Friday, 6 September 2024

Creationism Refuted - Consciousness Is Yielding Up Its Secrets To Science



Microtubules, seen in yellow in this image, are part of the skeleton of plant and animal cells
Wellesley - Wellesley team’s new research on anesthesia unlocks important clues about the nature of consciousness | Wellesley College

If there is one thing that creationists get right it is that science is a threat to their childish superstition, so they have two main lines of argument: firstly they tell us how their religion disagrees with science, using Bible quotes as though they are indisputable facts, not just claims written down and declared to be true; secondly they attack science as though finding fault with one aspect or another of science somehow invalidates all of it and their superstition wins by default.

Neither of these tactics ever provide any evidence for creationism of course because there is none to produce, but they have the desired effect of making the creationist feel superior to those clever-dicky, elitist scientists with their big words.

And one of their favourite lines of attack is to claim that 'science can't explain consciousness', conveniently forgetting to add the word 'yet' to the end of their claim. A basic understanding of science and the history of science, would tell them that not yet understanding something doesn't invalidate science, it invalidates ignorance. Science never used to understand lightening or earthquakes, or diseases, or atoms, or biodiversity and the appearance of kinship between species, but now it does.

And now we are beginning to understand consciousness too. We know, for example, that it doesn't exist independently of a fully-functional brain because it can be abolished with chemicals and by injury, so we know that whatever the mechanism, it is a function of neurophysiology and so amenable to scientific investigation and explanation. The questions are the 'how' and the 'what' that makes up all scientific investigation.

Thursday, 5 September 2024

Refuting Creationism - How Modern Humans Spread Across Europe Thousands Of Years Before 'Creation Week'


The distributions of density in (P 100 km−2) for a 43, b 42, c 41, d 40, e 39 and f 38 ka are shown. The symbols represent the AUR archaeological sites for different phases (full black dots: Phase 1; open circle: Phase 2; and red triangles: Core sites).
New population model identifies phases of human dispersal across Europe

There are of course, very many things Bible-literalist creationists need to ignore, lie about and/or misrepresent to maintain the delusion of Earth being just a few thousand years old, not the least of which is the abundant geological and archaeological evidence of human activity long before they believe Earth was created by magic out of nothing in the so-called 'Creation Week'.

Their handicap is in trying to compress the entire 13.8 billion year history of the Universe, the 3.8 billion year history of planet Earth and the 2-3 million year history of human evolution, into 10,000 or fewer years, and then trying to ignore the evidence of continuous, unbroken cultural history extending from way before a global genocidal flood, right through it and continuing to modern times, as though such a flood never happened.

And, as is normal with science, a paper just published in Nature Communications, gives them more evidence to ignore, lie about and/or misrepresent. It shows the history of early modern human migration across Europe during the Aurignacian (43,000 -32,000 years ago). The research comes from a team from the University of Cologne, Germany, led by Professor Dr Yaping Shao. It is explained in a University of Cologne press release:

Malevolent Design - How A Human Mouth Bacterium Is 'Designed' For Super-Fast Proliferation


Open Wide: Human Mouth Bacteria Reproduce through Rare Form of Cell Division | Marine Biological Laboratory
Cellular elongation at the tips of the filamentous bacteria Corynebacterium matruchotii.
Most cells, either single-celled organisms like bacteria or the eukaryote cells of multicellular organisms, reproduce by simple division into two daughter cells. Under favourable conditions, this means a cell can produce a population of descendants that grows exponentially 1 → 2 → 4 → 8 → 16 → 32→64 … etc. (population = 2n; where n= the number of generations)

But the trick a bacterium, Corynebacterium matruchotii, that is only found in the human mouth uses is to divide into multiple new cells at each generation. For example, assuming it splits into 10 daughter cell at each generation, its growth rate from a single founder cell will be 1 → 10 → 100 → 1000 → 10,000 → 100,000 → 1,000,000 … etc., (population = 10n). But scientists have found it can do better than that, producing up to 14 new cells at each generation.

In 6 generations in favourable conditions, Corynebacterium matruchotii can produce 1 million or more offspring, against an 'ordinary' bacteria's 64, so rapidly out-pacing any other bacteria. C. matruchotii is an essential component of the plaque that quickly develops on teeth. It appears to have no other known function.

In some ways, C. matruchotii behaves more like fungal hyphae, growing at the tip to produce a long thin filament. It is this filament that then simply splits up into small sections, each of which becomes a new cell.
The filamentous bacteria C. matruchotii splitting into multiple cells at once, a rare kind of cell division called multiple fission.

