Human Behavior

FAMILY MATTERS: Trait talk: What’s inherited and what’s created – Andover Townsman

Dear Doctor,

I ran across your article after having a discussion with my fiance. She has a teenage son who is exhibiting some very selfish behaviors. Long story short, I feel that he can be set on the right path by reinforcing more altruistic behavior and creating more opportunities for these positive actions. She thinks that selfishness is a trait passed on from her sons fathers side in that some of their behavior is on the selfish side and, as such, nothing we do will change his behavior. I ran across your article because I was looking for something that would prove or disprove her mindset. I am not looking at the human nature survival point, but rather whether something like selfishness is a trait that can be passed on through the gene pool from parent to child. Your thoughts?

Future Stepdad

Dear Future,

Thank you for your provocative email. We are a combination of genetics and experience.

Personally, it seems to me there is ample evidence for traits. Being more selfish may be one, but is more likely a combination of inheritance and experience. For example, suppose ones neurology predisposes toward caution or awareness of the reaction of others. Then, through a variety of experiences, which might include overindulgence, a behavior of self-entitlement is created.

You allude, for example to altruism. In my opinion, no human behavior, no matter how saintly, is completely altruistic. There is always some degree of self-centered reward in any human act. This is healthy narcissism.

Of course, there is such a thing as malignant and character-disordered narcissism, but that is another column.

Dr. Larry Larsen is an Andover psychologist. If you would like to ask a question, or respond to one, email him at lrryllrsn@CS.com.

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FAMILY MATTERS: Trait talk: What's inherited and what's created - Andover Townsman

Human Behavior

Economic Intuitions Behind The Q-Factors – Seeking Alpha

In their groundbreaking paper "Digesting Anomalies: An Investment Approach," published in the March 2015 issue of The Review of Financial Studies, Kewei Hou, Chen Xue and Lu Zhang proposed a new four-factor asset pricing model that went a long way toward explaining many of the anomalies that neither the Fama-French three-factor model nor subsequent four-factor models could explain. The authors called their model the " q-factor" model. Specifically, their four factors are:

The market excess return (beta). The difference between the return on a portfolio of small-cap stocks and the return on a portfolio of large-cap stocks (size). The difference between the return on a portfolio of low-investment stocks and the return on a portfolio of high-investment stocks. The difference between the return on a portfolio of high return-on-equity (ROE) stocks and the return on a portfolio of low ROE stocks.

In our book Your Complete Guide to Factor-Based Investing, Andy Berkin and I established five criteria that should be required before you consider allocating to a factor. The criteria are: persistence across long periods of time; pervasiveness across industries, countries, regions and even asset classes; robustness to various definitions; implementability (survives transactions costs); and intuitive risk- or behavioral-based explanations that provide reasons for believing the premium should persist in the future. We prefer risk-based explanations because risk cannot be arbitraged away, although popularity and the resulting cash flows can reduce premiums. However, we are willing to accept behavioral explanations because of limits to arbitrage which, along with the tendency for human behavior to remain unchanged, allow anomalies, such as the poor performance of small growth stocks with high investment and low profitability, to persist.

Given that one of the five required criteria is having an intuitive explanation for the persistence of the premium (with a preference for a risk-based explanation), it is important to note that Hou, Xue and Zhang provided theoretical underpinnings for the investment and profitability factors. They explained: "Intuitively, investment predicts stock returns because given expected cash flows, high costs of capital mean low net present values of new projects and low investment, and low costs of capital mean high net present values of new projects and high investment. Profitability predicts stock returns because high expected cash flows relative to low investment must mean high discount rates. The high discount rates are necessary to offset the high expected cash flows to induce low net present values of new projects and low investment."

Among their important findings was that the investment and profitability (ROE) factors are almost totally uncorrelated, meaning that they are independent, or unique. In addition, the authors found that the alphas of the value and momentum factors in the q-factor model are small and insignificant. These two factors, and the role they play, have been replaced by the investment and ROE factors. They also found that the q-factor model outperforms the Fama-French three-factor and four-factor models in its ability to explain most anomalies. In fact, most anomalies become insignificant at the 5 percent level of statistical significance. In other words, "Many anomalies are basically different manifestations of the investment and ROE effects."

The authors did acknowledge, however, that "the q-factor model is by no means perfect in capturing all the anomalies." Like all models, even the q-factor model is flawed, or wrong. If a model were perfect, it would be called a law (as we have in physics).

Because of its empirical success, the use of the q-factor model by practitioners for performance evaluation and portfolio management has been increasing. In addition, Eugene Fama and Kenneth French built on the concepts from the q-factor model, incorporating a profitability factor and an investment factor into their five-factor model (market beta, size and value being the other factors) and a six-factor model, which added momentum.

Given the risks of data mining, it's important that any factor model has intuitive explanations for why the factors explain the variation in returns across diversified portfolios. Otherwise, there will be questions about the theoretical soundness of the model.

Suresh Rajput and Muhammad Ilyas contribute to the literature on factor models with their January 2020 study "Do the Q-Factors Proxy for Surprises in Economic State Variables? They investigated whether the q-factors of ME (size), I/A (investment/assets) and ROE correlate with surprises in economic variables within the framework of the intertemporal capital asset pricing model (ICAPM). They ask if the q-factors are in line with the intertemporal asset pricing theory, which theorizes that average returns are explained by the responsiveness of returns to the changes in expected investment opportunities. They chose a set of important economic state variables that have been shown in the literature to help explain the mean and variance of stock returns, such as term spread, short-term T-bill yield, default spread and dividend yield, to describe the changes in expected investment opportunities. The term spread is the spread of 10-year and one-year government bonds. The dividend yield is the sum of the last 12 months' dividends divided by the level of the index. The default spread is the spread of long-term Baa and long-term government bonds. And the risk-free rate is the yield of a one-month Treasury bill. Their data sample covered the U.S. market over the period January 1967 to December 2018. Following is a summary of their findings, each of which was significant at least at the 5 percent confidence level:

There is a significant correlation between q-factors and shocks in state variables. ME correlates with the surprises in default spread, term spread and Treasury bill yield. I/A is related to the surprises in aggregate dividend yield. ROE correlates with surprises in term spread and default spread.

These findings led the authors to conclude: "These findings suggest that the q-factors may act as a proxy for the surprises in economic state variables that describe the changes in the investment opportunity set."

Summarizing, Rajput and Ilyas provide evidence that the q-factors are related to surprises to economic variables that have been shown in the literature to help explain the mean and variance of stock returns, providing the important theoretical risk-based explanation for why investors should expect the premiums to persist, as risk cannot be arbitraged away.

Through their research, financial economists continue to advance our understanding of how financial markets work and how prices are set. The Fama-French three-factor model was a significant improvement on the single-factor capital asset pricing model (CAPM). Mark Carhart moved the needle further by adding momentum as a fourth factor. The authors of the q-theory made further significant advancements, which in turn motivated the development of the competing Fama-French five- and six-factor models.

The competition to find superior models is what helps advance our understanding not only of the markets but also our understanding about which factors to focus on when selecting the most appropriate investment vehicles and developing portfolios.

Disclosure: I/we have no positions in any stocks mentioned, and no plans to initiate any positions within the next 72 hours. I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it (other than from Seeking Alpha). I have no business relationship with any company whose stock is mentioned in this article.

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Economic Intuitions Behind The Q-Factors - Seeking Alpha

Human Behavior

Is Speciesism Driving the Coronavirus Pandemic? – Sentient Media

Reluctance to question humans exploitation of animals creates a dangerous disconnect in the publics understanding of COVID-19 and its ongoing risks. Lorelei Plotczyk shares her perspective.

Reading Time: 11 minutes

Reluctance to question humans exploitation of animals creates a dangerous disconnect in the publics understanding of COVID-19 and its ongoing risks. Lorelei Plotczyk shares her perspective.

During a global pandemic, likely caused by the exploitation of animals, humanitys relationship with other species continues largely unchanged: meat flies off the shelves and a docu-series trivializing the plight of captive wild animals is an Emmy-nominated success. What makes it possible for most humans to continue as normal instead of questioning our relationship with or use of non-human animals? Perhaps its thanks to the social construct we call speciesism.

