Tuesday 5 March 2024

Creationism in Crisis - "No! No! My God Is A Little God, And I Want Him To Stays That Way "


Webb Unlocks Secrets of One of the Most Distant Galaxies Ever Seen - NASA Science

Continuing a series showing how much more impressive the Universe is than religion's prophets ever thought it was.

How is it that hardly any major religion has looked at science and concluded, "This is better than we thought! The Universe is much bigger than our prophets said, grander, more subtle, more elegant?” Instead they say, “No, no, no! My god is a little god, and I want him to stay that way.” A religion, old or new, that stressed the magnificence of the Universe as revealed by modern science might be able to draw forth reserves of reverence and awe hardly tapped by the conventional faiths.

The James Webb Space Telescope (JWST) has just detected one of the most distant galaxies ever seen. Because the velocity of light through space is a finite quantity, this means that the radiation detected by the JWST left the galaxy when the Universe itself was only about 430 million years old, in other words about 3.4 billion years ago.

To put that into miles means calculating the distance light travels in a year and multiplying that by 3.4 billion. In one year, light will travel just over 16 billion miles, so the object the JWST has detected is about 50 trillion miles away, and, if it's still there, it will now be at least 3.4 billion years old - which is a really long time compared to the age the authors of the Abrahamic holy books thought.

To put that in perspective: here is how the Christian Bible describes the Universe:
The Universe as described in Genesis 1: 3-18
And God said, Let there be light: and there was light. And God saw the light, that it was good: and God divided the light from the darkness. And God called the light Day, and the darkness he called Night. And the evening and the morning were the first day. And God said, Let there be a firmament in the midst of the waters, and let it divide the waters from the waters. And God made the firmament, and divided the waters which were under the firmament from the waters which were above the firmament: and it was so. And God called the firmament Heaven. And the evening and the morning were the second day. And God said, Let the waters under the heaven be gathered together unto one place, and let the dry land appear: and it was so. And God called the dry land Earth; and the gathering together of the waters called he Seas: and God saw that it was good.

Gen 1:3-10

[…]

And God said, Let there be lights in the firmament of the heaven to divide the day from the night; and let them be for signs, and for seasons, and for days, and years: And let them be for lights in the firmament of the heaven to give light upon the earth: and it was so. And God made two great lights; the greater light to rule the day, and the lesser light to rule the night: he made the stars also. And God set them in the firmament of the heaven to give light upon the earth, And to rule over the day and over the night, and to divide the light from the darkness: and God saw that it was good.

Gen 1:14-18
And here is how the scientists at NASA using the JWST and the Hubble Space Telescope describe just a tiny portion of the universe
Looking deeply into space and time, two teams using NASA’s James Webb Space Telescope have studied the exceptionally luminous galaxy GN-z11, which existed when our 13.8 billion-year-old universe was only about 430 million years old.

Initially detected with NASA’s Hubble Space Telescope, this galaxy — one of the youngest and most distant ever observed — is so bright that it is challenging scientists to understand why. Now, GN-z11 is giving up some of its secrets.

Vigorous Black Hole Is Most Distant Ever Found

A team studying GN-z11 with Webb found the first clear evidence that the galaxy is hosting a central, supermassive black hole that is rapidly accreting matter. Their finding makes this the farthest active supermassive black hole spotted to date.

“We found extremely dense gas that is common in the vicinity of supermassive black holes accreting gas,” explained principal investigator Roberto Maiolino of the Cavendish Laboratory and the Kavli Institute of Cosmology at the University of Cambridge in the United Kingdom. “These were the first clear signatures that GN-z11 is hosting a black hole that is gobbling matter.”

Using Webb, the team also found indications of ionized chemical elements typically observed near accreting supermassive black holes. Additionally, they discovered a very powerful wind being expelled by the galaxy. Such high-velocity winds are typically driven by processes associated with vigorously accreting supermassive black holes.

“Webb’s NIRCam (Near-Infrared Camera) has revealed an extended component, tracing the host galaxy, and a central, compact source whose colors are consistent with those of an accretion disk surrounding a black hole,” said investigator Hannah Übler, also of the Cavendish Laboratory and the Kavli Institute.

Together, this evidence shows that GN-z11 hosts a 2-million-solar-mass, supermassive black hole in a very active phase of consuming matter, which is why it's so luminous.

Pristine Gas Clump in GN-z11’s Halo Intrigues Researchers
A second team, also led by Maiolino, used Webb’s NIRSpec (Near-Infrared Spectrograph) to find a gaseous clump of helium in the halo surrounding GN-z11.

“The fact that we don't see anything else beyond helium suggests that this clump must be fairly pristine,” said Maiolino. “This is something that was expected by theory and simulations in the vicinity of particularly massive galaxies from these epochs — that there should be pockets of pristine gas surviving in the halo, and these may collapse and form Population III star clusters.”

Finding the never-before-seen Population III stars — the first generation of stars formed almost entirely from hydrogen and helium — is one of the most important goals of modern astrophysics. These stars are anticipated to be very massive, very luminous, and very hot. Their expected signature is the presence of ionized helium and the absence of chemical elements heavier than helium.

The formation of the first stars and galaxies marks a fundamental shift in cosmic history, during which the universe evolved from a dark and relatively simple state into the highly structured and complex environment we see today.

In future Webb observations, Maiolino, Übler, and their team will explore GN-z11 in greater depth, and they hope to strengthen the case for the Population III stars that may be forming in its halo.

