Religion, Creationism, evolution, science and politics from a centre-left atheist humanist. The blog religious frauds tell lies about.
Sunday, 16 February 2025
Malevolent Designer News - How a Fungus Makes Its Host Destroy Its Own Brain
Fungus ‘hacks’ natural immune system causing neurodegeneration in fruit flies - University of Birmingham
If we are to believe creationists, their god created insects such as fruit flies, Colorado beetles, etc., and then set about devising ways to kill them with, amongst other pathogens, fungi that infect them and destroy them from inside.
One of the problems this supposedly intelligent designer had to overcome was the immune system it had given the insects in order to protect them from the pathogens it was designing to kill them.
According to an open access paper just published in PLOS Biology by a team led by Professor Alicia Hidalgo from School of Biosciences, The University of Birmingham, one species of parasitic fungus, Beauveria bassiana, cleverly turns its host's immune system against its host, making it destroy its own brain. Although this fungus does not affect mammals, so poses no threat to humans, the team warns that it is possible that another fungus could use a similar technique against mammals, including humans.
Thursday, 13 February 2025
Malevolent Designer News - How Cancer is Cleverly Designed to Trick Our Immune System
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There is an ongoing arms race between medical science and cancer - and guess whose side creationism's intelligent designer appears to be on.
Yep, it's the same intelligent designer who designed cancers in the first place by creating an error-prone DNA replication mechanism that goes wrong, as does the error-correction mechanism it designed to try to rectify its faulty design with an added layer of complexity. And one of the results of it going wrong is cancer.
One of the more hopeful treatments for cancer was a tailor-made immunotherapy in which specific antibodies to the cancer cells were used to attack the cancer and treat it like a parasitic pathogen, by training the immune system to recognise the cancer and attack and destroy it.
But, true to form, creationism's divine malevolence has hit back by designing a response by cancer cells to attack by cells of the immune system.
We can be sure this is the work of creationism's intelligent designer because William A Dembski, the Discovery Institute's flunky and pseudoscientist in residence, tells us that any genetic sequence that produces a function must have been given 'specified information' in the form of the DNA that codes for that specific protein because, so he claims, specified information is too complex to have evolved.
Wednesday, 5 February 2025
Malevolent Design - How Sudan Virus is Cleverly Designed to Kill 50% of Its Victims
New Study Reveals How Sudan Virus Binds to Human Cells | Midwest Antiviral Drug Discovery (AViDD) Center
It's shaping up to be a thrilling month for devotees of creationism's divine malevolence as science finds out just how brilliantly its nasty little parasites are designed to make us sick and increase the suffering in the world, although quite why any normal person would worship a hate-filled sadistic psychopath is even more of a mystery than the mechanism by which it designs and creates organisms.
The latest is the details of how the Sudan virus (a variant of Ebola with a 50% 'success' rate in terms of deaths of its victims) has an improved method of binding to our cells to gain entry and start the killing process. Like Ebola, it binds to receptors on the cell surface, but because it has just 4 different amino acids in its coat proteins, it binds much more efficiently - a factor which probably contributes to its high kill rate.
Tuesday, 4 February 2025
Malevolent Design - More Brilliance from Creationism's Divine Malevolence
Hijacking of plasmin by dengue virus for infection - NUS Faculty of Science | NUS Faculty of Science
If you're a creationists who follows the latest science (if there is such a thing), you must be bursting with admiration for the ingenuity of your beloved intelligent designer for the way its brilliance at making us sick and spreading more suffering in the world is being revealed by science.
In the last few days, I've reported on how HIV, the virus that causes AIDS, is designed to hijack our cell's metabolic processes to ensure its own survival, and how the zika virus that cause the serious birth defect, microcephaly, in children if their mothers become infected during pregnancy, is brilliantly designed to make our skin produce more of the scent that attracts mosquitoes, so ensuring it is spread as widely as possible.
Now we have a superb example of this skill in malevolent design revealed by researchers from the National University of Singapore (NUS) who have discovered how the dengue virus is designed to make sure as many people as possible are infected by it. And this is breath-taking in its ingenuity. It is spread by the divine malevolence's favourite insect vector - the mosquito.
Sunday, 2 February 2025
Malevolent Design - How Zika Is Designed to Spread Maximum Suffering.
Zika uses human skin as ‘mosquito magnet’ to spread virus further | LSTM
January was something of a joyous month for devotees of creationism's divine malevolence. Following closely behind the news of how it brilliantly designed HIV to use our cells defences against us so making it better at infecting and killing us, we have news of another breathtakingly brilliant design of a nasty little pathogen - the zika virus that causes microcephaly in children if their mothers become infected during pregnancy.
This news is that it turns our skin into a living 'magnet' to attract the vector that spreads it - mosquitos - so ensuring it gets transmitted to as many victims as possible. It does it by altering a gene and protein expression in dermal fibroblasts, causing the skin to produce odours that are attractive to mosquitoes. In effect, calling them to come and feed.
Before creationists start bleating unscientific and biologically non-sensical nonsense about 'genetic entropy' and devolution allowed by 'sin' I should point out that no mutation that conveys a benefit on an organism can be regarded as 'devolutionary'. It is classic evolution by natural selection. And, as per William Dembski's gibberish about 'specified complexity', any complex DNA or RNA sequence that codes for a specific function must be regarded as 'specified complexity', using his argument, so must have been specified by a magic designer, according to his misuse of statistics and probability. Or perhaps a creationist could explain why such a highly specific function of converting a human gene to make special mosquito-attracting scents, is not an example of Dembski's 'specified complexity'.
So, how was this, in creationist terms, intelligently designed virus, discovered to have this touch of brilliance in its design? That was the result if a new study by an international team led by Liverpool School of Tropical Medicine. Their findings are published, open access, in Communications Biology.