Speciesism is defined as the assumption of human superiority leading to the exploitation of animals. It is an implicit bias that spans across cultures and renders humans unable or unwilling to connect animal exploitation to the resulting consequencescurrent catastrophe included. Diseases originating from animals, called zoonoses, have caused nearly every pandemic in human history per TIME Magazine, yet that causal relation is largely relegated to scientific and activist discussions that dont permeate the popular conversation. Widespread reluctance to examine the root cause of the pandemic is creating a disconnect in the prevailing discourse.

Humanitys relentless exploitation of animals, especially for food, dramatically increases opportunities for zoonoses to infect people. Given the scope and scale of that undertaking, the truly shocking thing about the COVID-19 pandemic is that it didnt happen sooner. By exploiting animals, humans willfully perpetuate the largest vector for zoonotic disease that would not otherwise exist. And while no longer interfering with animals is logically the best approach to prevent future zoonotic pandemics, many people are reluctant to give up the resulting pleasures, especially animal products. Societys collective failure to change accordingly would be akin to continuing to smoke after a lung cancer diagnosiswith the whole world obligated to pay the price.

Zoonoses outbreaks, which are mediated by human action in most cases per 2012 research, have quadrupled in the past 50 years. A 2013 United Nations Food and Agriculture Organization (UN FAO) report calls much of this surge directly related to the human quest for more animal-sourced foodyet speciesism guides the narrative away from human culpability. Zoonotic pathogens are often described as jumping to humans due to contact or mixing with animals, while humanitys role is neutralized to detectives figuring out where problematic interactions occur. Such framing serves to mystify the primary reason for the interactions while masking their exploitative nature.

Humans predatory dominion over non-human animals is the reason why zoonoses now account for 75 percent of emerging infectious diseases. We annually breed, rear, and slaughter domesticated animals by the billions while destroying biodiverse habitats for grazing and feed crop production; we hunt, fish, trade, and even farm trillions more so-called wild animalsall while exploiting countless others for clothing, entertainment, experimentation, and sport. Worse, we do so despite having the tools and technology to phase out animal exploitation altogether. Widespread aversion to examining avoidable yet normalized violence against animals prevents honest discourse, and therefore meaningful conclusions, about the resulting scourges.

Zoonoses rose in prevalence whensurprise!humans began forcing wild animals into domestication, largely to serve as our own species living stock, around 10,000 years ago. Since then, researchers note, so-called livestock use has continued to present new health challenges and new opportunities for emergence of zoonotic pathogens. One such opportunity resulted in losing up to 90 percent of the Native American population to livestock-derived zoonotic diseases brought over by European colonists. Today, slaughterhouse workers and animal farmers are at the leading edge of the human-animal interface and more likely to become infected with a zoonotic virus per CNN. Yet ending that cycle by phasing out livestock use altogether is largely excluded from the general conversation. Politicians are unwilling to risk their popularity and scientists refuse to draw the logical conclusions to which their own research points, with rare exception.

Humanity has long focused on prevention and response measures for pandemics that avoid any honest reevaluation of the human behavior that is primarily driving them: animal exploitation. Instead of challenging the status quo, mainstream news organizations continue to reinforce this disconnect by omitting, or even distorting and blocking, vegan advocacy linking animal consumption to zoonoses. A recent Sentient Media survey finds that nearly all trending COVID-19 coverage omits the connection between animal exploitation and pandemics, at best using vague language like it came from animals. Like other oppressive mindsets, speciesism creates an insidious alternate reality in which we blame the victims (when we bother to consider them at all) instead of the victimizers.

The wildlife trade is widely implicated in unleashing the novel coronavirus, but conventional animal farming may have played an equally crucial role. Leading virologist Christian Drosten tells the Guardian that humans create opportunities for coronaviruses to switch hosts through our non-natural use of animalslivestock. At the China food market linked to early COVID-19 cases, wild animals mixed with livestocksomething TIME calls a big risk and the National Review a deadly combination. Per 2014 research, domesticated animals like livestock serve as amplifiers of pathogens that emerge from wild animals and are the central ones in the network of zoonotic disease transmission. A July 2020 UN report on preventing the next pandemic reiterates that although wild animals may harbor zoonotic diseases, livestock act as a bridge for transmission between the animal hosts and humans.

The novel coronavirus may have originated in bats, but it required an intermediary host to infect its first human. Farming advocacy group GRAIN calls farmed pigs an obvious candidate given their human-like immune systems, and Scientific American reveals that an earlier strain of coronavirus likely crossed from bats to pigs. The latter cites infectious disease epidemiologist Gregory Gray in warning that looking for novel coronaviruses in pigs should be a top priority due to the massive global scale of pig farming. Ceasing to breed and consume pigs and other animalsthese activities being the actual root of the problem, versus the bats or pigs themselveswould be far more effective. Whether or not COVID-19 is ever traced to humanitys bacon obsession, it appears inevitable that our appetites for animals will continue to unleash other diseases like swine flu and avian flu (despite the livestock sectors denial).

Science links zoonotic diseases to animal exploitation and especially to animal farming. A 2004 joint report by groups including the World Health Organization identifies increasing demand for animal protein as a common theme among the risk factors for zoonoses emergence. The Lancet published research in 2007 linking zoonoses to the environmental degradation associated with livestock and in 2012 to animal production systems. Reuters coverage of another 2012 study warns most human [zoonotic] infections are acquired from the worlds 24 billion livestock, adding that exploding global demand for livestock products means the problem is likely to get worse. Now that COVID-19 is here, the July UN report on pandemic prevention makes clear that increasing global meat demand only exacerbates future pandemic risk. Referring to the Spanish Flu of 1918-20 and the novel coronavirus, a group of doctors writing for the Journal of Disease Reversal and Prevention points out that the two largest pandemics in the past 100 years revolve around our food choicesspecifically, the consumption of animals. Sadly, such credible scientific research continues to prompt little meaningful action.

Experts have articulated for decades that livestock production risks catastrophic pandemics; Dr. Michael Greger, author of Bird Flu: A Virus of Our Own Hatching, details as much in an eerily prescient 2008 presentation. That same year, a GRAIN report on emerging viruses notes governments unwillingness to confront the dominant powers of industrial livestock farmingan unwillingness that evolutionary biologist Rob Wallace implicates as causing the current pandemic. He says that the likelihood of the livestock industry unleashing a virus that might kill a billion people is regarded as a worthy risk. A social media poll shows that many animal consumers willingly accept those terms.

The pandemic risk posed by meat and dairy production is not exclusive to the most intensive forms of animal farming (often referred to collectively as factory farming). Per the UN FAO, suggestions claiming otherwise are misleading. Its 2013 report states that disease emergence in livestock is not specific to large-scale, intensive systems and includes animals roaming freely over large areas. The 1918 influenza pandemic, after all, may have originated from pig and poultry barns predating todays highly-mechanized and concentrated animal feeding operations (CAFOs). Modern subsistence farming remains anything but industrial, yet it still contributes to the emergence of zoonoses; 2012 research finds a strong correlation among dependence on livestock, poverty, and zoonotic disease. Either way, planetary boundaries dictate that the vast majority of current global demand for animal products can only be met by CAFOs, which are known breeding grounds for pathogens.

Whether free-range or intensive, animal farming also unleashes zoonoses by destroying habitats. Despite dominating global land use, livestock production provides just 18 percent of humanitys calories and 37 percent of our protein. Extensively transforming forests for grazing and growing feed encourages emerging diseases by causing unnatural overlap of domestic and wild species, amplified disease activity in displaced animals, and disruptions in species populations that, when balanced, naturally keep diseases more contained. Livestock production is the single largest driver of habitat loss, a 2015 study states. A 2018 study finds that shifting to plant-based farming has the extraordinary ability to offset habitat loss by freeing up an area of land equivalent to the U.S., China, the European Union, and Australia combined. An evolution away from livestock reliance is an unparalleled solution for mitigating habitat loss.