The research on the pristine gas clump in GN-z11’s halo has been accepted for publication by Astronomy & Astrophysics. The results of the study of GN-z11’s black hole were published in the journal Nature on January 17, 2024. The data was obtained as part of the JWST Advanced Deep Extragalactic Survey (JADES), a joint project between the NIRCam and NIRSpec teams.
But it's not fair to blame the authors of the Bible for getting it so hopelessly wrong. They were doing their best with what little knowledge they had.

Creationism in Crisis - A Mystery In Plant Evolution - 125 Million Years In The Making In That Long Pre-'Creation Week' History Of Life On Earth



A 'Ginormous' tomato produced by an unregulated CLV3 gene.

An evolutionary mystery 125 million years in the making | Cold Spring Harbor Laboratory

In an example of one of those lovely gaps in the record of the evolution of a species into which creationists try to shoehorn their ever-shrinking and increasingly homeless little god, there is something about the evolution of tomatoes and Arabidopsis thaliana that scientists can't yet explain.

But the problem for creationists is that this gap is somewhere in the evolutionary history of these plants that occurred almost 125 million years before creationism’s god decided to create a small flat planet with a dome over it to keep the water above the sky out, centred on the Middle East, in what creationists like to call 'Creation Week'.

The problem comes from the fact that what creationists think is a science and history text book was written by ignorant people who knew nothing of the world outside their small part of it and who had no idea about the history of the planet or of life on it, so they wrote an imaginative story to fill the gap in their knowledge and understanding, and, quite understandably, got almost every aspect of it complete wrong.

And of course, they would never have imagined that one day someone almost as ignorant as they were, would gather their tales into a book and declare it to be the inerrant word of a god - an idea that would be hilarious if it wasn't taken seriously by adults who can become dangerously violent when their superstition is questions.

The mystery that Cold Spring Harbor Laboratory (CSHL) biologists have uncovered is that sometime during the last 125 million years, tomatoes and Arabidopsis thaliana plants experienced an extreme genetic makeover. Just what happened remains unclear. But the mystery surrounds CLV3, a gene key to healthy plant growth and development.

CLV3 controls the growth of fruit in these plants and, if uncontrolled will result in large, even gigantic, fruits, so there is an evolutionary trade-off between a few large fruits and lots of smaller fruits. The mystery is just how and why this balance was achieved differently in two distantly-related plants.

As the CSHL press release explains:

Monday 4 March 2024

Anti-Vaxxer Conspiracists News - How Trumpanzee Cult Conspiracists Are Risking People's Lives For Money While Feeding Populist Extremism


Anti-vaccine conspiracies fuel divisive political discourse | The University of Tokyo
According to a news item carried today by Agence France-Presse (AFP), US antivaxx conspiracists are deliberately spreading fear and disinformation to sell quack medical kits to gullible fools and in doing so are risking the lives of anyone foolish enough to believe them. And a recent paper published by a Japanese research group has shown how extremist parties are trading on growing antivaxx paranoia, originating in Trump-supporting conspiracists in the USA, by incorporating it into the political platforms.

This team of researchers recall how Donald Trump first of all tried to take credit for developing the mRNA vaccines against Covid-19, as though he had personally directed the research and invented the science behind mRNA vaccines, then switched to curry favour with the antivaxxers by casting doubt on the need for boosters. And of course, antivaxxer conspiracy theories became a central theme of the rabidly pro-Trump QAnon conspiracy theorists.

Firstly, the AFP report:

Saturday 2 March 2024

Creationism in Crisis - How Radiometric Dating Really Works - And Refutes Creationism


Example of a radioactive decay chain from lead-212 (212Pb) to lead-208 (208Pb) . Each parent nuclide spontaneously decays into a daughter nuclide (the decay product) via an α decay or a β− decay. The final decay product, lead-208 (208Pb), is stable and can no longer undergo spontaneous radioactive decay.
Source: Wikipedia

Creationism in Crisis - How Radiometric Dating Really Works - And Refutes Creationism

As a service to Creationists, I asked ChatGPT to outline the main geochronology techniques, how and when they are used by palaeontologists, what their limitations are, and how scientists allow for possible sources of error.

All creationists need do is explain how and where these techniques are wrong and what the source of error is that can make 10,000 years or less look like hundreds of millions, or billions of years, without claiming the fundamental forces which control the universe changed to such an extent that atoms would not have been able to form when the they believe the universe, Earth and all life on it were created.

Remember to supply the verified evidence because a claim made without evidence can be dismissed without evidence, and false claims will simply demonstrate what many people already know - that creationism is a cult for people gullible enough to believe falsehoods and ignorant enough not to know they've been fooled.

Unintelligent Design - The Heath-Robinson Workaround For A Design Fault In The Immune System


The “switch” that keeps the immune system from attacking the body - EPFL

A Machine for Testing Golf Drivers - William Heath-Robinson
A characteristic of designs by creationism's putative intelligent designer, is the needless complexity which often arises because earlier solutions were suboptimal and either didn't work very well or tended to cause problems that needed to be mitigated with another layer of (often suboptimal) complexity.

This is also a characteristic of systems 'designed' by a mindless natural process with no power or mechanism for scrapping a suboptimal design and starting again and no ability to predict the future and design for problems which will arise later.

In fact, what creationists think is evidence of a supreme intelligence, more often seems to resemble the designs of the British cartoonist and eccentric designer, William Heath-Robinson, who was famous for his machines designed to solve every-day problem, which were invariably far more complex than they need have been, and which incorporated everyday objects such as umbrellas, full coal-scuttles for counter-weights, lengths of knotted string and stepladders balanced on upright pianos to give them enough height. Take away any of these unlikely components and the whole machine would fail, in an almost perfect metaphor for how evolution can exapt pre-exiting structures from other processes and structures for novel functions, to give the appearance of irreducible complexity.