Tell me all about the zika virus, its evolution and recent spread, please. Zika virus (ZIKV) is a mosquito-borne flavivirus primarily transmitted by Aedes mosquitoes, particularly Aedes aegypti. First identified in 1947 in a rhesus monkey in Uganda's Zika Forest, it was subsequently detected in humans in 1952 in Uganda and the United Republic of Tanzania. (who.int).
Evolution and Lineages
Zika virus (ZIKV) is an RNA virus. Specifically, it is a positive-sense, single-stranded RNA virus belonging to the Flavivirus genus within the Flaviviridae family. Other notable flaviviruses include dengue, yellow fever, and West Nile viruses.
Because ZIKV has an RNA genome, it mutates and evolves more rapidly than DNA viruses, which may have contributed to its recent spread and ability to cause large outbreaks.
Phylogenetic studies have identified two main lineages of ZIKV: African and Asian. The virus remained relatively obscure for decades, causing only sporadic human infections in Africa and Asia. However, in 2007, a significant outbreak occurred on Yap Island in Micronesia, marking ZIKV's first major emergence outside its traditional endemic areas. (academic.oup.com)
The Asian lineage is particularly notable for its role in the outbreaks in the Pacific and the Americas. Genetic analyses suggest that mutations in the virus may have enhanced its ability to infect humans and spread more efficiently, contributing to its rapid dissemination. (frontiersin.org).
Global Spread and Recent Developments
Following the Yap Island outbreak, ZIKV caused significant epidemics in the Pacific, including in French Polynesia in 2013. In 2015, Brazil reported its first case, leading to a large outbreak associated with severe birth defects, such as microcephaly, and neurological disorders like Guillain-Barré syndrome. The virus then spread throughout the Americas, prompting the World Health Organization to declare it a Public Health Emergency of International Concern in 2016. (who.int).
As of May 2024, ZIKV transmission persists in several countries, though generally at low levels since 2018. Recent data indicate that three additional countries have reported autochthonous mosquito-borne transmission, and two more have established *Aedes aegypti* populations without documented ZIKV transmission. (who.int).
In January 2025, new research revealed that ZIKV can manipulate human skin to emit chemical signals attracting more mosquitoes, potentially facilitating further spread of the virus. (sciencedaily.com).
Prevention and Control
Preventing ZIKV infection primarily involves controlling mosquito populations and minimizing exposure to mosquito bites. This includes using insect repellent, wearing protective clothing, and eliminating standing water where mosquitoes breed. Given the association between ZIKV infection during pregnancy and birth defects, pregnant women are advised to avoid travel to areas with active ZIKV transmission. (who.int).
Despite ongoing research, there is currently no specific antiviral treatment or vaccine for ZIKV. Efforts to develop a vaccine have faced challenges, including fluctuating transmission rates and limited funding.
Zika uses human skin as ‘mosquito magnet’ to spread virus further
Zika virus hijacks the skin of its human host to send out chemical signals that lure more mosquitoes to infect and spread the disease further, new research shows.
Zika transmission has been reported more than 90 countries as the spread of the Aedes aegypti mosquito that carries the virus, as well as dengue and chikungunya, has increased over recent years as an effect of climate change and urbanisation. Yet surprisingly little is known about the factors that drive Zika transmission success.
A new study led by Liverpool School of Tropical Medicine and published in Communications Biology shows that Zika causes metabolic changes in human skin that essentially transforms it from a protective barrier to a magnet for mosquitoes.
Their research shows that the Zika virus alters gene and protein expression in dermal fibroblasts, the cell type responsible for maintaining structural integrity in the skin. These metabolic changes increase the production of certain chemicals emitted through the skin, known as volatile organic compounds (VOCs), that are attractive to mosquitoes and encourage them to bite. Their findings are supported by an extensive meta-proteome analysis, a technique that examines the overall effect of the interaction of different types of gene and protein within an organism.
Most Zika infections do not lead to disease, and those that do generally cause mild symptoms that last for 2-7 days.Our findings show that Zika virus isn’t just passively transmitted, but it actively manipulates human biology to ensure its survival. As Zika cases rise and Aedes mosquitoes expand their range, understanding the mechanisms by which they gain a transmission advantage could unlock new strategies for combating arboviruses. This could include developing genetic interventions that disrupt the signal transmitted through the skin which seems to be so attractive to mosquitoes. The possibilities are as intriguing as they are urgent.
Dr Noushin Emami, co-corresponding author Department of Molecular Bioscience
Wenner-Gren Institute
Stockholm University, Stockholm, Sweden
And Vector Biology Department (VBD)
Liverpool School of Tropical Medicine (LSTM)
Liverpool, UK.
Zika can occasionally cause more serious complications and can harm a developing baby if contracted by a pregnant woman.
This study was conducted in collaboration with Emami Lab at Stockholm University, alongside researchers from the Nature Research Centre in Vilnius, the University of Veterinary Medicine in Hanover, Molecular Attraction AB, Umeå University, Leibniz University Hannover, and the University of Greenwich.
AbstractObviously, to creationism's intelligent designer who designed mosquitoes to drink human blood and so spread several nasty parasites and viruses, and gave them the ability to detect and home in on the scents we give off, it was a simple matter to design the zika virus to enhance those scents to attract more mosquitoes and have the virus spread as widely as possible, to maximise the number of children born with microcephaly. At least, since that is about all the zika virus does, we have to assume that wehoever designed it, designed it with that specific function in mind.