Of the many experts connecting habitat loss to zoonoses, several specifically implicate livestock farming. One Health initiative co-founder Laura H. Kahn links livestock production with the widespread deforestation that has contributed to the emergence of zoonotic diseases. Pandemics expert Sonia Shah points out that replacing wild habitats with animal farming ratchets up the risk of disease emergence, yet, weve razed an area around the size of the continent of Africa to raise animals for slaughter. Global health expert Alanna Shaikh says that zoonotic outbreaks are encouraged by pushing into the last wild spaces on our planet, including when we burn and plow into the Amazon rainforest so that we can have cheap land for ranching. Againdespite the misleading vilification of vegan-associated foods like soy or even mainstream favorites like almonds and avocadosongoing large-scale deforestation and corresponding habitat destruction are unavoidable without a widespread dietary shift to plant-based foods.

Incredibly, the extreme biosecurity risks of animal use are not limited to zoonoses. Livestock production is also driving the rise of foodborne pathogens like salmonella and E. coli as well as worsening human antibiotic resistancecategorized by the U.N. as a developing crisis on par with AIDS and Ebola. Livestock vaccinations are now being touted as a solution to prevent zoonotic diseases, yet they only help to stop the spread of existing rather than novel viruses. In the words of bioethicist Jan Deckers, As high populations of farmed animals are maintained only because of human demand for their products, many consumers of animal products are more likely to impose diseases upon other human beings compared to those who refrain from such consumption. The prevalence of speciesism prevents most people from taking even a shred of ownership for the collective consequences of animal exploitation, no matter how extreme.

Rather than blaming those we otherize, both human and non-human, significantly decreasing the likelihood of future pandemics requires ceasing all forms of animal exploitation. Racist rhetoric blaming China for COVID-19 diverts attention away from humanitys collective behaviors that drive the emergence of novel zoonoses. Sam Scarpino, who advises public health agencies on controlling emerging epidemics, explains that despite the myopic public focus on Asia, new flu strains emerge from American livestock operations almost every summer. Farmed animals continue to be transported vast distances for slaughter in conditions that risk public health at facilities that prioritize profits over attempted disease reduction. Vested interests prompt some to decry any meaningful critique of animal agricultures necessity, instead invoking improved monitoring and regulationyet humanity has had over 10,000 years to get this right. The next zoonotic disease outbreak with the potential to infect humans is already spreading amongst farmed pigs.

The COVID-19 pandemic exemplifies the negative feedback loop often created when the powerful exploit the vulnerable. Using some animals for food subjects other animals to laboratory experiments in an attempt to control the resulting preventable zoonotic diseases and dooms others still to mass depopulation. Animals confined to fur farms and zoos for fashion and entertainment are even contracting this virus. As the human death toll continues to rise, the risk of exposure to COVID-19 compounds the routine exploitation of slaughterhouse employees. While no one is immune to the health and ecological consequences of animal exploitation, poor and marginalized people, primarily communities of color, are often hardest hit by its negative effects. COVID-19 is no exception.

Even in the midst of a pandemic linked to animal consumption, the U.S. government continues to favor animal farming over plant-based food production. As with already-existing farm subsidies, livestock producers are receiving the lions share of COVID-19 agricultural aid. Slaughterhouseswidely euphemized as meat plantsare now deemed critical infrastructure, prompting the Center for Biological Diversity to observe that Trump is willing to sacrifice workers lives to prop up the nations inhumane and environmentally destructive addiction to meat. Although its undeniably regressive to pretend as though abundant alternatives to animal products do not exist, this particular form of denial spans across the political parties.The media, in typical form,mischaracterized the predicted meat shortage as a crisis, rather than an uncannily-timed opportunity to socially distance ourselves from meat and dairy. A USA Today investigation has since exposed that the meat shortage scenario was highly exaggerated to keep slaughterhouses operating.

With so much of the current situation beyond our control, there is something humanity can do to avoid repeating history. The Lancets 2007 research advises that a reduction in livestock production would decrease human contact with new infectious agents, while its 2012 research finds wide-scale adoption of a plant-based diet may result in a decreased threat of zoonotic disease. Infectious diseases advisor Dr. Daniel Schar names mitigated risk from pandemic disease among the many planetary health dividends of plant-based diets, a sentiment that public health specialist Aysha Akhtar echoes in her 2014 TEDx Talk. One Healths Laura Kahn suggests consuming less meat (and raising fewer animals for food) and promoting meat alternatives or vegetarian diets. Among the lessons that can be gleaned from scientific documentation of how the novel coronavirus emerged, per Forbes Jeff McMahon, is that humanity needs to just eat plants. Scientist Liz Specht writes that plant-based and cultivated meat is helping to remove the food insecurity and zoonotic disease concerns inherent in animal-based food. A team of international wildlife and veterinary experts concludes in a June 2020 report that humanity can increase switching to plant-based foods to reduce consumption of, and demand for, animal products to reduce the risk of pandemics in a post-COVID-19 world. Ecologist Carl Safina argues, Whats needed to reduce the frequency of new diseases adapting to humans from animals is, basically, to stop farming and eating them. The group of doctors writing in the Journal of Disease Reversal and Prevention agrees, urging a reevaluation of, or even a moratorium on, eating animals. Scientist and physician Vural zdemir considers COVID-19 as a wake-up call to embrace veganism and animal sentience, and stop wildlife trade and commodification.

Signs of an urgently-needed change in animal consumption are starting to surface. At the very least, reports NPR, COVID-19 has more people rethinking their relationship with meat. Sierra Club notes that because COVID-19 struck at a time when global meat demand was [already] declining, plant-based eating is now becoming more widely accepted as a form of environmental and political engagement. A Psychology Today op-ed contemplates a more dramatic shift to veganism emerging from this pandemic. The New York Times decisively names slaughterhouses as the food chains weakest link while declaring that the end of meat is here. A Harvard Political Review headline calls just as bluntly for the end of animal agriculture. Other mainstream outlets report that COVID-19 is catalyzing less reliance on animal protein and more demand for plant-based meat (for which U.S retail demand surged in March and April). July headlines report the UNs projection that the biggest global meat-eating decline in decades is now underway, due in part to increasing public distrust of animal products. Many experts recommend purchasing mostly plant-based foods to stock up pantries while limiting grocery store trips. Per Specht, taking animals out of our food system is easier than we may thinkand now, as many are experiencing firsthand, so is taking them out of our kitchens. Systemic roadblocks to veganism, such as food deserts, remain as deterrents for those in underserved communities, but various collectives and nonprofits are addressing dietary inequities to better establish veganism as a right for all. The global benefits to be gained by making plant-based diets more accessible, in concert with a widespread rise of both anti-racism and anti-speciesism, would be transformative.

Contemplating the pandemics aftermath, a renowned epidemiologist told the media that he hopes people will realize that humans are all much more alike than different. Anti-speciesism simply extends this realization to other sentient species. Those we use and kill with impunity are at our mercy; now, we all are at the mercy of a virus unleashed by that abuse of power. The single and shared beating heart begging us to change our ways, as depicted in Kristin Flyntzs viral poem, belongs to animals, too. A global pandemic is just one type of catastrophe on a long list of those related to animal use. Imagine that its potable water (the depletion of which animal consumption is driving) instead of just hand sanitizer that were fighting over. Or, to quote one Twitter user, If you think COVID-19 is scary, wait until antibiotics no longer work. Embracing safer, more eco-friendly, and more ethical alternatives to animal exploitation is our best defense against the next potential pandemic and countless other preventable emergencies in the making. The idea that anyone should willfully default to animal violence persists due to nothing but a stale social construct.

So lets aim to never get back to normal. The truly transformative wake-up call of COVID-19 would be for humanity to finally acknowledge the disastrous consequences of all oppressive hierarchies, including speciesism, and begin to dismantle them, together, for the benefit of all sentient beings.

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Is Speciesism Driving the Coronavirus Pandemic? - Sentient Media

Human Behavior

Vaccines undergo strict safety testing before they are licensed for use in the US and many other countries; no validity to the claim of a 33% death…

CLAIM

Would you take a vaccine with a 33% death rate to feel safe from a virus with a .06% death rate?