And yet they work, or at least look as though they would if anyone ever made one.

An example of a Heath-Robinson machine in mammalian 'design' was revealed by a scientists working at the Swiss École polytechnique fédérale de Lausanne (EPFL), who have discovered how the body prevents the immune system from attacking itself.

But, as the very many auto-immune diseases show, this system is far from perfect and frequently fails, sometime with serious, even fatal, consequences.

But the whole immune system is only needed because something designed pathogens such as bacteria, viruses and other parasites, apparently to attack us and make us sick in the first place. Parasites are a source of conflict for creationists who have to believe both that the putative designer god is the only entity capable of designing living things, and that something else created parasites because their god wouldn't do such a thing, and both that their god is omnipotent, but powerless against that other designer.

So, what is this mechanism the EPFL researchers have discovered?

Their findings are the subject of an open access paper in Nature and is explained in an EPFL news release:

How Science Works - A Fossil Whale Is Not What Was Thought - But It Still Refutes Creationism!


Size comparison of a modern blue whale (Balaenoptera musculus) and the extinct Perucetus colossus, known from a fossil discovered in Peru.

Image by Cullen Townsend (https://www.cullentownsenddesign.com/)
Slimming Down a Colossal Fossil Whale | UC Davis

Scientists may have got it wrong when they thought they had the fossilised remains of the heaviest thing that ever lived, in the form of a 39 million-year-old fossil whale from the Peruvian Middle Eocene, which they called Perucetus colossus.

But, before creationists get over-excited, thinking it's the 30 million years they got wrong, they need to read on; it isn't the age they got wrong, but the estimated mass.

A new analysis by palaeontologist at the University of California Davis has put Perucetus colossus back into the same range as modern whales and lighter than the blue whale, which retains its position as the largest and heaviest organism ever to exist on Earth, dwarfing even the largest dinosaurs.

How they went about it is the subject of an open access paper in PeerJ and a news release from UC Davis:

Friday 1 March 2024

Abiogenesis News - That God-Shaped Gap Just Keeps On Shrinking


Scripps Research scientists reveal how first cells could have formed on Earth | Scripps Research

It's been a bad week so far for creationists. Coming so soon after scientist announced they had solved the 'chirality problem, is news that another team have shown how simple cells could plausibly have formed in the pre-biotic conditions that pertained on early Earth.

Creationists are generally black & white thinkers who value certainty above truth, so, for them there is no such thing as a plausible explanation; either something is proven beyond doubt, even passing an especially impossible standard of evidence, or it is wrong (so God did it!).

And one of their 'certainties' is their absolute faith in the slogan, "You can't get life from non-life!", which is chanted like a protective mantra in any debate about evolution (conveniently switching the debate from evolution to what they think is safer ground, abiogenesis). But ask them to define 'life' in such a way that you can test for it to tell if something is alive or not, or to explain how the non-living food they eat gets converted into living tissues, if that's impossible, and you're likely to get an ad hominem or an indignant, condescending flounce and a swift termination of the conversation.

It is an essential ingredient of creationism that the belief that abiogenesis is 'impossible' be maintained as the last refuge for their ever-shrinking creator god to be located in, as all the other gaps are closed to it.

So, having committed themselves to the certainty that abiogenesis is 'impossible', they have unwittingly committed themselves to accepting that any plausible process which can be shown to be viable, refutes the notion of impossibility and everything they conclude from it. So, their next step is the intellectually bankrupt technique of moving the goal-posts or demanding scientist provide an impossible standard of evidence such as showing it happening - billions of years ago. Never will they concede that evidence of plausibility refutes the claim of impossibility because, to a black & white thinker, plausibility doesn't give enough certainty, so can be dismissed until proven.

So, we can expect that predictable display of intellectual bankruptcy in response to the news that scientists at the Scripps Institute, La Jolla, CA, USA have discovered a plausible mechanism for the formation of simple self-replicating cells in the prebiotic conditions that pertained on early Earth.

Their findings are published in the Cell Press journal Chem and are the subject of a Cripps Institute press release:

Malevolent Designer News - How Creationism's Divine Malevolence Is Adapting The Avian Flu Virus to Kill Marine Mammals


Avian Influenza Virus Is Adapting to Spread to Marine Mammals | UC Davis

Elephant seals lie dead on a beach in Argentina following an outbreak of avian influenza in the region.
Photo: Maxi Jonas.
As an example of creationist double-think and intellectual bankruptcy, their attitude toward parasites like viruses is a classic:
  • "Only God is capable of designing organisms, so "Look at the trees!" and "What about irreducible complexity?"
  • "Something else created parasites like bacteria, worms and viruses, because God wouldn't do something like that!"

Simultaneously committing blasphemy and refuting their own argument from teleology!

I wonder then how that rarest of animals, the intellectually honest creationist copes with the news that the creator of the avian flu virus, H5N1, is in the process of adapting it to kill marine mammals such as elephant seals, just as it adapted the SARS-CoV-2 virus from a bat virus to one that could kill humans and cause economic collapse.

Evidence that it is doing so, if you believe viruses are created and don't evolve naturally, which dogma forbids a creationist from believing, comes in the form of a study by scientists from University of California, Davis, and the National Institute of Agricultural Technology (INTA) in Argentina. The study, the first genomic characterization of H5N1 in marine wildlife on the Atlantic shore of South America, is published in the journal Emerging Infectious Diseases and is described in a UC Davis news release:

Thursday 29 February 2024

Malevolent Designer News - Creationism's Divine Malevolence Is Still Victimising Frogs


Foothill yellow-legged frog, Rana boylii

Photo: Rebecca Fabbri/USFWS
Scientists assemble a richer picture of the plight and resilience of the foothill yellow-legged frog | The Current

Almost unnoticed by the general public and noticed only by biologists and wildlife conservationists, is a pandemic far more deadly than the Covid-19 pandemic, or even the Medieval Black Death.