Transmission of Zika virus (ZIKV) has been reported in 92 countries and the geographical spread of invasive virus-borne vectors has increased in recent years. Arboviruses naturally survive between vertebrate hosts and arthropod vectors. Transmission success requires the mosquito to feed on viraemic hosts. There is little specific understanding of factors that may promote ZIKV transmission-success. Here we show that mosquito host-seeking behaviour is impacted by viral infection of the vertebrae host and may be essential for the effective transmission of arboviruses like ZIKV. Human skin fibroblasts produce a variety of metabolites, and we show that ZIKV immediately alters gene/protein expression patterns in infected-dermal fibroblasts, altering their metabolism to increase the release of mosquito-attractive volatile organic compounds (VOCs), which improves its transmission success. We demonstrate that at the invasion stage, ZIKV differentially altered the emission of VOCs by significantly increasing or decreasing their amounts, while at the transmission stage of the virus, all VOCs are significantly increased. The findings are complemented by an extensive meta-proteome analysis. Overall, we demonstrate a multifaceted role of virus-host interaction and shed light on how arboviruses may influence the behaviour of their vectors as an evolved means of improving transmission-success
Introduction
The human body comprises around 40 trillion (3.7 × 1013) cells1, which produce an enormous variety of metabolites including volatile organic compounds (VOCs). The qualitative and quantitative changes in VOC profiles reflect the optimum status of healthy cells. The skin is the body’s largest organ, serving multiple essential functions, including acting as a physical barrier for protection, a site for sensory perception, and a centre for vitamin synthesis. The release of VOCs through the skin, which contributes to the distinct odours of the human body, is a familiar part of our daily experience2. These VOCs include a large number of volatiles that can be listed as carboxylic acids, aldehydes, alcohols or ketones3. Dermal fibroblasts are the main cell type present in skin connective tissue (dermis)4. These mesenchymal/stromal cells derived from the embryonic mesoderm, reside in the dermal layer of skin. They produce extracellular matrix proteins to strengthen the dermal compartment and interact with epidermal cells5.
Zika virus (ZIKV) had not been widely known until a series of outbreaks occurred with severe clinical complications that made it a matter of global public health concern. The emergence of ZIKV followed a typical pattern of a vector-borne disease being introduced into a new ecosystem and host population and spreading rapidly with severe implications for human health. ZIKV is a mosquito-borne virus belonging to the genus Flavivirus and is transmitted to humans by mosquitoes of the genus Aedes. Both Aedes aegypti and Aedes albopictus are the primary vectors for ZIKV transmission in nature6. Vector-mediated transmission of ZIKV is initiated when a blood-feeding female Aedes mosquito injects the virus into the skin of its mammalian host, followed by infection of a wide range of permissive cells. Indeed, skin cells, including dermal fibroblasts were found to be permissive to ZIKV infection. Infection of skin fibroblasts rapidly resulted in the presence of high RNA copy numbers and a gradual increase in the production of ZIKV particles over time, indicating an active viral replication stage. In humans, the incubation period from mosquito bite to symptom onset is ≈3–12 days7. Accumulating data indicate that ZIKV alters the biochemical processes of the infected cells by modifying glucose8,9 and fatty acid10 metabolism. However, no published data has yet revealed any changes in the composition of infected cell volatome. While Zhang and colleagues11 demonstrated that flaviviruses can manipulate host skin microbiota to produce an odour that attracts mosquitoes, the specific role of infected human skin cells in manipulating mosquitoes’ behaviour remains unclear.
Mosquitoes have made themselves at home in new geographical regions throughout recent years, bringing with them some historically exotic diseases. Epidemiologic and laboratory studies have implicated various Aedes spp. mosquitoes as ZIKV vectors11. In mosquitoes, it appears that the viral load is initially high on the day of feeding, but then decreases to undetectable levels for about ten days. After this incubation period, the viral content increases again by day 15 and remains high from days 20 to 60. This is important because it suggests that it takes about 10 days for the virus to reach the salivary glands of the mosquito where it can potentially be transmitted to humans7. There is currently no specific treatment or vaccine available to mitigate or prevent ZIKV infection. Prevention measures, particularly conventional vector control, are currently the priority while we await these and other advances in control of the substantial harm caused by this virus. The World Health Organization has issued recommendations on this matter12.
To further understand this complex issue, this study aims to demonstrate how ZIKV manipulate vector behaviour by altering gene/protein expression in human dermal fibroblasts at different stages of infection. These changes lead to an increased release of mosquito-attractive VOCs, ultimately enhancing transmission success. Here, we describe how ZIKV infection of human host cells provoked the modified feeding behaviour of its tiger mosquito vector in a manner that plausibly results in enhanced transmission success.
And William Dembski insists that whatever a DNA/RNA sequence produces it must have been intelligently specified to produce that outcome. The malice of this designer knows no bounds apparently. That's if you believe what creationists claim.
If you believe what science says, it's easy to see how genes mutating and being selected for when they convey an advantage can produce this sort of host-parasite arms race over time, especially if it only takes a few tweaks of the RNA sequence to manipulate one of our genes, and suddenly, lots more mosquitoes are homing in and spreading the new variant far and wide.
Thursday, 12 December 2024
Malevolent Design - The Sneak Tactics of Toxoplasma gondii
Toxoplasma gondii parasite uses unconventional method to make proteins for evasion of drug treatment
Here we are with yet another example of an organism that, if there is a designer behind it, that designer can only be described as malevolent and determined to maximise the suffering and misery in the world.
It is, of course, another example of a nasty little parasite which, if you subscribe to the creationist view that complexity 'proves' design, has been designed to ensure we are as vulnerable to is as possible by helping it evade the immune system and other mechanisms, supposedly designed by the same designer god to protect us from the parasites it designs to harm us.
This example is the parasite Toxoplasma gondii, which is notorious for manipulating its natural victims, which are felines and their prey species. For example, mice infected with T. gondii lose their fear of cats so they get eten and the parasite gets into its primary host; infected chimpanzees develop a liking for the smell of leopard urine.
Humans are not the natural secondary host, but the parasite readily infects us as we catch it from cats. It is thought that about one third of humans are infected. Once infected it is impossible to get rid of from the body because, even if antibodies are produced by our immune system, the parasites go into a dormant state as cysts which can form in any organs of the body, including the brain.
Saturday, 7 December 2024
Malevolent Design - How Malaria Is Being Redesigned to Keep On Killing Children
Study uncovers first evidence of resistance to standard malaria treatment in African children with severe malaria
In another twist of the arms race with human medical science Plasmodium falciparum, the malevolently designed parasite that causes malaria and kills hundreds of thousands of children a year, mostly in Africa, has developed resistance to Artemisinin. Scientists were already aware that resistance had arisen in cases of uncomplicated malaria, but this is the first such incidence of resistance in the more severe form of the disease.