DETAILS

Inaccurate: The claim that a COVID-19 vaccine has a 33% death rate is not supported by scientific evidence. This claim is likely based on a separate false claim about a nonexistent COVID-19 vaccine trial from Ukraine.

KEY TAKE AWAY

More than a hundred COVID-19 vaccine candidates are in the midst of testing worldwide. The claim that a COVID-19 vaccine has a 33% death rate is false; there is no evidence to support it. The claim is most likely based on a separate false claim that five out of 15 volunteersamong whom were four Ukrainian soldiersdied in a vaccine trial in Ukraine, which was refuted by the Ukrainian military. Despite efforts to accelerate the usual timelines used in vaccine development, COVID-19 vaccines are not being approved by public health authorities until they undergo rigorous testing for safety and effectiveness. A vaccine with a demonstrated 33% death rate has not been and would never be approved for use in the U.S. or most other countries.

REVIEW Facebook posts (example) asking the question Would you take a vaccine with a 33% death rate to feel safe from a virus with a 0.06% death rate? began circulating in late July 2020, and have received more than 10,000 interactions on Facebook, according to the social media analytics tool CrowdTangle. The identity of the virus and the vaccine are not explicitly stated in the post, but it most likely refers to the virus SARS-CoV-2 and the COVID-19 vaccine.

The question posed in the post introduces the false premise that a COVID-19 vaccine has been developed and found to cause death in 33% of people who receive it. Although the Facebook posts do not provide any information about the source of this figure, it is most likely based on a recent false claim that five of 15 test subjects died in a clinical trial conducted in Ukraine which tested a COVID-19 vaccine supposedly developed in the U.S. The claim, which was attributed to the Lugansk Media Centre (example) and the Lugansk Peoples Republic, was debunked in fact-checks published by Vox Ukraine and AFP Fact Check. Lugansk is a city in eastern Ukraine which is involved in a territorial dispute between Ukraine and Russia. The claim was also published by News Front, an outlet known for publishing pro-Russia disinformation, according to PolitiFact.

PolitiFact reported finding no record of a COVID-19 vaccine trial taking place in Ukraine in ClinicalTrials.gov, a database of privately and publicly funded clinical studies conducted around the world, which is run by the U.S. National Library of Medicine. Similarly, the ISRCTN Registry, a clinical trial registry recognized by the World Health Organization and the International Committee of Medical Journal Editors, contains no record of any such study. Vox Ukraine also stated, There is no confirmed information on the beginning of the COVID-19 vaccination in Ukraine and The Ministry of Defence hasnt reported [about COVID-19 vaccination], either.

According to AFP Fact Check, the Ukrainian military has also refuted the claim, with spokesperson Oleksiy Mazepa confirming, There are no tests with our soldiers. This is obvious fake news. This is the way Russian propaganda works.

The involvement of the Lugansk Media Centre and the Lugansk Peoples Republic in the propagation of this claim suggests that it may have originated as part of a Russian disinformation campaign. Outlets with links to the Russian government have had a track record of promoting misinformation about vaccines and COVID-19, among other topics. EUvsDisinfo, a project of the European External Active Services EastStratCom Task Force, which addresses Russian disinformation campaigns, has documented these ongoing campaigns here and here.

In a 2018 study published in the American Journal of Public Health, researchers from the George Washington University who studied more than 1.7 million tweets found that Russian trolls and bots contributed to online vaccine misinformation by promoting discord and false equivalency, fostering the appearance of a genuine public debate over vaccines, and driving vaccine hesitancy[1].

As of 9 August 2020, more than 165 COVID-19 vaccine candidates are in development around the world, according to the New York Times Coronavirus Vaccine Tracker. A vaccine remains the only way to achieve herd immunity safely, as Carl Bergstrom, a biologist at the University of Washington, and Natalie Dean, a biostatistician at the University of Florida, state in a New York Times opinion piece.

It is challenging to determine the exact percentage of immune individuals needed to achieve herd immunity to COVID-19 in a population because the number depends on many biological and social variables, as Marm Kilpatrick, an epidemiologist and professor at University of California Santa Cruz, explains in this Twitter thread. One study published in Science used a mathematical model that considered variations in human behavior to estimate that herd immunity would be reached when 43% of a population was immune to the disease[2]. In contrast, an article published in Immunity estimated that approximately 67% of the population needs to be immune[3]. However, this estimate is based on the model of classical herd immunity, and the authors cautioned that this model relies on simplifying assumptions, such as homogeneous population mixing and uniform sterilizing immunity in recovered individuals across demographic groups, which are unlikely to hold true [in real life].

Although there is pressure to develop a COVID-19 vaccine quickly, scientists emphasize that vaccine safety must remain a top priority. You really have to test a vaccine carefully, and not just roll it out because people are clamoring for it with an epidemic underway, said Marc Lipsitch, an epidemiologist at the Harvard Chan School of Public Health, in a PNAS news article published 30 March 2020.

Shibo Jiang, a virologist at Fudan University, also warned of significant repercussions if vaccines and therapies reach the market before adequate safety testing. The publics willingness to back quarantines and other public health measures to slow spread tends to correlate with how much people trust the governments health advice. A rush into potentially risky vaccines and therapies will betray that trust and discourage work to develop better assessments, he wrote in a Nature article.

Vaccine candidates, including those for COVID-19, must pass several stages of clinical trials that demonstrate their safety and efficacy before they are approved for public use in the U.S. (see figure below), the U.K., Australia, the European Union, and other parts of the world.

A COVID-19 vaccine that kills one in three people would not pass clinical trials or be licensed by health authorities, as this would be considered an unacceptably high risk of serious adverse effects.

Overall, the claim that a COVID-19 vaccine has a 33% death rate is false and unsupported by scientific evidence. It is likely based on a separate claim, which was refuted by multiple sources.

Although it remains unclear which, if any, of the COVID-19 vaccine candidates currently undergoing testing will ultimately be licensed for public use, there has been a surge of misinformation about COVID-19 vaccines on social media. Health Feedback reviewed some of these claims, including the false claims that RNA vaccines alter our DNA and that a volunteer died during a vaccine trial in April. The proliferation of such misinformation has left its mark. According to an article published in Science on 30 June, as few as 50% of Americans plan to get a COVID-19 vaccine, while in France more than 25% said they would not get a vaccine. In the United Kingdom, about 16% of people surveyed said they would refuse a vaccine and another 16% said they were uncertain.

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Vaccines undergo strict safety testing before they are licensed for use in the US and many other countries; no validity to the claim of a 33% death...

Human Behavior

Quietly waiting in the background of the pandemic, AI is about to become a big part of our lives – The Province

Way back in December, before the world started paying attention to the novel coronavirus, a Toronto-based company called BlueDot Inc. noticed the first hints that something was amiss.

By applying an artificial intelligence algorithm to analyze news reports and airline ticket data, BlueDot noted a significant disease outbreak brewing before even the World Health Organization raised the alarm.

An AI epidemiologist sent the first warnings of the Wuhan virus, a Wired headline reported in late January, flagging BlueDots achievement.

BlueDot earned another round of media coverage in March when the rest of the world caught up in understanding the seriousness of the COVID-19 pandemic.

Our weird behavior during the pandemic is messing with AI models

The companys use of artificial intelligence was the sort of application where the technology can shine: taking in large amounts of data to then find subtle patterns beyond what humans can come up with themselves.

But a couple of months later, the technology press was telling a different story.

Our weird behavior during the pandemic is messing with AI models, an MIT Technology Review headline declared.

AI systems designed to predict the rhythms of human behaviour based on historical data were no longer working, because those rhythms had been turned upside down by the pandemic-induced lockdown.

In spite of the hype and excitement among technologists in the past few years, AI has also been largely absent from the conversation about how to fight the coronavirus, with even the most ardent adherents acknowledging the technology has largely faded into the background during the pandemic.

The most significant public health measures have been decidedly low-tech, such as social distancing, cloth masks and track-and-trace epidemiology, but experts say the dip in attention wont last too long.

Indeed, the longer the pandemic lasts, the more important artificial intelligence will become, they say, and it will likely play a big part in the economic recovery.