It kills a very high percentage of its victims, has already exterminated whole populations of frogs and other amphibians, and has contributed significantly to the global mass extinction currently underway.

It is, of course, the chytrid fungus Batrachochytrium dendrobatidis, which, along with a closely-related fungus, B. salamandrivorans, causes the fatal disease, chytridiomycosis, in frogs and other amphibians.

As an example of the work of creationism's divine malevolence, it takes some beating for its sheer malevolent nastiness. It infects the skin of these amphibians, through which they breath, and causes it to thicken and fail as a respiratory organ, leading to suffocation, multiple organ failure and death. Here is how I described it in my illustrated book, The Malevolent Designer: Why Nature's God is not Good:
Exterminating Frogs with a Fungus.

Most of the examples I’ve talked about so far have been organisms and viruses that affect humans, but we are far from being the only species that Creationism’s putative intelligent designer seems to have taken an intense dislike to. For example, the world’s frogs and other amphibians are currently being decimated by chytridiomycosis, caused by a couple of related Chytrid fungi, Batrachochytrium dendrobatidis and B. salamandrivorans. It has been estimated that over 500 different species have been severely reduced in number by this fungal plague, with over 90 extinctions.

These fungi seem to have originated in an area of Southeast Asia by modification of a common, harmless, soil fungus. In that part of the world, the local population of amphibians seems to be resistant to the pathogenic forms of the fungi, suggesting that these fungi frequently become pathogenic and the local population have built up resistance to it.

According to research carried out by a team from the Fenner School of Environment and Society, Australian National University, ACT, Australia, it was resistance in the local population which probably kept the disease from spreading more widely, until human agency intervened to change the environment. They have related the increased trade in amphibian species to the spread of the fungi all over the world where they found species with no evolved resistance (42).

Figure 5 Frog Victims of Chytrid Fungus

Illustration: Catherine Webber-Hounslow
Recently, another team found that one of the factors that could have made these fungi so successful is that the frog’s immune response seems to have worked against it. Researchers from the University of Central Florida and the Smithsonian Conservation Biology Institute (SCBI) found that, in the frog Rana yavapaiensis, a species known to vary in its ability to survive attack by these fungi, those which showed an elevated immune response had a worse outcome that those with a lower response (43). Somehow, the frog’s ‘designed’ immune system was working against it and the fungi had been ‘designed’ to exploit this.

ID advocates would have us believe that, for reasons unknown, their putative intelligent designer has deliberately redesigned a soil fungus so it can overcome the immune system it designed to protect frogs from infections, and so exterminate over 90 species of amphibians that it designed earlier and severely endanger some 500 species in what has been described as the biggest single loss of biodiversity, albeit, aided and abetted by humans in this endeavour. Creationism’s intelligent designer must really hate the frogs it designed. Maybe a private definition of the word ‘intelligent’ is being employed here.
Now a team of researchers from multiple American wildlife and conservation agencies have looked in detail at the spread of this fungus in one particular frog which has declined so rapidly it is now an endangered species - the foothill yellow-legged frog, Rana boylii. This small frog's range once extended from Oregon to Baja California.

They have shown that human agency is implicated in the spread of this fungus by not only spreading it around the world in trade, as the earlier Australian study found (42), but with regard to the foothill yellow-legged frog specifically, by global warming, climate change and habitat destruction as more land is converted to agriculture. They have published their work, open access, in Royal Society Open Science. It is also explained in a University of California Santa Barbara, news release:

Up to only a few inches in length, with a lemon-hued belly, the foothill yellow-legged frog may seem unassuming. But its range once stretched from central Oregon to Baja California. In 2023, it was listed under the federal Endangered Species Act. Its rapidly decreasing range is due in part to a fungal pathogen called Batrachochytrium dendrobatidis, or Bd, that has devastated amphibians around the world.

A team of researchers, including UC Santa Barbara’s Andrea Adams, has conducted the most comprehensive study to date of disease dynamics in foothill yellow-legged frogs. The team’s data — sourced from both wild frogs and specimens in museum collections — enabled them to track patterns of infection across a large geographic range. In a study published in Royal Society Open Science, the researchers reveal that drought, rising temperatures and the increasing conversion of land for agriculture appear to be the largest factors driving Bd infection in this species.

The researchers aimed to assemble as much data as they could, both in space and time. They surveyed in the creeks and rivers of California and Oregon, where they swabbed wild yellow-legged frogs for the presence of Bd. It also led them into fluorescent-lit museum collections to sample specimens from as far back as the 1890s.

The team leveraged a large network of people and institutions to amass this wealth of samples.

Many foothill yellow-legged frog field researchers had data that they weren’t actively analyzing, and so we were able to bring all of this data together and get it into a usable format that we could use to paint a much bigger picture of what is, and was, going on with Bd in this species.

Andrea J. Adams, co-author.
Earth Research Institute
University of California, Santa Barbara, CA, USA.
The researchers swabbed each frog’s skin to determine if the animal was infected. To test for Bd, they used a PCR test, similar to some tests for COVID. By searching for Bd DNA from thousands of samples, the researchers were able to identify infection rates and severity. Co-lead author Ryan Peek ran this information through statistical models, which accounted for climatic, geographic, biologic and land use variables. This enabled the team to track disease patterns across a large geographic range over roughly 120 years.

The team discovered that disease patterns of Bd aligned with historical frog declines. The pathogen began to spread in the 1940s from the southern coast of California, moving northward and eventually affecting nearly the entire region. The biggest factors driving infection seem to be drought, increasing temperatures and the use of ever more land for agriculture.