Indiana University School of Medicine researchers, in collaboration with colleagues at Makerere University in Uganda have discovered a case of complicated malaria in a child in Uganda.
Wednesday, 27 November 2024
Mallevolent Design - How Salmonella Sneaks Past Our Defences To Make Us Sick
New study shows how salmonella tricks gut defenses to cause infection
There is a simple paradox at the heart of creationism that I have never even seen an attempt to resolve. It all comes from two beliefs: there is only one designer god capable of designing living organisms and that designer god designed us complete with our immune system with which we can attempt to resist attack by pathogens, and that pathogens are not the work of this design, but are the result of 'genetic entropy' and 'devolution' since Adam & Eve let 'sin' into the world. The fact that Michael J. Behe, who invented that excuse, has let slip that ID Creationism is Bible literalism in a lab coat seems to be lost on his followers who still dutifully insist that it is a scientific alternative to evolution and should be taught in school science class (presumably now with the tale of Adam & Eve taught as real history and 'sin' as a real force in science).
The paradox is, did the designer god give Adam & Eve an immune system, or did it design an upgrade when 'sin' allowed pathogens to exist? If the former, it was anticipating and planning for the so-called 'fall'; if the latter, it lacked foresight so is not omniscient.
But however creationists resolve this paradox they still have to explain why the 'intelligently designed' immune system doesn't work very well and why whatever is designing pathogens seems to be able to overcome it.
The nonsense about 'sin', 'the fall', etc., is trivially easy to refute because any improvement in a parasite's ability to parasitise its host can't possibly be regarded as a devolution from some assumed initial perfection because an improvement can't be worse that what it's an improvement on. The whole nonsense of 'devolution' is biological gobbledygook, intelligently designed to appeal to scientifically illiterate simpletons who want to fit the Bible superstition somewhere in the reasoning without bothering too much about the logic or the biology.
So, the paradox boils down to why an intelligent designer would be having an arms race with itself so the parasites it creates can continue to parasitise the victims it creates complete with their immune system it created to stop them. Creationists normally flee in terror at the mere mention of arms races, which is why you'll never see them discussed in the cult literature apart from where pathogens are waved aside as 'caused by sin', blah, blah, blah...
So, it would be refreshing indeed to see a genuine attempt by an intelligent design creationist try to give some rational explanation, and hopefully without giving away the fact that ID creationism is merely Christian fundamentalism in disguise, for the discovery by a new UC Davis Health study that shows how the Salmonella bacteria, a major cause of food poisoning, can invade the gut even when protective bacteria are present.
As an added embarrassment for creationists, Salmonella is closely related to Escherichia coli (E.coli) that they usually cite Michael J. Behe as 'proving' it must have been designed by their god because its flagellum is 'irreducibly complex'.
First a little AI background information about Salmonella, where it came from and what it does to us:
Sunday, 3 November 2024
Malevolent Design - How Sleeping Sickness Parasites Are 'Designed' to Evade Our Immune System
Discovery Illuminates How Sleeping Sickness Parasite Outsmarts Immune Response | Johns Hopkins | Bloomberg School of Public Health
Trypanosoma brucei is a blood-borne eukaryote parasite that should leave believers in an intelligent designer, open-mouthed in admiration for its inventive genius. Christian fundamentalist creationists of the white supremacist persuasion should also admire the racist that, through T. brucei, has managed to keep large parts of Africa technologically under-developed due to the difficult in maintaining herds of domestic animals where the vector of these parasites - the tsetse fly - is common.
As a vector, the tsetse fly is a triumph of malevolent design which I mentioned in my popular book, The Unintelligent Designer: Refuting the Intelligent Design Hoax, but it would have been all for nothing without the nasty little T. brucei to cause sleeping sickness in humans and the debilitating disease "nagana" in cattle.
What creationist admires of the divine malevolence they believe designs these things should now be marveling at is the sheer brilliance of the design by which it manages to evade the immune system, which they believe was created by the same designer god which now regards his design as a problem to be overcome oh parasites like T. brucei can continue making Africans and their cattle sick.
Thursday, 17 October 2024
Malevolent Designer News - Stand By For The Next Move In The Mpox Arms Race
Fort Detrick, Maryland.
Mpox Vaccine Is Safe and Generates a Robust Antibody Response in Adolescents | NIAID: National Institute of Allergy and Infectious Diseases
As Medical science announces success in the search for a vaccine against the mpox virus currently spreading misery and suffering around the globe, we can be as sure as can be that creationism’s divine malevolence is working on a variant with an inbuilt way to evade the antibodies the vaccine produces, in just the same way it did with COVID-19 - if you believe a magic designer is behind these things, the way intelligent [sic] design creationists do.
Tuesday, 15 October 2024
Unintelligent Design - The Blunder That Causes Cancers
Ludwig Cancer Research
It has often been a theme of my blog posts how, if we regard cells as the result of conscious (I won't use the term 'intelligent' as that's singularly inappropriate, as we shall see) design then the picture quickly emerges of a bungling incompetent, cobbling together Heath-Robinson solutions to problems of its own incompetent making and lack of foresight.
The entire system of epigenetics, for example, is only necessary in a multicellular organism with its cell specialisation because specialised cells only need a small subset of the entire genome, yet, because cells replicate using exactly the same process that single-celled organisms use, where the entire genome needs to be replicated in every daughter cell, the cells of multicellular organisms such as humans each receive the entire species genome. So, most of it needs to be turned off.
This is where the epigenetic system comes in where methyl groups are attached to key bases in the DNA which prevents that section being transcribed into RNA, effectively switching the gene off. There are other components to the epigenetic system, but that is the pertinent component as far as this particular blunder is concerned.
The problem starts when a methyl group is attached to a cytosine base (C in the CGTA genetic code) which is next to a guanine(G) base.