I would tend to agree with you that the real-world impact has been relatively minimal, and theres different reasons for that, said Jean-Franois Gagn, chief executive of Element AI, a Toronto-based AI software developer.

Theres just only so much an algorithm can do in figuring out risk and uncertainty when things are so volatile.

Artificial intelligence is a hazily defined term for a collection of technologies, but most of the excitement in the past decade has been around deep learning, which uses computer programming structures loosely modelled on the neural networks in human brains.

Its possible to train an algorithm to identify patterns and make predictions by feeding vast amounts of data into these computerized neural networks.

This technology can be used for tasks such as image recognition. By showing a neural network a million photos, some with cats in the image and some without cats, you can train the system to recognize patterns in the data that look like cats. After a while, you have a computer that can reliably identify cats.

The same process can be applied to many different situations. For example, a neural network could take all the data about your internet browsing history, spot patterns in both your data and other customers data and then feed it into a recommendation algorithm so that an e-commerce company can show you products youre likely to buy.

Gagn and several other experts who spoke to the Financial Post said the success of AI is largely confined to such specific functions. He said that when you try to do something ambitious, such as running a whole shipping network with machine learning, it gets really difficult.

What we are all realizing is that describing the world and giving good examples to models is hard, he said. Most of our forecasting systems out there right now in the industry, broadly speaking, are very simple techniques that have been trained on a few months of data that often are at the daily level, with very few variables that describe the outside world.

In practice, this means that AI tends to work well as the special sauce inside a larger system.

For example, deep learning might improve your phone by analyzing the patterns in all your touchscreen inputs and then personalizing the sensitivity to better recognize a deliberate finger press as opposed to a palm brushing against the corner of the screen.

The vast majority of the time, (AI) is not transformative. The vast majority of the time, its a tool for a task that makes you more efficient, said Avi Goldfarb, a professor at the Rotman School of Management at the University of Toronto, and co-author of Prediction Machines, a book about the economics of AI.

Sometimes that means cost reduction, but often it means serving your customers better than you were before because you can personalize something.

But its one thing to analyze inputs on a touchscreen, quite another thing when problems become bigger and more complex.

AI might be used for self-driving cars someday, but the algorithm to do so would need to consider a vast array of possibilities in order to navigate a vehicle through city streets, and the stakes are much higher because a mistake could kill somebody.

The big, ambitious ideas for AI, such as self-driving cars or robots that make better stock picks, tend to be the ones where marketing hype and grandiose claims attract investment dollars and customer interest. But those problems are difficult to solve and require enormous amounts of data.

The sci-fi vision of artificial intelligence, while good at attracting attention, misses the mark, because it makes AI seem like something that hasnt yet proven its worth. Similarly, its easy to think that AI is absent from the pandemic because its not being used in spectacular ways.

Goldfarb said AI is already present in many of the tools being used to fight COVID-19, but its embedded in larger technology systems.

Some thermal cameras and thermometers to test for fever have machine learning embedded in their software to give more accurate results, and can even aggregate anonymized data to predict future infection flare-ups.

The machine learning function makes the tools in those systems work a bit better, but its not flashy enough to get the same marketing hype a robot would.

But, eventually, AI will become just a routine part of software development whenever theres a task that can use data for pattern recognition, said Wally Trenholm, chief executive of Toronto-based Sightline Innovation Inc. and a senior fellow at the Centre for International Governance Innovation.

Trenholm said deep learning will be embedded in everything and become so normal that nobody will even talk about it.

I look at AI as kind of a multipurpose technology, kind of like the databases of the 1970s, he said. If you look at every piece of software right now, its got a database in it, and probably 40 years from now, every piece of software will have AI in it.

The current pandemic might even accelerate the path to a future of ubiquitous AI.

Goldfarb said one of the side effects of the COVID-19 lockdown and the shift to remote work is that people are creating far more data than they were before.

The meeting that used to happen in an office conference room is now happening over Zoom, and in-person conversations between coworkers have shifted to Slack.

The last few months have led to a massive digitization of work. A lot of things that used to happen either face to face or in ways that werent recordable are now digitized, Goldfarb said. Once information is digitized, you can use machine learning to help.

Already, as the pandemic stretches on past the initial crisis phase and becomes an ongoing challenge, scientists and technologists are finding ways to use data and neural networks to fight the disease.

In July, the University of Toronto highlighted the work of two researchers who are using deep learning to identify molecules from previous drug candidates and therapies that might work well to fight COVID-19.

Instead of taking a slow, methodical approach, they can use data to predict which potential drugs are the most promising, thereby speeding up the typical research process.

We normally take a linear approach, going step by step, selecting a few candidate drugs or therapies and slowly moving them forward with testing over several years, Jean-Philippe Julien, an associate professor at the University of Toronto, said on the universitys website.

But now, with COVID, we all understand that this approach is not possible. Everyone accepts that we have to move much faster.

Email: jmcleod@nationalpost.com | Twitter:

Continued here:
Quietly waiting in the background of the pandemic, AI is about to become a big part of our lives - The Province

Human Behavior

Monkeys’ Attraction to Burned Grasslands May Offer Clues to Human Ancestors’ Mastery of Fire – Smithsonian Magazine

When human ancestors first made fire, they turned a force of nature into a handy tool. The pivotal breakthrough allowed our predecessors to cook, clear land and fend off fierce predators.

Scientists will never know with certainty the story behind that initial spark lit by homininsliving and fossil species on the human branch of the primate family tree. But some researchers assume clever hominins learned to control flames by watching wildfires that tore through their African homelands. Perhaps human ancestors tasted a naturally seared carcass and became determined to light their own paleo-cookout 1 million years ago or so.

Since scientists cant ask ancient hominins what drew them to fire, several years ago anthropologist Nicole Herzog turned to the next best thing. The professor at the University of Denver began studying primates who live near frequently ablaze habitats to see if our evolutionary cousins reap any benefits from scorched lands. Fire's a frightening and dangerous and scary thing, she says. What would motivate a critter to actually want to go near it or associate with it in the way that humans do?

One key benefit may be safety from predators, according to Herzogs latest study, published this month in the Journal of Evolution. For the study, the anthropologist tracked the behavior of South Africas vervet monkeys before, during and after fires. It turns out the monkeys sensed fewer predators in fire-swept savannah compared to unburned grasslands, where leopards and other stealth killers hide. The openness of burned ground may deter carnivores and offer a safe haven for these primates.

The finding that living primates benefit from blazes in this way means its possible ancient hominins did too, according to Herzog and her coauthors. The scientists think human ancestors initially ventured into fire prone grasslands, at least in part, to avoid predators. That could explain why hominins came to frequently encounter and eventually master fire.

Archaeologist Sally Hoare of the University of Liverpool praised the study for documenting primates that face multiple predator species in a savannah environment, which might be similar to the habitats of some hominin species. She says studying non-human primates is the only way we can actually look at how the early uptake of fire may have occurred, what may have attracted hominins to these environments.

Others show more skepticism. Its an important question how primates in general approach fire and fire areas, says biological anthropologist Rick Potts of the Smithsonians National Museum of Natural History. It may have relevance to human evolution.

Herzog conceived the study with colleagues from the University of Utah while she was a doctoral student there. They had read reports, mostly anecdotal, describing primates reactions to fire, but they had not seen any studies attempt to measure the benefits of burned lands.

To do so, Herzog focused on a troop of 25 vervet monkeys that roamed freely in South Africas Loskop Dam Nature Reserve. The plucky monkeys, with salt-and-pepper pelts and black faces, are famous among anthropologists for their language-like communications. Vervets sound distinct alarm calls for different predators and troop members respond with appropriate defensive moves. They climb high trees after the leopard call, scan the brush after the snake call, and dive into vegetation upon hearing an eagle call. They have this vocal repertoire, Herzog explains. When you hear those calls you have a good idea of what's going on.