Bd is a fungus that is spread through spores in the water, but that spread may occur differently in foothill yellow-legged frogs in different regions and climates, the researchers found. In some places, drought increased infection, while in others, it did not, possibly because of the presence or absence of other species that can carry Bd and share the same water, such as American bullfrogs, a species introduced from eastern North America.

If you combine the fact that there are bullfrogs building up the number of spores that these frogs are exposed to, and then they’re all kind of stuck in these small pools together, that explains why drought matters. They are suddenly getting hit with a really large number of spores and getting sick and dying.

These findings open more questions about what was stopping transmission and what allowed it to happen later.

Dr. Anat M. Belasen, co-first author
Department of Integrative Biology
University of Texas at Austin, Austin, TX, USA
And Department of Ecology and Evolutionary Biology,
Cornell University, Ithaca, NY, USA.
What’s more, foothill yellow-legged frogs live exclusively in streams and rivers, not ponds and lakes. So the species is already stressed when these waterways shrink into isolated pools.

The progression of Bd in the foothill yellow-legged frog also differed from its course in other western amphibians. In many other species, the disease radiated from urban centers, rather than this clear south-to-north trend. What’s more, the disease showed up later in the foothill yellow-legged frog than in other species in its range.

Frogs switch from herbivores as tadpoles to carnivores as adults, which means they connect different nutrient cycles together in the food web. Their position at the center of the food chain also influences the ecosystem.

When you remove frogs from an ecosystem, what you get is less control of insects, things that the frogs would eat. There is also less food for things that eat the frogs, like snakes, birds and small mammals. It really throws things off and makes the ecosystem less stable and less functional.

“There are areas that have wet soils that would be alongside suitable habitat. In areas where more of those lands have been converted to agriculture, we see a higher risk of frogs being infected with the fungus.

Dr. Anat M. Belasen.
Co-author Jamie Bettaso swabs a wild foothill yellow-legged frog to test for fungal infection.

Photo Credit: Jamie Bettaso
The conversion of land for agriculture was another major factor influencing the spread of Bd. for these frogs.

In addition to disease hotspots, the team also identified a number of cold spots — areas where the pathogen is present but less influential. The existence of so many cold spots in different areas is a good sign, as it may mean that many areas have conditions suitable for keeping disease rates low, even as climate change increases temperatures and patterns of drought.

The authors are curious what might explain this clustering, especially when cold spots appear in unexpected locations: for example, places with similar habitat, land-use and climatic impacts as hotspots. It suggests there may be some genetic basis for the differences, whether on the pathogen side or the host side. Adams is currently researching the feasibility of reintroducing foothill yellow-legged frogs to Southern California.

The results of this paper shed a lot of light on the dynamics of where Bd occurs, what drives its spread and how the pathogen and frog may interact in the future.

We took a big snapshot of this species’ disease relationship through time. Earlier studies provided the researchers with glimpses into disease patterns in smaller geographic regions, “but now we have a much larger dataset that further confirms many of these patterns, and expands on them.

Andrea J. Adams.
More detail is given in the team's open access paper in Royal Society Open Science:
Abstract

Species with extensive geographical ranges pose special challenges to assessing drivers of wildlife disease, necessitating collaborative and large-scale analyses. The imperilled foothill yellow-legged frog (Rana boylii) inhabits a wide geographical range and variable conditions in rivers of California and Oregon (USA), and is considered threatened by the pathogen Batrachochytrium dendrobatidis (Bd). To assess drivers of Bd infections over time and space, we compiled over 2000 datapoints from R. boylii museum specimens (collected 1897–2005) and field samples (2005–2021) spanning 9° of latitude. We observed a south-to-north spread of Bd detections beginning in the 1940s and increase in prevalence from the 1940s to 1970s, coinciding with extirpation from southern latitudes. We detected eight high-prevalence geographical clusters through time that span the species' geographical range. Field-sampled male R. boylii exhibited the highest prevalence, and juveniles sampled in autumn exhibited the highest loads. Bd infection risk was highest in lower elevation rain-dominated watersheds, and with cool temperatures and low stream-flow conditions at the end of the dry season. Through a holistic assessment of relationships between infection risk, geographical context and time, we identify the locations and time periods where Bd mitigation and monitoring will be critical for conservation of this imperilled species.

1. Introduction

Threatened species with large geographical ranges often require unique, regional conservation strategies to combat stressors such as infectious disease. Pathogen surveys and reporting have become standard for North American wildlife diseases [1,2]; however, relative risk across a landscape and among populations within species remains difficult to anticipate, especially when data are collected by separate research groups [3]. Central reporting databases [4], synthetic analyses and retrospective surveys can help assess disease threats and identify high-risk populations.

Among the most significant wildlife diseases, amphibian chytridiomycosis caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd) has contributed to declines of hundreds of species worldwide [5]; but see [6]. In North America, notable Bd-associated declines have occurred across the west including the southern Rocky Mountains [7,8], Arizona and New Mexico [9,10], Nevada [11] and California [1214]. In several of these cases, infection outcomes varied widely among populations due to host-related and environmental factors including genetics, prior Bd exposure and abiotic conditions [1517].