Monday, 14 October 2024
Unintelligent Design Or Sheer Malevolence? - Defective Sperm Puts Mother And Baby At Risk
Defective sperm doubles the risk of preeclampsia | Lund University
Christian superstition insists that every person conceived is a creation of their omniscient, omnipotent god who knows and has always known, exactly who is going to be born and has an oven-ready plan for their entire existence. Each baby conceived was exactly as the Christian god intended, down to the last detail of the DNA Exactly which sperm fertilizes which egg when, is part of the god's omniscient, perfect plan.
Leaving aside the absurdity of throwing millions of sperms at a single egg to produce that conception, when only a predetermined one was going to be the winner in order to produce the predetermined genome, when a single sperm would have been just as effective, we are left with the disturbing idea that any and all genetic defects were the intended outcome of that conception; the intention of a supposedly omnibenevolent god.
Now, it might, in fact it definitely is possible for a Christian to imagine some ultimate good will come from a child with a genetic defect, but what if a defect in the sperm causes harm not just to the baby, but to the mother? Are we to conclude that a mother whose life is put at risk by a defective sperm from her partner was the intended victim of an 'all-loving' god? What possible good can come from a mother's (and almost invariably her baby's) life being in danger from something beyond her control? What possible good can come from preeclampsia?
Saturday, 12 October 2024
Malevolent Design - How Chlamydia Is 'Designed' to Cause Maximum Sufferring.
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The problem of parasites for creationists is one that, despite the best efforts of apologists like Michael J Behe of the Deception Institute, just won't go away.
Sadly, Behe shot himself in the foot with his original claim to have proven 'intelligent [sic] design in living organisms with his choice of the bacterial flagellum in E. coli, where he persuaded his willing audience that these nasty little pathogens had been intelligently designed - and by unspoken assumption, designed by the locally-popular god.
Now creationists wave his 'proof' of design as evidence for their creator god because only their god is capable of creating living organisms.
But, with characteristic double-think, creationists also argue that their god is omnibenevolent, so something else must have created parasites like E. coli, and, courtesy again of Michael J. Behe, they cite 'Sin' causing 'genetic entropy' and the absurd idea of 'devolution' this supposedly causes, as the cause of parasites and pathogens (but not the bacterial flagellum, obviously!).
The problem with that notion is that they need to do their double-think trick one more time and believe that a trait with improves a pathogens ability to live and reproduce in its host makes it somehow less perfect that one without that trait. So, in the creationist's world, an improvement is a move away from perfection!
But, with a cult that appears to believe learning is a move away from the 'perfection' of pristine ignorance (from whence comes expertise in all aspects of science), that's probably not too difficult a feat of mental gymnastics for a creationist to perform.
Thursday, 10 October 2024
Refuting Creationism - Even More Signs of The Divine Malevolence's Obsessive Compulsive Disorder?
Over 160,000 new virus species discovered by AI - The University of Sydney
This is the second paper today to show the apparent obsession creationism's putative designer has with creating viruses, if you believe that superstition.
The first paper dealt with the discovery that there are some 600 different viruses to be found on a used toothbrush and on the shower heads in US bathrooms; this one reports on a discovery that makes that finding pale into insignificance. It is the discovery, using the machine learning of AI, of 161,979 new viruses!
This is just tip of the iceberg as the authors say the method just scratches the surface of biodiversity and opens up a world of discovery with millions more to be discovered.
Refuting Creationism - Is Creationism's Divine Malevolence Sufferring from Obsessive-Compulsive Disorder?
Viruses are teeming on your toothbrush, showerhead - Northwestern Now
Creationism's putative creator is nothing if not obsessive.
One of its obsessions appears to be designing ever-more exquisite ways to kill its creation as almost nothing in nature exists that doesn't have something that lives on or in it, often killing it in the process or at least weakening it in some way.
Its most visible obsession seems to be with designing beetles of which there are some 500,000 species with more being discovered almost daily. It's highly likely that there may be as many as a million different beetles in the world, many of which catch and devour other arthropods.
But it's in the field of virology that we find another obsession with designing variations on a general theme. Not only are there literally hundreds of thousands of viruses but every species has multiple variants - look at the number of different variants of the SARS-CoV-2 virus that have emerged since the initial wave of the COVID-19 pandemic!
Tuesday, 8 October 2024
Malevolent Design - How The Black Widow Spider's Toxins Harm Us Mammals
Scientists decode black widow spider venom
Black widow spiders have a cocktail of toxins, most of which are effective against their arthropod prey such as insects, but one of them, α-latrotoxin, is very effective against vertebrates, including humans, although even the smallest vertebrates don't normally feature in the black widow's diet.
So why did this toxin evolve?
Normally, a species which is capable of delivering a nasty, even lethal, bite to a threat, rather than to prey, evolves strategies for avoiding doing so, while warning that it could if it wanted to - rather like a creationists avoiding answering a question while pretending they could if they wanted to, only without the pretense. Most species do this with warning colours or, in the case of the rattlesnake, a warning rattle. This is because using venom against a threat might mean there isn't enough left if the next potential meal wanders by, so it's better to warn and threaten than to actually bite.
But not so the black widow, except for the strikingly marked European species, Latrodectus tredecimguttatus, and the South American, Latrodectus curacaviensis. If anything, the black widow is cryptocamoflaged to not be noticed in the dark places they inhabit.
Saturday, 5 October 2024
Unintelligent Designe - Creationism's Blundering Heath-Robinson 'Designer' Strikes Again - And Causes Cancer
How Cells Recognize and Repair DNA Damage -
One thing you can depend on with creationism's putative designer is that there will never be a simple solution when there is a more complicated way to solve the problem it just created, and just like William Heath-Robinson, it will try to use pre-existing structures that were designed for an entirely different function, like a pile of books under the legs of a ladder to make it tall enough, and every piece of string holding things together will have knots in it.