In 2012, park staff lit controlled fires to improve habitat conditions and reduce the risk of natural wildfires. The researchers observed the animals during the two days the fires raged, plus 90 days before and after. Over that 6-month span, during 107 hours of logged observations, the scientists documented the troop members minute-by-minute locations and activities like feeding, resting and bickering. But the scientists were most interested in behaviors signaling the monkeys had either spotted or were looking out for predators. In addition to the alarm calls, when a vervet first senses danger, it may scale a tree or stand on its hind limbs and visually scan the surroundings.

During the study, Herzogs team didnt witness any lethal attacks. But they did glimpse vervet killers, including black mamba, python, viper snakes, leopards and baboonsbigger monkeys that sometimes eat vervets. The reserve is also home to African wildcats, jackals, eagles and crocodiles. Based on earlier research, vervets most common killers are leopards, which hunt by sneak attack in dense vegetation. Herzog predicted fire would transform treacherous grasslands into open ground, where monkeys could spot predators well in advance. What she didnt know is if the monkeys themselves would realize that charred earth offered protection in this way.

The results suggest the monkeys did in fact feel safer from carnivores in the burned zones. Of the 72 anti-predator behaviors observed, only 10 happened on burned ground. They logged eight scans of the surroundings, two instances of fleeing and zero alarm calls. This could mean there were actually fewer carnivores in the areas post-fire. Or, the monkeys relaxed their vigilance measures, knowing they could spot a predator before it posed serious danger. The vervets also entered grassy parts of the park, now charred, where theyd never been seen before. Generally the troop congregates near rivers lined with canopy trees. But, burning that grass was like turning this key and it opened up an entirely new area to them, says Herzog.

The troop appeared nonplussed near active, raging fires, says Herzog. She fondly recalls one decrepit old male that perched on a branch and watched a fire, seemingly for entertainment, until it nearly reached the trees base. This fits with observations of chimpanzees around brush fires in Senegal, previously reported by Herzog and Texas State University anthropologist Jill Pruetz. Both the chimps in Senegal and vervets in South Africa appeared to grasp fire safety. Near a blaze, they continued feeding, grooming and resting without signs of stress or fearfor example, having their hairs stand upright. When the flames came close enough to pose danger, the groups calmly relocated. They key into things about each particular fire that tell them whether they need to get out of there, or whether they can sit and watch it pass, says Herzog.

Herzog cautions that the new study tracked one troop of vervets for several months. She says more studies are needed on diverse primates in different environments before scientists can make any big claims about fire in human evolution.

Still, the vervet data adds one brick of support to a big idea posed by the study authors a few years back. According to their pyrophilic primate hypothesis, hominins faced frequent wildfires 2 to 3 million years ago. Eventually human ancestors adapted to and benefited from these conditions for several possible reasons: Burning made grasslands easier to traverse, exposed hidden food resources like seeds and tubers, or reduced predator risksas seems to be the case for vervets today.

The last point may have been especially important a few million years ago, when the African carnivore guild was far more terrifying that today. Archaeologist Sally Hoare points out that predators were bigger, like Pachycrocuta, the largest hyena to ever walk the earth, and Agriotherium, a carnivorous bear nearly twice the size of a lion. Hoare says predators were also more diverse. At least ten genera of large mammal predators stalked Africa then, compared to five today. As for hominins, roughly three-to-four feet tall Lucy-like Australopiths, Hoare remarks, You kind of wonder how any of them actually survived.

Potts takes issue with the timing of this scenario. Carnivore numbers begin to drop around 2.8 million years ago, whereas fire prone grasslands dont appear widespread until after 2 million years ago, he says.

The date when human ancestors mastered fire is hotly contested. Archaeologists identify hominin-made fires by using biochemical analyses to identify sediment, bones and artifacts that show signs of high-heat alteration. Using these methods, scientists have shown human ancestors built campfires by nearly 800,000 years ago, based on circular concentrations of burned wood, seeds and stone tools at the site of Gesher Benot Yaaqov, Israel. Some scientists think hominins mastered fire between 1 and 1.5 million years ago because of scattered burnt bone, plant ash or reddened sediments detected at African sites, including South Africas Wonderwerk and Swartkrans and Kenyas Koobi Fora and Chesowanja. But for these sites more than 1 million years old, researchers debate whether hominins ignited their own flames or wildfires burned the materials.

Some scientists push our lineages mastery of fire earlier than that in-the-dirt evidence. Harvard University anthropologist Richard Wrangham and others contend hominins became pyro-masters around 2 million years ago based on changes in the appearance of fossils. Around this time hominin body and brain size nearly doubled, while teeth and jaws got smaller. Wrangham and colleagues attribute these changes to the invention of cooking, which makes food easier to chew, explaining the smaller dentition, and more energy-rich, to fuel bigger bodies and brains. They say these hominins must have mastered fire for cooking.

I vigorously disagree about that because the must have argument is not evidence, says Potts. He sees direct physical evidence for hearths and burned artifacts as the only way to set the date for hominin control of fire. And other scientists propose the skeletal changes, which form the basis of Wranghams cooking hypothesis, were because hominins started hunting and regularly eating meat 2 million years back

Even if scientists do eventually settle when our ancestors mastered fire, that wont necessarily explain the how and why of it. Nor will watching vervets and other primates provide a definitive answer. But the hope is such studies will spark hypotheses about what drew our ancestors to the flames, and thats important because theres at least one point anthropologists agree upon: mastery of fire was a major milestone that set human ancestors apart from other species. The way that we take advantage of fire and dependence that we have on it says Herzog. Probably has been incredibly influential in shaping human evolution.

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Monkeys' Attraction to Burned Grasslands May Offer Clues to Human Ancestors' Mastery of Fire - Smithsonian Magazine

Cell Biology

New tools catch and release molecules at the flip of a light switch – Science Codex

A Princeton team has developed a class of light-switchable, highly adaptable molecular tools with new capabilities to control cellular activities. The antibody-like proteins, called OptoBinders, allow researchers to rapidly control processes inside and outside of cells by directing their localization, with potential applications including protein purification, the improved production of biofuels, and new types of targeted cancer therapies.

In a pair of papers published Aug. 13 in Nature Communications, the researchers describe the creation of OptoBinders that can specifically latch onto a variety of proteins both inside and outside of cells. OptoBinders can bind or release their targets in response to blue light. The team reported that one type of OptoBinder changed its affinity for its target molecules up to 330-fold when shifted from dark to blue light conditions, while others showed a five-fold difference in binding affinity -- all of which could be useful to researchers seeking to understand and engineer the behaviors of cells.

Crucially, OptoBinders can target proteins that are naturally present in cells, and their binding is easily reversible by changing light conditions -- "a new capability that is not available to normal antibodies," said co-author Jos Avalos, an assistant professor of chemical and biological engineering and the Andlinger Center for Energy and the Environment. "The ability to let go [of a target protein] is actually very valuable for many applications," said Avalos, including engineering cells' metabolisms, purifying proteins or potentially making biotherapeutics.

The new technique is the latest in a collaboration between Avalos and Jared Toettcher, an assistant professor of molecular biology. Both joined the Princeton faculty in 2015, and soon began working together on new ways to apply optogenetics -- a set of techniques that introduce genes encoding light-responsive proteins to control cells' behaviors.

"We hope that this is going to be the beginning of the next era of optogenetics, opening the door to light-sensitive proteins that can interface with virtually any protein in biology, either inside or outside of cells," said Toettcher, the James A. Elkins, Jr. '41 Preceptor in Molecular Biology.

Avalos and his team hope to use OptoBinders to control the metabolisms of yeast and bacteria to improve the production of biofuels and other renewable chemicals, while Toettcher's lab is interested in the molecules' potential to control signaling pathways involved in cancer.

The two papers describe different types of light-switchable binders: opto-nanobodies and opto-monobodies. Nanobodies are derived from the antibodies of camelids, the family of animals that includes camels, llamas and alpacas, which produce some antibodies that are smaller (hence the name nanobody) and simpler in structure than those of humans or other animals.

Nanobodies' small size makes them more adaptable and easier to work with than traditional antibodies; they recently received attention for their potential as a COVID-19 therapy. Monobodies, on the other hand, are engineered pieces of human fibronectin, a large protein that forms part of the matrix between cells.