For the stream-dwelling foothill yellow-legged frog, Rana boylii, Bd's role in the species' changing abundance across its endemic range (California and Oregon, USA) is not well-understood. The species has declined for at least the last half-century, with extirpations reported from xeric lower latitudes [18], at the wetter northern range limit [19] and downstream of large dams range-wide [20]. A mix of abiotic and biotic factors influence Bd infection risk and disease dynamics in many systems, including elevation, latitude, climate, habitat quality and host characteristics [21]. The relative importance of these factors remains unclear in rivers with winter flood/summer drought flow regimes typical across R. boylii's geographical range. Bd is considered a significant potential threat to R. boylii [22] because it is implicated in the species' disappearance from rivers of California's South Coast [23] and in recent autumn die-offs of R. boylii in Central Coast streams [24,25]. A large-scale assessment of Bd infections is needed to clarify how infections relate to historical declines in some regions' rivers and persistence in others, identify clusters of increased infection risk across the species’ range, and evaluate how infection incidence and severity changes with the seasonality of the Mediterranean climate and across the diverse ecoregions that R. boylii occupies.

Here, we leverage data from over 2000 field and museum samples covering 124 years to synthesize knowledge and evaluate patterns of Bd infections in R. boylii. We use a combination of modelling approaches and spatial scan statistics to ask: (i) how are Bd detections in R. boylii are distributed over space and time, (ii) whether watersheds with high versus low Bd infection risk clustered historically and today, and (iii) how Bd infections are related to biotic and abiotic factors. Our results highlight priority populations for Bd mitigation, regions that are data-deficient and warrant further sampling and monitoring, and remaining gaps in our knowledge about Bd susceptibility in R. boylii. Our study serves as a resource for wildlife managers implementing disease mitigation and species recovery projects, such as re-introductions, and as an example of collaborative research to address conservation challenges in wide-ranging imperilled species.

Figure 1.
Distribution of R. boylii samples assayed for Bd infection. Diamonds show museum samples (collected 1897–2005), circles show field samples (2005–2021). Filled symbols indicate Bd-positive samples. (a) Sampling locations across California and Oregon, USA. Symbols overlap in some localities; see inset barplots for sample sizes. Rana boylii clades are outlined and labelled, with California Endangered Species Act status abbreviated in parentheses: SSC = Species of Special Concern, TH = Threatened, EN = Endangered. (b) Spatio-temporal spread of Bd detections. Symbol size indicates sample size at the HUC-12 (sub-watershed) level. Generalized additive model (GAM) of latitude∼capture year + sample size in Bd-positive samples is shown with black curved line (R2 = 0.133).

Photo of R. boylii in Napa County, CA by Marina De León.
It must be thrilling for devotees of the putative divine malevolence to see the stunning success it is having exterminating so many species of frog, but one can't help but wonder what the ancestral frog did to incur this wrath. Did it maybe eat a forbidden mosquito or spawn out of wedlock?

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ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

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The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

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Creationism in Crisis - Biological Chirality Explained - And Another Favourite Creationist Gap Slams Shut With No God(s) Found


How molecular “handedness” emerged in early biology | Scripps Research

Back in the 1980's when I first encountered (mostly) American creationists on the emerging Internet, one of their arguments from personal incredulity was that 'no-one can explain' why amino acids occur naturally in two stereo forms, yet only one is found in nature (therefore God did it!).

This 'problem' for evolutionary biologist now seems to have dropped out of favour with creationists, probably because, as more and more former creationists realise they've been fooled, only the lower tail-end of the IQ bell curve remain, and this phenomenon, known as chirality, is a little difficult to understand and requires a modicum of understanding of chemistry.

Basically, at the heart of an amino acid is a carbon atom with four different atoms of groups attached. This structure can be thought of as a pyramid with a triangular base (known as a tetrahedron) with the carbon atom in the centre and each of the four atoms or groups at each point of the tetrahedron. These groups can be attached to the carbon in two separate ways so that one is a mirror image of the other. These are known as chiral forms or stereo-isomers. No matter how you rotate one, it can never be the same as its opposite chiral form.

These chiral forms have the same chemical properties and the same physical properties apart from one - the way they interact with polarised light. One form causes the plane of polarity of polarised light to rotate in one direction, the other in the other direction; so they are also known as optical isomers.

The chiral forms of amino acids are prefixed with 'D' or 'L' (upper case; Dextro and Laevo (right and left)) according to the physical structure, or 'd' and 'l' (lower case) according to which direction they rotate the plane of polarity of polarized light.

ChatGPT explains it more succinctly:

Creationism in Crisis - Evolution By Loss Of Complexity - How A Mutation Cost Our Ancestors Their Tails


Change in Genetic Code May Explain How Human Ancestors Lost Tails | NYU Langone News

In that distant, pre-'Creation Week' history of Life On Earth, 25 million years before creationists think Earth was created out of nothing, and all living things on it were magicked into existence without ancestors, a 'jumping gene' inserted a short length of DNA termed AluY, into the gene which controls tail length in monkeys, and the resulting tailless monkeys went on to diversify into the apes - gibbons, siamangs, orangutans, gorillas, chimpanzees, bonobos, and the hominins which were to evolve into the Australopithecines and the Homo genus, including Homo sapiens, all of which still possess that short insertion in the TBXT gene, which otherwise is identical to one of the gene which grow the tail of the simians.

As an example of design, it is one of the least intelligent, since, instead of removing all the genes required to grow a tail, the 'designer' simply broke an essential gene and left all the others to do nothing apart from having to be replicated in every cell in every ape that ever lived, as an example of the massive waste and unnecessary complexity that characterises an evolved process and gives the lie to any notion of any intelligence being involved.

By inserting the AluY snippet into a mouse BBXT gene the researchers found a variety of tail effects, including mice born without tails. They also showed that there was a small increase in the incidence on neural tube defects (spina bifida) in mice.

