Maybe you shouldn’t blindly believe everything you read? Even if the source has a pretty solid reputation?
Nature magazine has censored over 1,000 articles at the request of the Chinese government over the past several years. And it seems pretty clear that their recent article, “The proximal origin of SARS-CoV-2” is just one more example of their influence.
China bought off the head of Harvard’s chemistry department, you don’t think they could buy off run-of-the-mill research scientists scrambling for tenure and funding and publication? It’s absolutely horrific that so many scientists and researchers are taking part in what’s really clearly a disinformation campaign orchestrated by the Chinese Communist Party, and willfully spreading a smokescreen about something that’s already killed thousands and is projected to kill millions more across the planet.
And while the mainstream corporate media mindlessly regurgitates claims from the Chinese government that are falsifiable with the simplest of google searches, allowing the public to be lulled into a false sense of security and complacency, and Reddit rapidly censors and moderates anything that might indicate that this virus leaked from a Chinese lab and so the Chinese government is to blame for this pandemic – sites like ZeroHedge, that have been at the forefront of keeping the lines of investigation open, have been banished from Twitter and marginalized.
Below is a takedown of that article, and the good news is a much more nuanced and honest look at the origins of COVID-19, the Wuhan Strain of coronavirus is just a click away.
Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.
As our report mentions right at the start, scientists passed the H5N1 Bird Flu through a series of ferret hosts until it gained ACE2 affinity and then became incredibly virulent, which is what’s seen with COVID-19 since its affinity to ACE2 is orders of magnitude higher than SARS. That process would leave a genome that appears “natural” and not purposeful as well since it wouldn’t leave a genomic smoking gun and would simply appear to be the result of “natural” selection. However the addition of artificial generations produced by this process of passing through ferrets in the lab would create a lot of genetic distance from any possible relatives – precisely what is seen in COVID-19: it forms its own clade and appears very distant from all other bat coronaviruses. So this is lazy research, they’re either unaware of the Bird Flu study or are willfully ignoring it.
Given the level of genetic variation in the spike, it is likely that SARS-CoV-2-like viruses with partial or full polybasic cleavage sites will be discovered in other species.
This seems like pretty intentional dissimulation. It’s “likely” that other viruses with this cleavage site will be found? What? How likely? 1 in 10? 1 in 10 million? Is it likely that if my aunt grew balls she’d become my uncle? Is it “likely” that a natural intermediate animal vector will be found? Well… likely or not, until it happens it seems incredibly disingenuous to state that “likely” means a damn thing here.
The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown, and it will be important to determine its impact on transmissibility and pathogenesis in animal models. Experiments with SARS-CoV have shown that insertion of a furin cleavage site at the S1–S2 junction enhances cell–cell fusion without affecting viral entry14.
This doesn’t seem to address the virus’s provenance at all, but just as an aside it seems like a lot of the viruses with furin cleavage sites engage in ADE, which COVID-19 appears to be doing from a clinical perspective: neurological damage, the second infection is worse, and areas like Wuhan with extended infections have much higher CFRs as infections overlap.
The acquisition of polybasic cleavage sites by HA has also been observed after repeated passage in cell culture or through animals17.
Exactly. Passage through a series of ferret hosts in a lab would have given COVID-19 this distinct cleavage site.
It is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. As noted above, the RBD of SARS-CoV-2 is optimized for binding to human ACE2 with an efficient solution different from those previously predicted7,11.
Yes, again we aren’t arguing that this thing was built nucleotide-by-nucleotide as the perfect bespoke bio-weapon. This efficient solution is exactly the kind of thing that would be selected for after passage through ferrets in lab, which was already done to the Bird Flu that created a horrifically virulent strain. Isn’t it funny that no one’s mentioning that experiment? Or Baric’s work at UNC? How come every single public-facing virologist seems to be leaving these studies out? Are they really unaware of them? That seems exceedingly hard to believe when I was able to find them on the front page of a single google search. Seems a lot more likely everyone’s just covering each other’s asses since they realize the magnitude of what’s happening and how deep into the cover-up they already are.