And when we look beneath the superficial resemblance of design in, for example, a living cell, we find all manner of if-it-works-it'll-do solutions to problems, like the solution to the problem of breaking DNA that a team of scientists, led by Kaspar Burger, from Julius-Maximilians-Universität Würzburg (JMU) in Bavaria, Germany, have discovered.
The problem arises of course because the method for replicating DNA as cells divide is poorly designed and unnecessarily complicated in the first place. If the putative designer had devised a more sensible method for replicating cells in multicellular organisms than that used for replicating single cells where the whole genome needs to be replicated, many of the problems of erroneous copying wouldn't arise because only a small subset of the genome is needed for specialised cells.
Sunday, 29 September 2024
Malevolent Design - What Creationism's Divine Malevolence Chose Not To Give Us But Lets Us To Suffer Instead
Stowers scientists uncover a… | Stowers Institute for Medical Research
"God never restore an amputated limb". This fact, better than anything, illustrates either the limit of the power of prayer and 'faith healing' or the limit of power of the god being prayed to. There are no authenticated examples of a restored limb or of the spontaneous healing of a transected spinal cord, despite the steady supply of victims seeking a cure to 'miracle' site such as Lourdes, and the fervent prayers of victims and the families. (We can dismiss the 'Miracle of Calanda' as far too transparent a hoax to be taken seriously.) It just never happens!
An omniscience, omnipotent, omnibenevolent designer would work to minimise the suffering in its creation. To do otherwise tells us that the alleged creator is:
- Unaware of it, in which case it is not omniscient.
- Aware of it but powerless to prevent it, in which case it is not omnipotent.
- Aware of it but indifferent to it, in which case it is not omnibenevolent.
The facts are not permitted to overrule the sacred dogma - which is creationism in a nutshell.
If you believe in the creationist notion of magic creation, where every species was designed according to some perfect plan, then the fact that some species lack abilities with which other species have, and with which clearly the putative designer knew how to provide, should raise some questions about why the designer made the choice not to provide them.
And if, as most self-centered fundamentalist believe, humans were at the apex of this creator god's design, then it should have the best of everything, and yet there are a myriad of examples of other species being better than humans. (See the AI panel for examples):
Many species have abilities which would be beneficial to humans if we too possessed them* Do you have a list of examples of this? Yes! Many species have evolved unique traits that, if humans possessed them, could greatly enhance our abilities or solve certain challenges. Here's a list of some remarkable examples:These abilities, if adapted for human use, could offer enormous benefits in fields ranging from medicine and survival to transportation and energy efficiency.
- Regeneration (Axolotl, Starfish)
- Benefit: The ability to regrow limbs or even vital organs.
- Species Example: Axolotls and starfish can regenerate entire body parts. This could help humans recover from amputations, spinal cord injuries, or organ damage.
- Echolocation (Bats, Dolphins)
- Benefit: Enhanced navigation and perception in low-visibility conditions.
- Species Example: Bats and dolphins use echolocation to navigate in darkness or murky waters. This would allow humans to navigate dangerous environments or see without light.
- Photosynthesis (Plants, Algae)
- Benefit: The ability to convert sunlight directly into energy.
- Species Example: Plants and algae can photosynthesize, which could eliminate the need for food in some situations, reducing hunger and energy concerns.
- Extreme Durability (Tardigrades)
- Benefit: Surviving extreme environments such as radiation, freezing temperatures, dehydration, and even space.
- Species Example: Tardigrades (water bears) can endure near-death conditions. This would make humans far more resistant to extreme climates or space travel.
- Camouflage (Chameleons, Cuttlefish)
- Benefit: Blending into environments for protection or hunting.
- Species Example: Chameleons and cuttlefish can change color and texture. Humans with this ability could avoid detection in dangerous situations or during combat.
- Electricity Generation (Electric Eel)
- Benefit: Generating electrical energy for self-defense or powering devices.
- Species Example: Electric eels produce electric shocks. This could allow humans to power small devices or defend against threats using natural electricity.
- Hyper-Speed Healing (Deer Antlers, Certain Lizards)
- Benefit: Rapid recovery from wounds and injuries.
- Species Example: Deer regrow antlers each year at an incredibly fast rate. Some lizards regrow tails. Enhanced human healing could lead to faster recovery after surgeries or injuries.
- UV Vision (Birds, Insects)
- Benefit: Seeing ultraviolet light to detect environmental changes or patterns invisible to the human eye.
- Species Example: Many birds and insects can see ultraviolet light, which helps them find food and mates. Humans with this ability could have enhanced perception of their surroundings.
- Extreme Longevity (Greenland Shark, Tortoises)
- Benefit: Significantly extended lifespan.
- Species Example: The Greenland shark can live for centuries, and tortoises often live over 100 years. If humans possessed this trait, we could extend lifespans, allowing more time for knowledge acquisition and creativity.
- Poison Resistance (Mongoose)
- Benefit: Immunity to toxins and venoms.
- Species Example: The mongoose is resistant to snake venom, allowing it to hunt poisonous snakes. This could protect humans from dangerous toxins or make certain medical treatments less risky.
- Hibernation (Bears, Ground Squirrels)
- Benefit: Surviving long periods without food and conserving energy.
- Species Example: Bears and ground squirrels hibernate during the winter. Humans with this ability could endure long periods without food, which would be useful in survival situations or space travel.
- Rapid Adaptation to High Altitudes (Bar-Headed Geese)
- Benefit: Increased oxygen efficiency in high-altitude or low-oxygen environments.
- Species Example: Bar-headed geese can fly over the Himalayas at altitudes that would be deadly to most animals. This would allow humans to thrive in high-altitude environments or survive with less oxygen.
- Flight (Birds, Bats)
- Benefit: Self-powered aerial travel.
- Species Example: Birds and bats have evolved to fly, which could enable humans to travel independently through the air, revolutionizing transportation and exploration.
- Magnetic Field Detection (Migratory Birds, Turtles)
- Benefit: Natural GPS and navigation using Earth’s magnetic fields.