Quite why tailless would have been selected for during the evolution of these ancestors of the modern apes is a matter for speculation; maybe a tail was becoming an encumbrance for a brachiating mode of locomotion as opposed to running along the top of branches and jumping from branch to branch, which the smaller monkeys used, where a tail was an important balance organ. For a heavier ape hanging beneath the branches by its arms, there would have been less need for a balance organ and a tail would have been liable to damage and infection.

How this was discovered by a team led by researchers at New York University Grossman School of Medicine, is the subject of an open access paper in Nature and a NYU Langone Health news release:

Wednesday 28 February 2024

Covidiot News - How the mRNA Vaccines Give Long-Term Protection Against COVID-19


Long-Term Data Reveals SARS-CoV-2 Infection and Vaccine-Induced Antibody Responses Are Long-Lasting | Mount Sinai - New York

If you listen to antivaxxer covidiots you would believe:
  • COVID-19 is no worse than the common cold.
  • The SARS-CoV-2 virus which causes COVID-19, is a deadly organism developed by the Chinese for biological warfare.
  • COVID-19 was a hoax (which even normally hostile nations had signed up to, apparently).
  • God sent the virus to punish America for legalising same-sex marriage (and the rest of the world was collateral damage)
  • The vaccines developed against it don't work (regardless of what the clinic trials showed).
  • The vaccines contain microchips and special genes to make you become gay and/or subject to satellite control.
  • The vaccines contain deadly viruses that can be activated via the 5G phone network.
  • Millions of people have died or will die soon because they've been vaccinated.
  • [Fill in your own crackpot theory because someone will already have claimed it to be true].

The truth is, however, that millions of people died of COVID-19 in the first year of the pandemic, before a vaccine was generally available and this death rate fell to low levels following the roll out of the first vaccines and subsequent boosters to allow for new variants. Although the virus is still very much with us, people have been able to resume normal activities and the economic and health impact of the virus is now no more than that of seasonal flu, but there were concerns that antibody levels produced in response to the mRNA vaccines were short-lived, giving only temporary protection.

Now a large-scale analysis conducted by leading microbiologists at the Icahn School of Medicine at Mount Sinai has shown that antibody responses induced by COVId-19 vaccines are long-lasting. The results of this analysis are published, open access, in the Cell Press journal, Immunity, and are discussed in a Mount Sinai press release:
The emergence of SARS-CoV-2, the virus that causes COVID-19, in late 2019 sparked the global pandemic that is now in its fifth year. Vaccines that were developed at record speed have saved millions of lives. However, the emergence of SARS-CoV-2 variants and waning immunity have decreased the effectiveness of the vaccines against symptomatic disease. The common perception now is that mRNA-based vaccine-induced immunity wanes quickly. However, this assumption is largely based on data from short-term studies that include a very limited number of data points following peak responses.

The Mount Sinai research team’s analysis of more than 8,000 samples collected over a three-year period in New York City examined how antibody responses to the virus’s spike protein changed after infections, during the primary immunization series, during monovalent and bivalent booster vaccination, and during breakthrough infections.

They found that upon primary immunization, participants with pre-existing immunity (those who had previously been infected with the virus) mounted higher antibody responses faster and achieved higher steady-state antibody titers than individuals who had not been previously infected. The waning of antibody response was characterized by two phases: an initial rapid decay from the strong peak after vaccination, followed by a stabilization phase with very slow decay, suggesting that antibody levels were very long-lasting. Booster vaccination equalized the differences in antibody concentration between participants with and without pre-existing immunity. Breakthrough infections increased antibodies to similar levels as an additional vaccine dose in individuals who had not previously been infected.

This investigation represents one of the most extensive and in-depth assessments of the longevity of SARS-CoV-2 immune responses to date. Its major conclusion is that changes in the virus that allow it to evade immunity, rather than waning immunity, are the major reason for breakthrough infections.

Ours is one of the longest-running COVID-19 studies out there. Following the same group of people monthly over time is rare and powerful because you can compare immune responses on an individual level. SARS-CoV-2 continues to evolve, so this research is important to provide an understanding about the impact of new variants and new vaccine doses on a healthy immune system, and to guide all of us to make the best choices to maintain protection against the virus that continues to circulate in our communities.

Professor Viviana Simon, MD, PhD, lead author
Professor of Microbiology, Medicine and Pathology, Molecular and Cell-Based Medicine
Department of Microbiology
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
This in-depth analysis was made possible through the Protection Associated with Rapid Immunity to SARS-CoV-2 (PARIS) study, an observational, longitudinal cohort of health care workers of the Mount Sinai Health System that was initiated in April 2020. At that time, the densely populated New York metropolitan area was hit with an exponential increase in severe SARS-CoV-2 infections, and essential workers in the health care system were at high risk for infection. In response to the crisis, a team of leading virologists, physician-scientists, and pathologists at Mount Sinai established a specific and sensitive SARS-CoV-2 binding enzyme-linked immunosorbent assay to accurately measure the SARS-CoV-2 antibody titers. This test was used to measure immune responses in the PARIS cohort in order to determine how quickly the antibody defenses were mounted and much these changed over the months and years of follow up.

In addition to showing the impact on a person’s individual antibody response to vaccines based on the type of vaccine received and whether or not they were infected before receiving the first dose, the PARIS study made possible the development of a mathematical model that can be used to predict and characterize antibody responses of both individual people and populations.

People have pandemic fatigue and vaccine uptake has slowed, especially after the vaccines started to be charged to insurance*. We were pleasantly surprised to see that the booster doses promoted a large antibody response regardless of a person’s personal infection history, so we are hopeful that our study findings will encourage people to get their vaccine boosters when eligible and to stay engaged in research. Our work also showcases the impact of viral evolution over time and why it’s critical to keep studies like this going, despite the pandemic fatigue.