Furthermore, if genetic manipulation had been performed, one of the several reverse-genetic systems available for betacoronaviruses would probably have been used19
This is an utterly vacuous statement. Probably doesn’t mean a damn thing in science. “Okay folks, we probably won’t get an earthquake anytime soon, so no reason to prepare for one or try and detect one coming!” Seriously?
Instead, we propose two scenarios that can plausibly explain the origin of SARS-CoV-2: (i) natural selection in an animal host before zoonotic transfer; and (ii) natural selection in humans following zoonotic transfer.
As we’ve explained before, there was no trace of this virus before November 2019, and full zoonotic jumps don’t just magically happen, especially not of a virus that’s so incredibly adapted to humans and able to infect us undetected and spread undetected, and then kill us after more than enough time has passed to find multiple new hosts. It’s funny so many virologists are throwing out the book of how zoonotic jumps happen… all that money in gain-of-function research must be quite blinding. Kind of amazing they don’t matter how many thousands of people are dying. As far as the intermediate animal host goes: It might as well be a unicorn at this point. Until someone finds it, it’s just conjecture.
Malayan pangolins (Manis javanica) illegally imported into Guangdong province contain coronaviruses similar to SARS-CoV-221. Although the RaTG13 bat virus remains the closest to SARS-CoV-2 across the genome1, some pangolin coronaviruses exhibit strong similarity to SARS-CoV-2 in the RBD, including all six key RBD residues21 (Fig. 1). This clearly shows that the SARS-CoV-2 spike protein optimized for binding to human-like ACE2 is the result of natural selection.
The most recent study, covered in our article, that examines the neutral sites that are assumed to best show heritage found that pangolins are “very unlikely” to have served as a host at all. Their assertion that natural natural selection is clearly shown is raw steamy bullshit. Serial passage through ferrets fits the overall big picture far better than this pangolin crap.
For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.
WAIT WAIT WAIT!! You mean exactly like a bunch of ferrets, which have the same ACE2 receptor as humans, all jammed into a bunch of cages together and then infected over and over again in a lab?! That’s crazy talk!! Other than the fact it was exactly the process used to make the Bird Flu into something that “could make the 1918 pandemic look like a pesky cold.”
It is possible that a progenitor of SARS-CoV-2 jumped into humans, acquiring the genomic features described above through adaptation during undetected human-to-human transmission. Once acquired, these adaptations would enable the pandemic to take off and produce a sufficiently large cluster of cases to trigger the surveillance system that detected it.
Hence, this scenario presumes a period of unrecognized transmission in humans between the initial zoonotic event and the acquisition of the polybasic cleavage site. Sufficient opportunity could have arisen if there had been many prior zoonotic events that produced short chains of human-to-human transmission over an extended period.
Sure this would be plausible… other than the fact that, as we cover in our report, that statistical analysis shows that this thing didn’t hit humans until November of 2019, which this article agrees with. But zoonotic jumps only occur after a genomic trial-and-error process where the virus jumps to one host, spreads to a few new hosts, and then fizzles out. There is absolutely no evidence anywhere of this occurring. Every single data points to this thing hitting humans in November and being immediately adapted and dangerous. There is no trace whatsoever of it creating small clusters of infections and dying out – stating there could have been doesn’t mean it’s been seen. It hasn’t. And as our report covers, this would require sustained interaction with the intermediate host – how does that happen in the middle of a massive modern urban metropolis the size of NYC? And where is this intermediate host anyways? If an intermediate host isn’t needed, is it some magical sleep-flying bat that decided not to hibernate and fight crime in Wuhan when it’s buddies were all hibernating, creating the sustained interactions with humans as it fought for Justice? Because that’s about as plausible as what’s being proposed here.
The presence in pangolins of an RBD very similar to that of SARS-CoV-2 means that we can infer this was also probably in the virus that jumped to humans.
