouldn’t be mindful of your performance after a bad night’s sleep. Halson says that in long endurance events or team sports, where there are more cognitive and emotional components than, say, a 100-meter sprint, a sleep-deprived brain can play tricks on the body. The best thing you can do: Remind yourself that you’ve put in the work and that the cloudiness you’re feeling is more likely than not just your brain asking for sleep.

https://getpocket.com/explore/item/what-happens-to-your-body-on-no-sleep

NASA Tries to Save Hubble, Again

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Cumulatively, Ingenuity has now flown more than 3 km across the surface of Mars.

NASA’s stalwart Mars helicopter is back and better than ever

• Google is using the new Business Profile to solicit small business opposition to pending antitrust legislation.
• Using search features to sway small business sentiment reflects a new, more aggressive Google policy towards regulation.
• Unfortunately, the authorities Google is using to support its position are largely astroturfed.

Google recently rebranded Google My Business as "Business Profile." They have been heavily promoting the new name and features via email to get small businesses to interact with the new search and maps interface. Clicking though I discovered Google had an additional and more nefarious use for this campaign.

I was shocked that the first call to action wasn't an invitation to edit my listing or even an incentive to buy Google Ads. It was a call to support Google's fight against possible antitrust regulations.

With all of the buzz around the rebranding, Google apparently couldn't resist the opportunity, however brazen, deceptive and totally misguided, to enlist the small business community in its antitrust fights.

Propaganda Plain and Simple

We are all used to Facebook crying wolf about how small businesses will be hurt by Apple's app-privacy initiatives. Now Google has apparently taken a page from Facebook's playbook.

When clicked, the call to action takes you to a page titled: Understand the impact new legislation could have on your business. On that page Google details, in a very Meta/Facebook-like fashion, all the pain small businesses will face if the government successfully manages to put in place a regulatory framework to limit Google's unprecedented power and reach.

First up was a call to join an email list to help with advocacy on behalf of Google. After signing up the page notes, "Together, we can help shape the policy conversation and have an impact on regulations that affect you — and your business." I assume that is the royal we.

They proceed to list the "costs" in time and money that small businesses would incur if these new laws are allowed to pass:

• Making it harder for customers to find you because your business listing (including your phone number, address, and business hours) may no longer appear on Google Search and Maps.
• Making your digital marketing less effective if Google Ads products are disconnected from each other and from Google Analytics.
• Hurting your productivity if Gmail, Docs, and Calendar are split up and they no longer work together seamlessly.

Search has never been objective, it has long reflected Google's editorial choices regarding what should and should not be shown. But deceptively using a new(ish) search feature to promote Google's clearly self-interested antitrust agenda and attempt to manipulate traditionally conservative small businesses to support that position moves search results from editorial content to something more like propaganda, plain and simple.

There seems to be no better way to prove Yelp right about Google's inappropriate control of search results than by this brazen political appeal. Clearly this "feature"  is not for the betterment of the user, as Google frequently claims. It's about bamboozling small businesses to support Google in their fight to remain a monopoly.

Takes Astroturfing to a New Level

Google provides what appear to be three authoritative references to buttress their position that the bills before Congress are bad for small business:

"For even more information on these bills, see why the Connected Commerce Council, Chamber of Progress, and US Chamber of Commerce oppose these bills."

You are probably familiar with the US Chamber of Commerce, one of our country's largest big business lobbying groups, spending roughly $100,000,000 million annually. Until 2019 they were climate deniers and actively fought against mild mannered climate bills. More recently they have opposed voting rights legislation. They have a long stood against worker's rights and stood for the interests of big business. To say, as Wikipedia does, that "politically, the US Chamber of Commerce is considered to be on the political right" is an understatement.

Google is not just a member of the US Chamber of Commerce but they actively promote it as well. There is an old adage: "You are who you hang with, so choose your friends carefully." Obviously Google has chosen.

But to assure left-leaning businesses that Google doesn't just hang with the right politically, Google offers another "authoritative" source: the Chamber of Progress, a "coalition of technology firms that supports pro-business public policies and left-of-center cultural values."

Yet the Chamber of Progress is funded by a rogues' list of Silicon Valley companies including Uber, Instacart, Grubhub, and Doordash as well as Google, Amazon, Facebook, and Twitter. "The Chamber’s founder and chief executive officer is Adam Kovacevich, who previously led the public policy team at Google." Independent they are not.