"These papers go hand in hand," said Avalos. "The opto-nanobodies take advantage of the immune systems of these animals, and the monobodies have the advantage of being synthetic, which gives us opportunities to further engineer them in different ways."

The two types of OptoBinders both incorporate a light-sensitive domain from a protein found in oat plants.

"When you turn the light on and off, these tools bind and release their target almost immediately, so that brings another level of control" that was not previously possible, said co-author Csar Carrasco-Lpez, an associate research scholar in Avalos' lab. "Whenever you are analyzing things as complex as metabolism, you need tools that allow you to control these processes in a complex way in order to understand what is happening."

In principle, OptoBinders could be engineered to target any protein found in a cell. With most existing optogenetic systems, "you always had to genetically manipulate your target protein in a cell for each particular application," said co-author Agnieszka Gil, a postdoctoral research fellow in Toettcher's lab. "We wanted to develop an optogenetic binder that did not depend on additional genetic manipulation of the target protein."

In a proof of principle, the researchers created an opto-nanobody that binds to actin, a major component of the cytoskeleton that allows cells to move, divide and respond to their environment. The opto-nanobody strongly bound to actin in the dark, but released its hold within two minutes in the presence of blue light. Actin proteins normally join together to form filaments just inside the cell membrane and networks of stress fibers that traverse the cell. In the dark, the opto-nanobody against actin binds to these fibers; in the light, these binding interactions are disrupted, causing the opto-nanobody to scatter throughout the cell. The researchers could even manipulate binding interactions on just one side of a cell -- a level of localized control that opens new possibilities for cell biology research.

OptoBinders stand to unlock scores of innovative, previously inaccessible uses in cell biology and biotechnology, said Andreas Mglich, a professor of biochemistry at the University of Bayreuth in Germany who was not involved in the studies. But, Mglich said, "there is much more to the research" because the design strategy can be readily translated to other molecules, paving the way to an even wider repertoire of customized, light-sensitive binders.

"The impressive results mark a significant advance," he said.

"Future applications will depend on being able to generate more OptoBinders" against a variety of target proteins, said Carrasco-Lpez. "We are going to try to generate a platform so we can select OptoBinders against different targets" using a standardized, high-throughput protocol, he said, adding that this is among the first priorities for the team as they resume their experiments after lab research was halted this spring due to COVID-19.

Beyond applications that involve manipulating cell metabolism for microbial chemical production, Avalos said, OptoBinders could someday be used to design biomaterials whose properties can be changed by light.

The technology also holds promise as way to reduce side effects of drugs by focusing their action to a specific site in the body or adjusting dosages in real time, said Toettcher, who noted that applying light inside the body would require a device such as an implant. "There aren't many ways to do spatial targeting with normal pharmacology or other techniques, so having that kind of capability for antibodies and therapeutic binders would be a really cool thing," he said. "We think of this as a sea change in what sorts of processes can be placed under optogenetic control."

Continued here:
New tools catch and release molecules at the flip of a light switch - Science Codex

Cell Biology

To understand the machinery of life, this scientist breaks it on purpose – Newswise

Newswise "I'm fascinated with life, and that's why I want to break it."

This is how Betl Kaar, an assistant professor at the University of Arizona with appointments in the Department of Molecular and Cellular Biology, Department of Astronomy and the Lunar and Planetary Laboratory, describes her research. What may sound callous is a legitimate scientific approach in astrobiology. Known as ancestral sequencing, the idea is to "resurrect" genetic sequences from the dawn of life, put them to work in the cellular pathways of modern microbes - think Jurassic Park but with extinct genes in place of dinosaurs, and study how the organism copes.

In a recent paper published in theProceedings of the National Academy of Sciences, Kaar's research team reports an unexpected discovery: Evolution, it seems, is not very good at multitasking.

Kaar uses ancestral sequencing to find out what makes life tick and how organisms are shaped by evolutionary selection pressure. The insights gained may, in turn, offer clues as to what it takes for organic precursor molecules to give rise to life - be it on Earth or faraway worlds. In her lab, Kaar specializes in designing molecules that act like tiny invisible wrenches, wreaking havoc with the delicate cellular machinery that allows organisms to eat, move and multiply - in short, to live.

Kaar has focused her attention on the translation machinery, a labyrinthine molecular clockwork that translates the information encoded in the bacteria's DNA into proteins. All organisms - from microbes to algae to trees to humans - possess this piece of machinery in their cells.

"We approximate everything about the past based on what we have today," Kaar said. "All life needs a coding system - something that takes information and turns it into molecules that can perform tasks - and the translational machinery does just that. It creates life's alphabet. That's why we think of it as a fossil that has remained largely unchanged, at least at its core. If we ever find life elsewhere, you bet that the first thing we'll look at is its information processing systems, and the translational machinery is just that."

So critical is the translational machinery to life on Earth that even over the course of more than 3.5 billion years of evolution, its parts have undergone little substantial change. Scientists have referred to it as "an evolutionary accident frozen in time."

"I guess I tend to mess with things I'm not supposed to," Kaar said. "Locked in time? Let's unlock it. Breaking it would lead the cell to destruction? Let's break it."

The researchers took six different strains of Escherichia coli bacteria and genetically engineered the cells with mutated components of their translational machinery. They targeted the step that feeds the unit with genetic information by swapping the shuttle protein with evolutionary cousins taken from other microbes, including a reconstructed ancestor from about 700 million years ago.

"We get into the heart of the heart of what we think is one of the earliest machineries of life," Kaar said. "We purposely break it a little, and a lot, to see how the cells deal with this problem. In doing this, we think we create an urgent problem for the cell, and it will fix that."

Next, the team mimicked evolution by having the manipulated bacterial strains compete with each other - like a microbial version of "The Hunger Games." A thousand generations later, some strains fared better than others, as was expected. But when Kaar's team analyzed exactly how the bacteria responded to perturbations in their translational components, they discovered something unexpected: Initially, natural selection improved the compromised translational machinery, but its focus shifted away to other cellular modules before the machinery's performance was fully restored.

To find out why, Kaar enlisted Sandeep Venkataram, a population genetics expert at the University of California, San Diego.

Venkataram likens the process to a game of whack-a-mole, with each mole representing a cellular module. Whenever a module experiences a mutation, it pops up. The hammer smashing it back down is the action of natural selection. Mutations are randomly spread across all modules, so that all moles pop up randomly.

"We expected that the hammer of natural selection also comes down randomly, but that is not what we found," he said. "Rather, it does not act randomly but has a strong bias, favoring those mutations that provide the largest fitness advantage while it smashes down other less beneficial mutations, even though they also provide a benefit to the organism."

In other words, evolution is not a multitasker when it comes to fixing problems.

"It seems that evolution is myopic," Venkataram said. "It focuses on the most immediate problem, puts a Band-Aid on and then it moves on to the next problem, without thoroughly finishing the problem it was working on before."

"It turns out the cells do fix their problems but not in the way we might fix them," Kaar added. "In a way, it's a bit like organizing a delivery truck as it drives down a bumpy road. You can stack and organize only so many boxes at a time before they inevitably get jumbled around. You never really get the chance to make any large, orderly arrangement."

Why natural selection acts in this way remains to be studied, but what the research showed is that, overall, the process results in what the authors call "evolutionary stalling" - while evolution is busy fixing one problem, it does at the expense of all other issues that need fixing. They conclude that at least in rapidly evolving populations, such as bacteria, adaptation in some modules would stall despite the availability of beneficial mutations. This results in a situation in which organisms can never reach a fully optimized state.

"The system has to be capable of being less than optimal so that evolution has something to act on in the face of disturbance - in other words, there needs to be room for improvement," Kaar said.

Kaar believes this feature of evolution may be a signature of any self-organizing system, and she suspects that this principle has counterparts at all levels of biological hierarchy, going back to life's beginnings, possibly even to prebiotic times when life had not yet materialized.

With continued funding from the John Templeton Foundation and NASA, the research group is now working on using ancestral sequencing to go back even further in time, Kaar said.

"We want to strip things down even more and create systems that start out as what we would consider pre-life and then transition into what we consider life."

###

The paper is online athttps://www.pnas.org/content/117/31/18582.