Again, analysis of the neutral sites shows that pangolins were almost certainly not in play.
Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described
This means nothing. There is no open-source shared database of viruses. No one has any idea what viruses are in China’s BSL-4 lab, where they’ve been collecting these viruses for years. As mentioned, one of our persons-of-interest was the very first person to isolate a coronavirus from a bat that uses the ACE2 receptor. He also worked at UNC in Baric’s lab making the hyper-virulent bat coronavirus in 2015.
Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.
The fuck it hasn’t.
Retrospective serological studies could also be informative, and a few such studies have been conducted showing low-level exposures to SARS-CoV-like coronaviruses in certain areas of China26. Further serological studies should be conducted to determine the extent of prior human exposure to SARS-CoV-2.
Beyond the statistical analysis that indicates it only hit humans in November in 2019, is the fact that the version of COVID-19 found in the first few dozen hosts was exactly the same – there aren’t any variants whatsoever, just one version. This is not what would be found with the genomic trial-and-error of a full zoonotic jump, which requires sustained human-to-human transmission as different variants of the virus try and fail to adapt to human biology. Here, only one variant was found in all the initial infected humans, instead of the multiple variants that would be expected. But does fit what would happen if a virus that already had high affinity to the ACE2 receptor, which is the same in human and ferrets, leaked out of a lab. But addressing this point in particular, oh weird, the study they cite from March of 2018 was done mostly on people who live in villages barely a kilometer away from bat caves. A far cry from a massive urban city bout the size of NYC. Oh, and how many of these villagers, who live about a kilometer or less from bat caves, had antibodies indicating exposure to bat coronaviruses? Two-point-seven percent. (There is hand-waving about how long antibodies persist in humans, but I’m pretty sure it’s more than long enough.) That study actually sampled people living in Wuhan too and found… no evidence whatsoever of exposure to “SARS-CoV-like coronaviruses.” So are these peer-reviewers just straight chugging lead paint, or are they on the take too?
The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation1
Again, just demonstrably false.
Get the real story here.
Showing posts with label nature. Show all posts
Showing posts with label nature. Show all posts
Saturday, March 21, 2020
Inside the Chinese lab poised to study world's most dangerous pathogens
via Nature
Maximum-security biolab is part of plan to build network of BSL-4 facilities across China.
A laboratory in Wuhan is on the cusp of being cleared to work with the world’s most dangerous pathogens. The move is part of a plan to build between five and seven biosafety level-4 (BSL-4) labs across the Chinese mainland by 2025, and has generated much excitement, as well as some concerns.
Some scientists outside China worry about pathogens escaping, and the addition of a biological dimension to geopolitical tensions between China and other nations. But Chinese microbiologists are celebrating their entrance to the elite cadre empowered to wrestle with the world’s greatest biological threats.
“It will offer more opportunities for Chinese researchers, and our contribution on the BSL‑4-level pathogens will benefit the world,” says George Gao, director of the Chinese Academy of Sciences Key Laboratory of Pathogenic Microbiology and Immunology in Beijing. There are already two BSL-4 labs in Taiwan, but the National Bio-safety Laboratory, Wuhan, would be the first on the Chinese mainland.
The lab was certified as meeting the standards and criteria of BSL-4 by the China National Accreditation Service for Conformity Assessment (CNAS) in January. The CNAS examined the lab’s infrastructure, equipment and management, says a CNAS representative, paving the way for the Ministry of Health to give its approval. A representative from the ministry says it will move slowly and cautiously; if the assessment goes smoothly, it could approve the laboratory by the end of June.
BSL-4 is the highest level of biocontainment: its criteria include filtering air and treating water and waste before they leave the laboratory, and stipulating that researchers change clothes and shower before and after using lab facilities. Such labs are often controversial. The first BSL-4 lab in Japan was built in 1981, but operated with lower-risk pathogens until 2015, when safety concerns were finally overcome.
The expansion of BSL-4-lab networks in the United States and Europe over the past 15 years — with more than a dozen now in operation or under construction in each region — also met with resistance, including questions about the need for so many facilities.