The third source referenced, the Connected Commerce Council, has but a single, noble goal: "To promote small businesses’ access to essential digital technologies and tools." It is also funded by big tech companies, Google, Amazon and Square, and has been called out by the Campaign for Accountability as Big Tech's Latest Astroturf Campaign. They have the look of a small business advocacy group but clearly serve other masters.

Search as a Political Tool

Previously, I had been somewhat ambivalent about Google's role as a monopoly. I have long felt that the Business Profile has helped many businesses grow and prosper. The choices Google made, while hurting some businesses, did seem to offer faster and cleaner information that benefitted many local businesses and  consumers.

Google results have historically reflected their discretionary editorial decisions and were well received by users. The monopoly that they had created, if not abused, would not be illegal.

Google has been more discreet in pursuit of their political goals and subtler in their managing of the press. They have always been able to get what they wanted from most political entities without too heavy a hand. However, the overt and blatant use of a search feature to promote a clearly political agenda, to help Google maintain its overwhelming monopoly, is "beyond the pale." Either Google has become desperate to regain control of the narrative or is becoming more obviously pugilistic to achieve its goals – or perhaps both.

This effort to manipulate small business folks with astroturfing is a whole new level of deception. It lays bare Google's intentions to protect their monopoly at all costs. Their attempt to buttress arguments with manufactured alliances, for legitimacy, adds fuel to an obvious fire.

Social Good to Self-Interest

Google has clearly moved from the commercial realm of search into using it to influence the political realm. While Google seems to be able to deliver websites and businesses to searchers, I have no faith that they can equitably deliver political solutions or political opinions via their search tools. Nor should they be in a position to use their monopoly to influence the body politic.

Yet Google is doing just that; using search to tilt the political playing field. They are not attempting to improve the political discussion, toward some social good. Rather Google is focused on its own, narrowly defined well-being. They obviously do all this with one interest in mind: their own, not the small businesses they are recruiting and certainly not the society at large.

Monopoly if not abused is not illegal. Monopoly used to disadvantage competitors is illegal. Monopoly used for self-interested social manipulation is immoral.

Update: Google seems to be a/b testing which delivery mode delivers the most sign ups and support for their politicking. Darren Shaw of Whitespark.ca) just surfaced an email with similar intent:

Google email to pitch SMBs on supporting Google's anti anti-trust agenda.

Source

More than a century later, in a paper published today in Cell, the neuroimmunologist Asya Rolls has shown that a similar kind of conditioning extends to immune responses. Using state-of-the-art genetic tools in mice, her team at the Technion in Haifa, Israel, identified brain neurons that became active during experimentally induced inflammation in the abdomen. Later, the researchers showed that restimulating those neurons could trigger the same types of inflammation again.

“This is an outstanding body of work,” said Kevin Tracey, a neurosurgeon and president of the Feinstein Institutes for Medical Research in Manhasset, New York. It “establishes that the classic concept of immunological memory can be represented in neurons.” Others before Rolls have suggested that the brain could remember and retrieve immune responses, he said, but “she proved it.”

Ruslan Medzhitov, an immunologist at the Yale School of Medicine in New Haven, Connecticut, considers the new research “very provocative.” But unlike other groundbreaking studies that push boundaries and challenge conventional concepts, he said that this one also evokes “the ‘Oh, it makes sense’ type of reaction.”

Decades of research and everyday experience offer striking examples of the interplay between mind and body. Around the time Pavlov was experimenting with drooling dogs, the American physician John Mackenzie watched one of his patients develop an itchy throat and struggle to breathe upon seeing an artificial rose — suggesting that the perception that pollen was present was enough to provoke her allergy symptoms. In the 1970s, scientists discovered a similar phenomenon while conducting taste-aversion experiments on rats: They repeatedly gave the animals an immunosuppressive drug along with the artificial sweetener saccharin; eventually, they found they could quell the animals’ immune activity with saccharin alone. Many of us can recall times when the mere scent of a food that once made us sick could trigger nausea anew.

But the mechanism responsible for these psychosomatic reactions has always been shadowy. Such experiences “cannot be guided by immunological memory as we know it,” said Rolls. Rather, it seems that these immune responses start in the brain, she said. “Somehow, there are these thoughts that initiate real physiological processes.”