Komal Srivastava, MS, Co-first author
Director of Strategy and Operation
Mount Sinai Center for Vaccine Research and Pandemic Preparedness.

According to the research team, the PARIS model has broad applications for studying the kinetics of antibodies produced to different COVID-19 vaccines in diverse populations. They stress much more work remains to analyze side effects, applications of the antibody model and continued research about new vaccines and viral variants.

This study adds an essential piece of data to understand the intricate immune response elicited by SARS-CoV-2 infection and COVID-19 vaccination. In light of the emerging viral variants, which predominantly induce a cross-reactive antibody response against the spike protein, it will be exciting to characterize in depth the role of these antibodies - in particular the non-neutralizing ones - in protection against the most recent circulating viral variants. Likewise, monitoring the induction of variant-specific antibodies after multiple exposures by breakthrough infections and by administration of updated COVID-19 vaccines, such as the XBB.1.5 monovalent booster, will be key to understand the evolution of the antibody response over time.

Assistant Professor Dr Juan Manuel Carreno Quiroz, PhD, Co-first author.
Department of Microbiology
Icahn School of Medicine at Mount Sinai, New York, NY, USA.


*Note: in the UK, vaccines are provided free by the NHS. Other non-US countries will have their own health-care systems which may or may not include charges for the vaccines.
More technical detail and the background to the research is given in the team's paper in Immunology:
Graphical abstract
Highlights
  • COVID-19-vaccine-induced immunity wanes but stabilizes at an individual setpoint
  • Pre-existing immunity results in rapid antibody responses upon vaccination
  • Boosters equalize antibody titers between individuals with and without hybrid immunity
  • Antibody kinetics show two phases: an initial rapid decay followed by a steady state

Summary

It is thought that mRNA-based vaccine-induced immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) wanes quickly, based mostly on short-term studies. Here, we analyzed the kinetics and durability of the humoral responses to SARS-CoV-2 infection and vaccination using >8,000 longitudinal samples collected over a 3-year period in New York City. Upon primary immunization, participants with pre-existing immunity mounted higher antibody responses faster and achieved higher steady-state antibody titers than naive individuals. Antibody kinetics were characterized by two phases: an initial rapid decay, followed by a stabilization phase with very slow decay. Booster vaccination equalized the differences in antibody concentration between participants with and without hybrid immunity, but the peak antibody titers decreased with each successive antigen exposure. Breakthrough infections increased antibodies to similar titers as an additional vaccine dose in naive individuals. Our study provides strong evidence that SARS-CoV-2 antibody responses are long lasting, with initial waning followed by stabilization.

Introduction

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in late 2019 sparked the global coronavirus disease 2019 (COVID-19) pandemic that is now in its 4th year. Vaccines to mitigate the impact of the pandemic were developed at record speed and have saved millions of lives. However, the emergence of SARS-CoV-2 variants1 and waning immunity2 have decreased the effectiveness of the vaccines against symptomatic disease.3 These two issues, the emergence of antigenically distinct SARS-CoV-2 variants and waning immunity, are often conflated and used interchangeably but represent two different phenomena.4 Most vaccines used in North America and Europe are based on lipid nanoparticles (LNPs) containing messenger RNA (mRNA) produced by Pfizer/BioNTech (BNT162b2) or Moderna (mRNA-1273), and the common perception now is that mRNA-based vaccine-induced immunity wanes quickly.5 However, this assumption is mostly based on data from short-term studies that include a very limited number of data points following peak responses.2,5

In March of 2020, the densely populated New York metropolitan area was hit with an exponential increase of severe SARS-CoV-2 infections, resulting in a staggering number of fatalities and a severely overburdened healthcare system.6,7,8 Due to shortages of personal protective equipment, essential workers in the health care system were at high risk for infection. In response to this crisis, we established (1) a specific and sensitive SARS-CoV-2 binding enzyme-linked immunosorbent assay (ELISA) to measure humoral immune responses,9 and (2) an observational longitudinal cohort of health care workers of the Mount Sinai Health System to determine the kinetics of these humoral responses. This study, named Protection Associated with Rapid Immunity to SARS-CoV-2 (PARIS),10 aims to capture the dynamics of SARS-CoV-2 antibody responses to infection as well as vaccinations, to determine re-infection rates, and to assess correlates of protection in the context of individual immune histories.

With over 8,000 longitudinal study visits across a single cohort during the first 3 years of the pandemic, our investigation represents one of the most extensive and in-depth assessments of the longevity of SARS-CoV-2 immune responses to date. Using this longitudinal cohort, we determined the kinetics of antibody responses to spike protein after infections, during the primary immunization series, during monovalent and bivalent booster vaccination, as well as during breakthrough infections. Our findings indicate that, in contrast to common perception, COVID-19 mRNA vaccination induces long-lasting antibody responses in humans. The PARIS Study also provides insights into the effect of booster vaccination and breakthrough infections on the stability of antibody responses.
What is clear from this study is that antibody levels remain at protective levels for very much longer that was previously thought and that they continue to give protection against the severe form of the disease. However, as the virus evolves in an environment in which the vast majority of possible victims have already been vaccinated or have had previous infections so have high antibody levels, the variants that can 'escape' this protection will continue to evolve and become the predominant variant.

This diagram from UK data shows how the different variants have evolved and either replaced earlier variants or have reached an equilibrium with them:
Changes in proportions of SARS-CoV-2 variants in UK over time. This diagram is a good illustration of how the proportions of different alleles of a gene change in a species gene pool over time as the species evolves.

It is essential then that regular boosters, which provide protection against the latest variants, should continue to be given. We are in a long-term struggle with this virus and vaccines keep us ahead of the game.

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