The Wuhan lab cost 300 million yuan (US$44 million), and to allay safety concerns it was built far above the flood plain and with the capacity to withstand a magnitude-7 earthquake, although the area has no history of strong earthquakes. It will focus on the control of emerging diseases, store purified viruses and act as a World Health Organization ‘reference laboratory’ linked to similar labs around the world. “It will be a key node in the global biosafety-lab network,” says lab director Yuan Zhiming.
The Chinese Academy of Sciences approved the construction of a BSL-4 laboratory in 2003, and the epidemic of SARS (severe acute respiratory syndrome) around the same time lent the project momentum. The lab was designed and constructed with French assistance as part of a 2004 cooperative agreement on the prevention and control of emerging infectious diseases. But the complexity of the project, China’s lack of experience, difficulty in maintaining funding and long government approval procedures meant that construction wasn’t finished until the end of 2014.
The lab’s first project will be to study the BSL-3 pathogen that causes Crimean–Congo haemorrhagic fever: a deadly tick-borne virus that affects livestock across the world, including in northwest China, and that can jump to people.
Future plans include studying the pathogen that causes SARS, which also doesn’t require a BSL-4 lab, before moving on to Ebola and the West African Lassa virus, which do. Some one million Chinese people work in Africa; the country needs to be ready for any eventuality, says Yuan. “Viruses don’t know borders.”
Gao travelled to Sierra Leone during the recent Ebola outbreak, allowing his team to report the speed with which the virus mutated into new strains1. The Wuhan lab will give his group a chance to study how such viruses cause disease, and to develop treatments based on antibodies and small molecules, he says.
The opportunities for international collaboration, meanwhile, will aid the genetic analysis and epidemiology of emergent diseases. “The world is facing more new emerging viruses, and we need more contribution from China,” says Gao. In particular, the emergence of zoonotic viruses — those that jump to humans from animals, such as SARS or Ebola — is a concern, says Bruno Lina, director of the VirPath virology lab in Lyon, France.
Many staff from the Wuhan lab have been training at a BSL-4 lab in Lyon, which some scientists find reassuring. And the facility has already carried out a test-run using a low-risk virus.
But worries surround the Chinese lab, too. The SARS virus has escaped from high-level containment facilities in Beijing multiple times, notes Richard Ebright, a molecular biologist at Rutgers University in Piscataway, New Jersey. Tim Trevan, founder of CHROME Biosafety and Biosecurity Consulting in Damascus, Maryland, says that an open culture is important to keeping BSL-4 labs safe, and he questions how easy this will be in China, where society emphasizes hierarchy. “Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important,” he says.
Yuan says that he has worked to address this issue with staff. “We tell them the most important thing is that they report what they have or haven’t done,” he says. And the lab’s international collaborations will increase openness. “Transparency is the basis of the lab,” he adds.
The plan to expand into a network heightens such concerns. One BSL-4 lab in Harbin is already awaiting accreditation; the next two are expected to be in Beijing and Kunming, the latter focused on using monkey models to study disease.
Lina says that China’s size justifies this scale, and that the opportunity to combine BSL-4 research with an abundance of research monkeys — Chinese researchers face less red tape than those in the West when it comes to research on primates — could be powerful. “If you want to test vaccines or antivirals, you need a non-human primate model,” says Lina.
But Ebright is not convinced of the need for more than one BSL-4 lab in mainland China. He suspects that the expansion there is a reaction to the networks in the United States and Europe, which he says are also unwarranted. He adds that governments will assume that such excess capacity is for the potential development of bioweapons.
“These facilities are inherently dual use,” he says. The prospect of ramping up opportunities to inject monkeys with pathogens also worries, rather than excites, him: “They can run, they can scratch, they can bite.”
Trevan says China’s investment in a BSL-4 lab may, above all, be a way to prove to the world that the nation is competitive. “It is a big status symbol in biology,” he says, “whether it’s a need or not.”