- Species Example: Some birds and turtles can detect the Earth’s magnetic field for navigation during migration. Humans could use this ability for more accurate navigation without technology.
- Temperature Regulation (Camels, Arctic Foxes)
- Benefit: Surviving extreme heat or cold without external aid.
- Species Example: Camels can endure extreme desert heat, and arctic foxes thrive in freezing conditions. Humans with this ability could survive in more hostile climates with ease.
It's in the area of rapid repair and regeneration that research is being concentrated in order to gain a scientific understanding of the processes involved and particularly why they have been lost. One recent example was the discovery that zebra fish can not only repair a transected spinal cord but can regenerate a missing section of their spinal cord and restore it to full functionality.
And now we have another piece of research into how the African killifish can regenerate a missing section of fin, and in particular how the process restores just the missing tissues, no more and no less. This research from the Stowers Institute for Medical Research has just been published, open access, in the Cell Press journal iScience and announced in a Stowers Institute press release:
Stowers scientists uncover a critical component that helps killifish regenerate their fins
The findings are a step toward closing the gap on how we could one day deploy regenerative medicine in humans
Spontaneous injuries like the loss of a limb or damage to the spinal cord are impossible for humans to repair. Yet, some animals have an extraordinary capacity to regenerate after injury, a response that requires a precise sequence of cellular events. Now, new research from the Stowers Institute for Medical Research has unveiled a critical timing factor—specifically how long cells actively respond to injury—involved in regulating regeneration.
A recent study published in iScience on September 20, 2024, sought to understand exactly how an organism knows how much tissue has been lost post-injury. Led by former Predoctoral Researcher Augusto Ortega Granillo, Ph.D., in the lab of Stowers President and Chief Scientific Officer Alejandro Sánchez Alvarado, Ph.D., the team investigated how African killifish properly regrow their tail fin following damage. By analyzing tissue dynamics during regrowth, they found that in addition to known factors, including how many cells are participating and where they are located, the length of time cells spend engaged in the repair process is also key.
One of the greatest unsolved mysteries of regeneration is how an organism knows what has been lost after injury. Essentially, the study points to a new variable in the equation of regeneration. If we can modulate the rate and the length of time that a tissue can launch a regenerative response, this could help us devise therapies that may activate and perhaps prolong the regenerative response of tissues that normally would not do so.
Dr. Alejandro Sánchez Alvarado, senior author.
Stowers Institute for Medical Research,
Kansas City, MO, USA.
Shortly after a killifish tail injury, the remaining tissue needs to know how much damage has occurred. Then, this tissue must enlist the right number of repair cells to the site of injury for the right amount of time. Damage sensing, repair cell recruitment, and timing somehow must work together to regrow the tail.If an animal that can regenerate extremities, like a tail, loses just a tiny portion, how does it know not to regenerate a whole new tail but just the missing piece?
Dr. Alejandro Sánchez Alvarado.
To address this question, the team probed different locations of injury in the killifish tail fin.
They found that skin cells both near an injury and in distant, uninjured regions launch a genetic program that primes the whole animal to prepare for a repair response. Then, skin cells at the site of injury sustain this response and temporarily change their state to modify the surrounding material called the extracellular matrix. Ortega Granillo likens this matrix to a sponge that absorbs secreted signals from the injured tissue that then guides repair cells to get to work. If the signals are not received or not interpreted correctly, the regeneration process may not restore the tail’s original shape and size.
Tail fin regeneration at 6 hours after injury. Fluorescence microscopy image shows skin cells (magenta), actively dividing cells (cyan), and transiently activated skin cell states (yellow).
We very clearly defined when and where—at 24 hours post-injury and in the extracellular matrix—the transient cell state is acting in the fin tissue. Knowing when and where to look allowed us to make genetic disruptions and gain a better understanding of the function of these cell states during regeneration.
Augusto Ortega Granillo, first author
Stowers Institute for Medical Research,
Kansas City, MO, USA.
To investigate whether these distinct cellular states communicate information to the extracellular matrix—the supportive structure surrounding cells—during the repair process, the researchers employed the CRISPR-Cas9 gene editing technique. They specifically targeted a gene known to modify the extracellular matrix, as they had observed its activation at the onset of the regeneration response. By disrupting the function of this gene, the team aimed to determine its role in relaying information from cells to the matrix during regeneration.
These modified animals no longer know how much tissue was lost. They still regenerated, but the speed of tissue growth was deficient. This is telling us that by changing the extracellular space, skin cells inform the tissue how much was lost and how fast it should grow.
Augusto Ortega Granillo.Indeed, the speed and amount of tissue regenerated in these genetically modified killifish increased regardless of whether the tail injury was mild or severe. This finding opens the possibility that cell states that modify the matrix increase regenerative regrowth. If the cell states could be adjusted, it may be a way to stimulate a more robust regeneration response.
Tail fin regeneration at 7 days post-injury. Fluorescence microscopy image shows skin cells (magenta), actively dividing cells (cyan), and transiently activated skin cell states (yellow), where these cell states are localized now only in the very tip of the fin.
From an evolutionary perspective, understanding why certain organisms excel at regeneration while others, such as humans, have limited regenerative abilities is a driving force in the field of regenerative biology. By identifying general principles in organisms with high regenerative capacity, researchers aim to potentially apply these insights to enhance regeneration in humans. This comparative approach not only sheds light on the evolutionary aspects of regeneration but also holds promise for developing novel therapeutic strategies in regenerative medicine.
Our goal is to understand how to shape and grow tissues. For people who sustain injuries or organ failure, regenerative therapies could restore function that was compromised during illness or following injury.
Augusto Ortega Granillo.Post-injury fin growth shown over time in the African killifish.
Additional authors include Daniel Zamora, Robert Schnittker, Allison Scott, Alessia Spluga, Jonathon Russell, Carolyn Brewster, Eric Ross, Daniel Acheampong, Ning Zhang, Ph.D., Kevin Ferro, Ph.D., Jason Morrison, Boris Rubinstein, Ph.D., Anoja Perera, and Wei Wang, Ph.D.