Read the original here:
To understand the machinery of life, this scientist breaks it on purpose - Newswise

Cell Biology

Dr. Suvas earns second R01 to explore cornea-based complication of herpes simplex virus-1 – The South End

Susmit Suvas, Ph.D.

A faculty member in the Wayne State University School of Medicines Department of Ophthalmology, Vision and Anatomical Sciences will use a new five-year, $1.88 million grant from the National Eye Institute to study how better to fight a chronic inflammation of the cornea that often leads to vision loss.

Associate Professor Susmit Suvas, Ph.D., is the principal investigator of Role of insulin-like growth factor binding proteins in the pathogenesis of herpes stromal keratitis.

Herpes simplex virus-1, or HSV-1, is an infection of the cornea that can cause the development of herpes stromal keratitis, a chronic inflammatory condition. HSK is a major cause of infection-induced vision loss in the United States, said Dr. Suvas, who also serves as the graduate officer of the Anatomy and Cell Biology Graduate Program.

Clinical signs of HSK include the development of new leaky blood vessels in a once-clear and transparent cornea. Newly formed leaky blood vessels bring a massive influx of immune cell types, such as neutrophils. These immune cells persist in the inflamed cornea and cause damage to corneal tissue. As a result, the cornea becomes opaque and thick.

The long-term goal of our research is to understand the pathogenesis of herpes stromal keratitis so that novel therapeutic approaches can be developed to better manage the condition of HSK and reduce the loss of vision, Dr. Suvas said.

The focus of our current grant application is to understand the role of insulin-like growth factor binding protein-3 (IGFBP-3) in inhibiting the survival of immune cells and development of new blood vessels (angiogenesis) in HSV-1 infected corneas," he added.

The National Eye Institute of the National Institutes of Health has continuously funded Dr. Suvass research on herpes stromal keratitis since 2009.

It is a great feeling to have simultaneously two five-year R01s supporting our research to understand the pathogenesis of HSK, he said. We anticipate that at the end of our study we will have a clear understanding of how IGFBP-3 protein reduces viral load, hemangiogenesis, and the survival and effector function of neutrophils in HSK developing corneas.

The grant number for this award is EY030129.

Read more:
Dr. Suvas earns second R01 to explore cornea-based complication of herpes simplex virus-1 - The South End

Cell Biology

Research Roundup: How the COVID-19 Virus Infects Other Cells and More – BioSpace

Every week there are numerous scientific studies published. Heres a look at some of the more interesting ones.

The Unusual Way the COVID-19 Virus Infects Other Cells

Researchers with the University of California, San Francisco found that when the SARS-CoV-2 virus infects a human cells, the infected cell grows multi-pronged tentacles that are studded with viral particles. These filaments, called filopodia, reach out to still-healthy neighboring cells, which then bore into the cells bodies and infect the healthy cells with virus. The research was published in the journal Cell.

Scientists previously believed the SARS-CoV-2 virus infected cells in a typical way, which is by finding receptors on the surface of cells in a persons mouth, nose, respiratory tract, lungs or blood vessels, and replicating and invading larger cells. Other viruses, such as smallpox, HIV and some influenza viruses also used filopodia to improve their ability to infect cells.

By conducting a systematic analysis of the changes in phosphorylation when SARS-CoV-2 infects a cell, we identified several key factors that will inform not only the next areas of biological study, but also treatments that may be repurposed to treat patients with COVID-19, said one of the studys authors, Nevan Krogan, professor, Department of Cellular Molecular Pharmacology at the UCSF School of Medicine.

They also tested 87 drugs and molecules by mapping global phosphorylation profiles to dysregulated kinases and pathways that have the potential for treating COVID-19. They then narrowed the list down to kinase inhibitors.

We narrowed in on about a dozen, Krogan told ABC News, and we highlighted about six or seven that look particularly potent in a laboratory setting. And were very excited now to try and take these into clinical trials.

Three of those drugs include Senhwa Biosciences silmitasertib, which is in clinical trials for bile duct cancer and other malignancies; Eli Lillys ralimetinib, a cancer drug being evaluated for ovarian cancer; and Astellas gilteritinib, which is used to treat acute myeloid leukemia and marketed under the brand name Xospata.

Predicting Which Babies Will Develop Type 1 Diabetes

Researchers at the University of Exeter with colleagues at seven international locations followed 7,798 children at high risk of developing type 1 diabetes from birth, over nine years. The TEDDY Study data was then used to develop an algorithm by combining multiple factors to determine if a child is likely to develop type 1 diabetes. The combined risk score melds genetics, family history, and islet autoantibody counts. It appeared to double current programs to screen newborns to prevent ketoacidosis, a potentially deadly consequence of type 1 diabetes.

COVID-19 Does Not Directly Damage Taste Buds

A common early symptom of COVID-19 is the loss of taste and smell. It was generally believed that the SARS-CoV-2 virus damaged the cells involved in taste and smell, which was the reason for this loss. Recent research suggests 20-25% of patients report a loss of taste. New research from the Regenerative Bioscience Center at the University of Georgia, however, suggests the damage is not caused directly by the virus, but indirectly by events induced during COVID-19 inflammation. The research found that taste bud cells are not vulnerable to the viral infection, because most do not express ACE2, the cell receptor that the virus uses to enter cells.

New Treatment for Osteoarthritis Shows Promise in Regrowing Cartilage

Researchers at NYU Langone Health/NYU School of Medicine conducted a study where they injected adenosine into the joints of rodents whose limbs had been damaged by inflammation caused by either traumatic injury or massive weight gain. The biological damage was similar to that seen in human osteoarthritis. Adenosine is typically used to store energy and plays a central role in metabolism. In the rodents, the eight weekly injections stimulated regrowth rates of cartilage tissue between 35% and 50%.

Llama-Inspired Nanobodies to Treat COVID-19

Researchers at the University of California, San Francisco (UCSF) have synthesized a molecule inspired by llama antibodies called nanobodies against SARS-CoV-2. They are approximately 25% of the size of human antibodies and from other animals, and they appear to be the most potent anti-coronavirus compound that has been tested in the laboratory so far. In addition, the nanobodies are extremely stable, which means they can be turned into a dry powder and aerosolized, which would make them much easier to administer than the human monoclonal antibodies being developed by companies such as Sorrento Therapeutics, Regeneron Pharmaceuticals and Eli Lilly.

Why People Have Different Responses to COVID-19

Researchers at McMaster University and the University of Waterloo discovered that ACE2 receptors exist in very low levels in human lung tissue. This challenges the generally accepted belief that the SARS-CoV-2 virus enters cells via ACE2, at least in the lungs. They published their research in the European Respiratory Journal and their findings were independently confirmed by other researchers and published in Molecular Systems Biology.

Our finding is somewhat controversial, as it suggests that there must be other ways, other receptors for the virus, that regulate its infection of the lungs, said Jeremy Hirota, co-lead scientist from the Research Institute of St. Joes Hamilton and an assistant professor of Medicine at McMaster. We were surprised that the fundamental characterization of the candidate receptors in human lung tissue had not yet been done in a systematic way with modern technologies.

Finding such low levels of ACE2 in lung tissue has important implications for how we think about this virus, said co-lead Andrew Doxey, professor of Biology at the University of Waterloo. ACE2 is not the full story and may be more relevant in other tissues such as the vascular system.

They are now exploring alternate additional infection pathways and why there are different patient responses to infection. To do so, they are using nasal swabs that were collected during COVID-19 diagnoses, which lets them analyze the genes expressed by the patients cells. They will correlate positive and negative COVID-19 cases with clinical outcomes and hope to develop predictive algorithms associated with morbidity and mortality.

It is clear that some individuals respond better than others to the same SARS-CoV-2 virus, said Hirota. The differential response to the same virus suggests that each individual patient, with their unique characteristics, heavily influences COVID-19 disease severity. We think it is the lung immune system that differs between COVID-19 patients, and by understanding which patients lung immune systems are helpful and which are harmful, we may be able to help physicians proactively manage the most at-risk patients.

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Research Roundup: How the COVID-19 Virus Infects Other Cells and More - BioSpace