Nature
542,
399–400
(23 February 2017)
doi:10.1038/nature.2017.21487
Maximum-security biolab is part of plan to build network of BSL-4 facilities across China.
A laboratory in Wuhan is on the cusp of being cleared to work with the world’s most dangerous pathogens. The move is part of a plan to build between five and seven biosafety level-4 (BSL-4) labs across the Chinese mainland by 2025, and has generated much excitement, as well as some concerns.
Some scientists outside China worry about pathogens escaping, and the addition of a biological dimension to geopolitical tensions between China and other nations. But Chinese microbiologists are celebrating their entrance to the elite cadre empowered to wrestle with the world’s greatest biological threats.
“It will offer more opportunities for Chinese researchers, and our contribution on the BSL‑4-level pathogens will benefit the world,” says George Gao, director of the Chinese Academy of Sciences Key Laboratory of Pathogenic Microbiology and Immunology in Beijing. There are already two BSL-4 labs in Taiwan, but the National Bio-safety Laboratory, Wuhan, would be the first on the Chinese mainland.
The lab was certified as meeting the standards and criteria of BSL-4 by the China National Accreditation Service for Conformity Assessment (CNAS) in January. The CNAS examined the lab’s infrastructure, equipment and management, says a CNAS representative, paving the way for the Ministry of Health to give its approval. A representative from the ministry says it will move slowly and cautiously; if the assessment goes smoothly, it could approve the laboratory by the end of June.
BSL-4 is the highest level of biocontainment: its criteria include filtering air and treating water and waste before they leave the laboratory, and stipulating that researchers change clothes and shower before and after using lab facilities. Such labs are often controversial. The first BSL-4 lab in Japan was built in 1981, but operated with lower-risk pathogens until 2015, when safety concerns were finally overcome.
The expansion of BSL-4-lab networks in the United States and Europe over the past 15 years — with more than a dozen now in operation or under construction in each region — also met with resistance, including questions about the need for so many facilities.
The Wuhan lab cost 300 million yuan (US$44 million), and to allay safety concerns it was built far above the flood plain and with the capacity to withstand a magnitude-7 earthquake, although the area has no history of strong earthquakes. It will focus on the control of emerging diseases, store purified viruses and act as a World Health Organization ‘reference laboratory’ linked to similar labs around the world. “It will be a key node in the global biosafety-lab network,” says lab director Yuan Zhiming.
The Chinese Academy of Sciences approved the construction of a BSL-4 laboratory in 2003, and the epidemic of SARS (severe acute respiratory syndrome) around the same time lent the project momentum. The lab was designed and constructed with French assistance as part of a 2004 cooperative agreement on the prevention and control of emerging infectious diseases. But the complexity of the project, China’s lack of experience, difficulty in maintaining funding and long government approval procedures meant that construction wasn’t finished until the end of 2014.
The lab’s first project will be to study the BSL-3 pathogen that causes Crimean–Congo haemorrhagic fever: a deadly tick-borne virus that affects livestock across the world, including in northwest China, and that can jump to people.
Future plans include studying the pathogen that causes SARS, which also doesn’t require a BSL-4 lab, before moving on to Ebola and the West African Lassa virus, which do. Some one million Chinese people work in Africa; the country needs to be ready for any eventuality, says Yuan. “Viruses don’t know borders.”
Gao travelled to Sierra Leone during the recent Ebola outbreak, allowing his team to report the speed with which the virus mutated into new strains1. The Wuhan lab will give his group a chance to study how such viruses cause disease, and to develop treatments based on antibodies and small molecules, he says.
The opportunities for international collaboration, meanwhile, will aid the genetic analysis and epidemiology of emergent diseases. “The world is facing more new emerging viruses, and we need more contribution from China,” says Gao. In particular, the emergence of zoonotic viruses — those that jump to humans from animals, such as SARS or Ebola — is a concern, says Bruno Lina, director of the VirPath virology lab in Lyon, France.