HighlightsIt's worth repeating what the Sowers Institute news release said at this point:
- Amputation position changes tissue-wide proliferation response
- Regeneration deploys transient regeneration-activated cell states.
- Sqstm1 slows down regenerative outgrowth in distal injuries.
- Prediction: positional information is transduced by ECM changes during regeneration.
Summary
Injury is common in the life of organisms. Because the extent of damage cannot be predicted, injured organisms must determine how much tissue needs to be restored. Although it is known that amputation position affects the regeneration speed of appendages, mechanisms conveying positional information remain unclear. We investigated tissue dynamics in regenerating caudal fins of the African killifish (Nothobranchius furzeri) and found position-specific, differential spatial distribution modulation, persistence, and magnitude of proliferation. Single-cell RNA sequencing revealed a transient regeneration-activated cell state (TRACS) in the basal epidermis that is amplified to match a given amputation position and expresses components and modifiers of the extracellular matrix (ECM). Notably, CRISPR-Cas9-mediated deletion of the ECM modifier sequestosome 1 (sqstm1) increased the regenerative capacity of distal injuries, suggesting that regeneration growth rate can be uncoupled from amputation position. We propose that basal epidermis TRACS transduce positional information to the regenerating blastema by remodeling the ECM.
Introduction
For many organisms, including humans, the preservation of anatomical form and function depends in great part on the periodic elimination and restoration of cells. This process is referred to as tissue homeostasis. In mammals, the rate of tissue homeostasis varies widely across organs; i.e., self-renewal of the intestinal and lung epithelia has been estimated to take 5 days and up to 6 months, respectively.1,2 As such, specific mechanisms exist in adult tissues responsible for sustaining specific rates of tissue homeostasis to mitigate normal, physiological wear and tear. The intricate balance of tissue homeostasis can be severely disrupted by injury. During their lifespans, all multicellular organisms are likely to experience some kind of injury. Unlike physiologically regulated tissue homeostasis, injuries and the extent of the damage incurred are unpredictable. This creates a challenge for organisms to monitor and deploy an anatomically specific regeneration response proportional to the magnitude of the injury.
During regeneration, a specialized structure known as blastema forms through the rapid proliferation and subsequent differentiation of multiple cell types to restore the missing tissue.3 For instance, it has been shown that osteoblast differentiation is accelerated in regenerating fins. Newly differentiated osteoblasts appear 4 days earlier in regenerated tissue compared to the pre-existing tissue, also referred to as the stump.4 It is not known whether there is a regeneration-specific osteoblast differentiation program or if differentiation trajectories used during tissue homeostasis can be accelerated during regeneration. Regeneration has also been shown to alter rates of tissue growth. In vertebrates, the speed of regeneration differs when different amounts of tissue are lost.5 For example, fish caudal fin amputations close to the base of the appendage, a proximal amputation, display higher growth rates than amputations performed further away from the base of the fin, a distal amputation.6,7
To date, it is not known how injured tissues detect amputation position and what processes may encode positional information during regeneration. Efforts to identify deposited positional information prior to injury led to the identification of transcripts and proteins that are differentially expressed along the proximo/distal (P/D) axis in the intact zebrafish fin.8 However, these differences are lost during regeneration, leading to the hypothesis that positional information must be redefined during regeneration.8 Alternatively, it has been proposed that migratory progenitor cells retain positional identity from their locations prior to injury. This opens up the possibility that progenitors communicate positional information to the new tissue to determine regeneration growth rate.9,10 But the mechanism of positional information retention and potential relay to other cells has not yet been identified.
Furthermore, it has been suggested that positional information is encoded in the tissue within the thickness of the bone at the plane of amputation11,12 and that mechanical distension of the epidermis during wound closure constitutes a direct measurement of the amputation position by the wound epidermis. A wave of mechanical distension in the basal epidermis was shown to propagate to different lengths according to the amputation position.13 To add to the complexity of this process, it was shown that there is a 2-day time window at the beginning of regeneration when positional information is possibly reestablished de novo. If blastemas are impaired in their proliferative ability during this time window, the wrong positional information is encoded in the regenerated appendage, so multiple rounds of regeneration consistently grow abnormal tissue sizes in the absence of any further impairment of proliferation.14 It is conceivable that independent mechanisms of positional information coordinating the regenerative response exist. There may be redundant and complementary means to adequately relay and deposit positional information into the new tissue. This would ensure that form and function are restored following diverse and unpredictable injury.
Here, we deploy spatial and temporal analysis of proliferation and single-cell transcriptomic profiling to measure molecular and cellular changes along the caudal fin P/D axis. We chose the African killifish Nothobranchius furzeri for our studies because of the reduced complexity of differential gene expression and gene regulation compared to the more broadly utilized zebrafish.15 We show that amputation position influences the length of time (persistence) it takes for tissues to progress through regeneration. We report on the discovery of a basal epidermal subpopulation that shows a transient regeneration-activated cell state (TRACS) likely to participate in mediating positional information in the regenerating blastema. Altogether, our study demonstrates that amputations along the P/D axis result in defined spatial and temporal rates of proliferation. We propose that such dynamics likely initiate the proportional changes in tissue architecture that may ultimately define the scale and rate of regeneration of amputated tissues.
From an evolutionary perspective, understanding why certain organisms excel at regeneration while others, such as humans, have limited regenerative abilities is a driving force in the field of regenerative biology.
No doubts there then on the part of the authors that the facts can't be explained by evolution and are better explained by creationism's childish superstition, and of course the Theory of Evolution explains it fully without the need to explain why something which evolved for one species or from a common ancestor is retained by one line but not another in terms of the intention, malevolent, benign or indifferent, of the mindless, directionless natural process that drives it.
Creationism, on the other hand, has to try to reconcile the reality with what they believe about their putative designer, which includes explaining why, if it isn't malevolent, it designs organisms to look as though a malevolent designer designed them.