In recent years Rolls’ lab has begun to get a handle on how thoughts and emotions could affect physical health. In 2018, she and her co-workers reported that stimulating neurons in the brain’s pleasure centers in mice disabled a subset of immune cells that suppress the body’s defenses; tumor growth slowed in those animals. In a study published in May, her team found that activating specific nerves in the colon prevented immune cells in the blood from entering the tissue — offering a mechanism for brain control over local inflammation.

Given that these groups of neurons regulated immune activity with such precision, Rolls couldn’t imagine that the brain would control a system without knowing its status. “So we wanted to see how the brain represents the state of the immune system,” she said.

Her team focused on the insular cortex, a structure deep within the brain that processes pain, emotions and the body’s inner physical sensations. “It would make perfect sense that the immune system would be part of this interoceptive information,” Rolls said.

To find out if that was true, the researchers slipped a chemical into the drinking water of laboratory mice to give them a weeklong bout of colitis.

The chemical disrupted the inner lining of the colon and triggered a rush of immune cells to the damage, which then harmfully spiraled out of control. A genetic modification in the mice enabled Rolls and her team to fluorescently label neurons active on the day the inflammation peaked, lighting up cells in the insula. They then used a second genetic tool to do something more powerful: They placed a molecular on/off switch onto the activated insula cells.

Then Rolls and her co-workers waited. Several weeks after the colitis subsided and the mice recovered, the researchers used their on/off switch to reactivate the neurons — and triggered a similar inflammatory response in the colon. They saw similar results in mice that had been induced to develop a different inflammatory disease, peritonitis, in the abdominal lining.

The immune responses sparked by neural stimulation “were reminiscent of the original” disease state, Rolls said. The similarities extended to the molecular level: In the mice with induced peritonitis, white blood cells carrying a specific receptor protein became more abundant in the abdominal lining during both the original inflammation and the inflammation evoked later.

The researchers also observed the opposite effect: When they instead inhibited the initial set of activated neurons, the animals’ disease symptoms weren’t as severe. This suggests that even during chemically induced inflammation, signals from the brain may be helping to determine its severity.

In a set of nerve-mapping experiments, the team determined that the insula neurons that kicked into action during the initial inflammation in fact “have a way to deliver a message all the way to the colon,” Rolls said.

In Tracey’s view, the new research shows “you can’t separate the state of the neuron activity from the state of the immune system activity. It’s a two-way street.”

In 2002, Tracey and his colleagues broke ground in this area with their discovery that the brain can send anti-inflammatory signals to other parts of the body through the vagus nerve. This line of research has advanced to the point where bioelectronic devices are being developed and studied to control inflammation in rheumatoid arthritis, pulmonary hypertension and other diseases.

Unlike the vagal nerve system, however, the insula neurons in Rolls’ mechanism sense the inflammation, remember that immune state and can reactivate it — a behavior that is more like Pavlovian conditioning than a negative feedback response, Medzhitov said. Tracey thinks of it this way: The vagus nerve is like a brake line in a car. Rolls’ study shows “there is a driver,” he said. “There is someone who decides whether to hit the brake or the gas pedal.”

However, as Rolls and her colleagues noted in their paper, they cannot yet say whether the insula neurons’ “memory” of the inflammation in some way describes the immune response itself, or if it’s instead a record of the sensations from the inflamed body tissues — in effect, the memory of what it felt like to be sick with that inflammation. They also can’t rule out that other parts of the brain could be involved in remembering the immune response too. What the study does show is that “this information is encoded even though it may not be consciously experienced,” said Medzhitov.

The research could have far-reaching implications. Describing an anatomical pathway that links “your emotional state all the way to the inflammation in the colon,” Medzhitov said, “that, to me, is probably the best demonstration available for psychosomatic control.”

The new findings also upend the common top-down view of the brain. “Most people tend to think, ‘We’re so smart, we decide what to do,’ and then we make our body do it,” Tracey said. “But that’s not how the nervous system works.” Instead, the brain receives and synthesizes information about changes in the body — an infection, a fever — and delivers a response.

Rolls’ work shows that “the brain is inseparable from the immune system,” said Tracey. “I think immunologists and neuroscientists both are going to be excited and surprised.”

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