Many staff from the Wuhan lab have been training at a BSL-4 lab in Lyon, which some scientists find reassuring. And the facility has already carried out a test-run using a low-risk virus.
But worries surround the Chinese lab, too. The SARS virus has escaped from high-level containment facilities in Beijing multiple times, notes Richard Ebright, a molecular biologist at Rutgers University in Piscataway, New Jersey. Tim Trevan, founder of CHROME Biosafety and Biosecurity Consulting in Damascus, Maryland, says that an open culture is important to keeping BSL-4 labs safe, and he questions how easy this will be in China, where society emphasizes hierarchy. “Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important,” he says.
Yuan says that he has worked to address this issue with staff. “We tell them the most important thing is that they report what they have or haven’t done,” he says. And the lab’s international collaborations will increase openness. “Transparency is the basis of the lab,” he adds.
The plan to expand into a network heightens such concerns. One BSL-4 lab in Harbin is already awaiting accreditation; the next two are expected to be in Beijing and Kunming, the latter focused on using monkey models to study disease.
Lina says that China’s size justifies this scale, and that the opportunity to combine BSL-4 research with an abundance of research monkeys — Chinese researchers face less red tape than those in the West when it comes to research on primates — could be powerful. “If you want to test vaccines or antivirals, you need a non-human primate model,” says Lina.
But Ebright is not convinced of the need for more than one BSL-4 lab in mainland China. He suspects that the expansion there is a reaction to the networks in the United States and Europe, which he says are also unwarranted. He adds that governments will assume that such excess capacity is for the potential development of bioweapons.
“These facilities are inherently dual use,” he says. The prospect of ramping up opportunities to inject monkeys with pathogens also worries, rather than excites, him: “They can run, they can scratch, they can bite.”
Trevan says China’s investment in a BSL-4 lab may, above all, be a way to prove to the world that the nation is competitive. “It is a big status symbol in biology,” he says, “whether it’s a need or not.”
Nature
542,
399–400
(23 February 2017)
doi:10.1038/nature.2017.21487
Wednesday, July 13, 2016
Leo Decaprio and the nature of reality: Crash Course Philosophy
Today Hank gains insight from that most philosophical of figures...Leonardo DiCaprio. In this episode, we’re talking about the process of philosophical discovery and questioning the relationship between appearance and reality by taking a look at Plato’s famous Myth of the Cave. All with a little help from our good pal Leo.
Tuesday, October 27, 2015
Did Humans Evolve to See Things as They Really Are?
via Scientific American
One of the deepest problems in epistemology is how we know the nature of reality. Over the millennia philosophers have offered many theories, from solipsism (only one's mind is known to exist) to the theory that natural selection shaped our senses to give us an accurate, or verdical, model of the world. Now a new theory by University of California, Irvine, cognitive scientist Donald Hoffman is garnering attention. (Google his scholarly papers and TED talk with more than 1.4 million views.) Grounded in evolutionary psychology, it is called the interface theory of perception (ITP) and argues that percepts act as a species-specific user interface that directs behavior toward survival and reproduction, not truth.
Hoffman's computer analogy is that physical space is like the desktop and that objects in it are like desktop icons, which are produced by the graphical user interface (GUI). Our senses, he says, form a biological user interface—a gooey GUI—between our brain and the outside world, transducing physical stimuli such as photons of light into neural impulses processed by the visual cortex as things in the environment. GUIs are useful because you don't need to know what is inside computers and brains. You just need to know how to interact with the interface well enough to accomplish your task. Adaptive function, not veridical perception, is what is important.
Hoffman's holotype is the Australian jewel beetle Julodimorpha bakewelli. Females are large, shiny, brown and dimpled. So, too, are discarded beer bottles dubbed “stubbies,” and males will mount them until they die by heat, starvation or ants. The species was on the brink of extinction because its senses and brain were designed by natural selection not to perceive reality (it's a beer bottle, you idiot!) but to mate with anything big, brown, shiny and dimply.
To test his theory, Hoffman ran thousands of evolutionary computer simulations in which digital organisms whose perceptual systems are tuned exclusively for truth are outcompeted by those tuned solely for fitness. Because natural selection depends only on expected fitness, evolution shaped our sensory systems toward fitter behavior, not truthful representation.
ITP is well worth serious consideration and testing, but I have my doubts. First, how could a more accurate perception of reality not be adaptive? Hoffman's answer is that evolution gave us an interface to hide the underlying reality because, for example, you don't need to know how neurons create images of snakes; you just need to jump out of the way of the snake icon. But how did the icon come to look like a snake in the first place? Natural selection. And why did some nonpoisonous snakes evolve to mimic poisonous species? Because predators avoid real poisonous snakes. Mimicry works only if there is an objective reality to mimic.
Hoffman has claimed that “a rock is an interface icon, not a constituent of objective reality.” But a real rock chipped into an arrow point and thrown at a four-legged meal works even if you don't know physics and calculus. Is that not veridical perception with adaptive significance?
see also:
Health: General Anesthesia Causes No Cognitive Deficit in Infants | Mind: Scientists Study Nomophobia — Fear of Being without a Mobile Phone | Sustainability: Exxon Knew about Climate Change Almost 40 Years Ago | Tech: Back to the Future, Part II Predicted Techno-Marvels of October 21, 2015
As for jewel beetles, stubbies are what ethologists call supernormal stimuli, which mimic objects that organisms evolved to respond to and elicit a stronger response in doing so, such as (for some people) silicone breast implants in women and testosterone-enhanced bodybuilding in men. Supernormal stimuli operate only because evolution designed us to respond to normal stimuli, which must be accurately portrayed by our senses to our brain to work.
Hoffman says that perception is species-specific and that we should take predators seriously but not literally. Yes, a dolphin's icon for “shark” no doubt looks different than a human's, but there really are sharks, and they really do have powerful tails on one end and a mouthful of teeth on the other end, and that is true no matter how your sensory system works.
Also, computer simulations are useful for modeling how evolution might have happened, but a real-world test of ITP would be to determine if most biological sensory interfaces create icons that resemble reality or distort it. I'm betting on reality. Data will tell.
Finally, why present this problem as an either-or choice between fitness and truth? Adaptations depend in large part on a relatively accurate model of reality. The fact that science progresses toward, say, eradicating diseases and landing spacecraft on Mars must mean that our perceptions of reality are growing ever closer to the truth, even if it is with a small “t.”
One of the deepest problems in epistemology is how we know the nature of reality. Over the millennia philosophers have offered many theories, from solipsism (only one's mind is known to exist) to the theory that natural selection shaped our senses to give us an accurate, or verdical, model of the world. Now a new theory by University of California, Irvine, cognitive scientist Donald Hoffman is garnering attention. (Google his scholarly papers and TED talk with more than 1.4 million views.) Grounded in evolutionary psychology, it is called the interface theory of perception (ITP) and argues that percepts act as a species-specific user interface that directs behavior toward survival and reproduction, not truth.
Hoffman's computer analogy is that physical space is like the desktop and that objects in it are like desktop icons, which are produced by the graphical user interface (GUI). Our senses, he says, form a biological user interface—a gooey GUI—between our brain and the outside world, transducing physical stimuli such as photons of light into neural impulses processed by the visual cortex as things in the environment. GUIs are useful because you don't need to know what is inside computers and brains. You just need to know how to interact with the interface well enough to accomplish your task. Adaptive function, not veridical perception, is what is important.
Hoffman's holotype is the Australian jewel beetle Julodimorpha bakewelli. Females are large, shiny, brown and dimpled. So, too, are discarded beer bottles dubbed “stubbies,” and males will mount them until they die by heat, starvation or ants. The species was on the brink of extinction because its senses and brain were designed by natural selection not to perceive reality (it's a beer bottle, you idiot!) but to mate with anything big, brown, shiny and dimply.
To test his theory, Hoffman ran thousands of evolutionary computer simulations in which digital organisms whose perceptual systems are tuned exclusively for truth are outcompeted by those tuned solely for fitness. Because natural selection depends only on expected fitness, evolution shaped our sensory systems toward fitter behavior, not truthful representation.
ITP is well worth serious consideration and testing, but I have my doubts. First, how could a more accurate perception of reality not be adaptive? Hoffman's answer is that evolution gave us an interface to hide the underlying reality because, for example, you don't need to know how neurons create images of snakes; you just need to jump out of the way of the snake icon. But how did the icon come to look like a snake in the first place? Natural selection. And why did some nonpoisonous snakes evolve to mimic poisonous species? Because predators avoid real poisonous snakes. Mimicry works only if there is an objective reality to mimic.
Hoffman has claimed that “a rock is an interface icon, not a constituent of objective reality.” But a real rock chipped into an arrow point and thrown at a four-legged meal works even if you don't know physics and calculus. Is that not veridical perception with adaptive significance?
see also:
Health: General Anesthesia Causes No Cognitive Deficit in Infants | Mind: Scientists Study Nomophobia — Fear of Being without a Mobile Phone | Sustainability: Exxon Knew about Climate Change Almost 40 Years Ago | Tech: Back to the Future, Part II Predicted Techno-Marvels of October 21, 2015
As for jewel beetles, stubbies are what ethologists call supernormal stimuli, which mimic objects that organisms evolved to respond to and elicit a stronger response in doing so, such as (for some people) silicone breast implants in women and testosterone-enhanced bodybuilding in men. Supernormal stimuli operate only because evolution designed us to respond to normal stimuli, which must be accurately portrayed by our senses to our brain to work.
Hoffman says that perception is species-specific and that we should take predators seriously but not literally. Yes, a dolphin's icon for “shark” no doubt looks different than a human's, but there really are sharks, and they really do have powerful tails on one end and a mouthful of teeth on the other end, and that is true no matter how your sensory system works.
Also, computer simulations are useful for modeling how evolution might have happened, but a real-world test of ITP would be to determine if most biological sensory interfaces create icons that resemble reality or distort it. I'm betting on reality. Data will tell.
Finally, why present this problem as an either-or choice between fitness and truth? Adaptations depend in large part on a relatively accurate model of reality. The fact that science progresses toward, say, eradicating diseases and landing spacecraft on Mars must mean that our perceptions of reality are growing ever closer to the truth, even if it is with a small “t.”
Saturday, February 21, 2015
Cymatics: When Science And Music Dance
From IFLScience :
When you weave science and music together, what happens?
Only some of the most mind blowing, jaw dropping visuals you’ll ever see.
Derived from the Greek word “wave”, Cymatics is defined by cymatic.org as revealing “a strange and beautiful symmetry at work in nature.” Commonly described as” visible sound”, it is a branch of modal phenomena originally created by Swiss doctor Hans Jenny.
Cymatics is achieved by vibrating a plate that is covered in a thin film of a medium, for example sand, water or iron fillings, by placing a frequency though it, commonly using tones or music. We can then observe the different frequencies displacing the medium, creating intricately stunning patterns or shapes.
Check out this unbelievable video by Nigel Stanford and his crew, demonstrating the incredible applications of Cymatics.
When you weave science and music together, what happens?
Only some of the most mind blowing, jaw dropping visuals you’ll ever see.
Derived from the Greek word “wave”, Cymatics is defined by cymatic.org as revealing “a strange and beautiful symmetry at work in nature.” Commonly described as” visible sound”, it is a branch of modal phenomena originally created by Swiss doctor Hans Jenny.
Cymatics is achieved by vibrating a plate that is covered in a thin film of a medium, for example sand, water or iron fillings, by placing a frequency though it, commonly using tones or music. We can then observe the different frequencies displacing the medium, creating intricately stunning patterns or shapes.
Check out this unbelievable video by Nigel Stanford and his crew, demonstrating the incredible applications of Cymatics.
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