Credit: Scott Chimileski, MBL
In 2020 a team of researchers showed how plaque is a highly structured and organised colony of different microorganisms which almost seems to be designed to allow Streptococcus mutans to get on with its job of dissolving the tooth enamel and causing caries. Creationists dogma insists that anything with a complex, organised structure must be intelligently designed because, so they assert, complexity and order can’t arise from disorder without intelligent intervention.

This latest discovery shows how the beginnings of this organised colony are established very quickly.

Wednesday, 4 September 2024

Malevolent Designer News - The Parasitic Nematodes 'Designed' To Carry Viruses


Virus RNA (red) in a B. malayi

Nematodes May Cause Disease Indirectly, via the Viruses They Carry

Not content with a whole range of parasitic worms to cause suffering, creationism's divine malevolence has also designed them to carry a payload of viruses to make their victims suffer even more.

This is the inescapable conclusion an honest creationist (if there is such a thing) would need to reach if he/she made an honest assessment of the facts just published by a team of researchers from the Centre for Neglected Tropical Diseases, Liverpool School of Tropical Medicine (LSTM), Liverpool, UK and the Global Health Institute, University of Antwerp, Antwerp, Belgium, in the journal Nature Microbiology.

This research team have identified a wide variety of viruses infecting nematodes and, most worryingly, the parasitic nematodes responsible for diseases in humans, so it is entirely possible that the diseases associated with infection by these nematodes could actually be caused by the viruses they carry. Related nematodes also show signs of virus-nematode co-evolution over millions of years in the form of a global distribution of nematode-virus associations.

Their research is explained in a press release from LSTM:

Tell me all about parasitic nematodes and the diseases they cause in humans, please. Parasitic nematodes (roundworms) are a diverse group of organisms that infect humans, animals, and plants. They can be found in various environments, from soil to water, and have adapted to parasitize a wide range of hosts. These nematodes can cause various diseases in humans, ranging from mild discomfort to severe and life-threatening conditions.

Overview of Parasitic Nematodes

Parasitic nematodes are classified under the phylum Nematoda. They are elongated, cylindrical, and non-segmented worms. Some of the most common parasitic nematodes that infect humans include:
  1. Ascaris lumbricoides (giant roundworm)
  2. Trichuris trichiura (whipworm)
  3. Ancylostoma duodenale and Necator americanus (hookworms)
  4. Strongyloides stercoralis (threadworm)
  5. Enterobius vermicularis (pinworm)
  6. Wuchereria bancrofti and Brugia malayi (filarial worms)
  7. Onchocerca volvulus (cause of river blindness)
  8. Dracunculus medinensis (Guinea worm)
  9. Toxocara spp (Toxocariasis)

Common Diseases Caused by Parasitic Nematodes in Humans
  1. Ascariasis
    • Causative agent: Ascaris lumbricoides
    • Symptoms: Often asymptomatic, but heavy infections can cause abdominal pain, malnutrition, growth retardation in children, intestinal obstruction, and respiratory issues (due to larval migration through the lungs).
    • Transmission: Ingestion of eggs from contaminated soil, water, or food.
    • Geographical distribution: Common in tropical and subtropical areas with poor sanitation.

  2. Trichuriasis (Whipworm Infection)
    • Causative agent: Trichuris trichiura
    • Symptoms: Asymptomatic in mild cases, but heavy infections can cause diarrhea, rectal prolapse, anemia, growth retardation in children, and malnutrition.
    • Transmission: Ingestion of eggs from contaminated soil, food, or water.
    • Geographical distribution: Widespread in tropical regions, especially in areas with poor sanitation.

  3. Hookworm Infections
    • Causative agents: Ancylostoma duodenale and Necator americanus
    • Symptoms: Anemia (due to blood loss in the intestines), abdominal pain, diarrhea, weight loss, and fatigue. Skin itching and rash can occur where larvae penetrate the skin.
    • Transmission: Larvae penetrate the skin, usually through bare feet when walking on contaminated soil.
    • Geographical distribution: Common in warm, moist climates, particularly in sub-Saharan Africa, Southeast Asia, and South America.

  4. Strongyloidiasis
    • Causative agent: Strongyloides stercoralis
    • Symptoms: Often asymptomatic, but can cause abdominal pain, diarrhea, skin rash, and severe life-threatening hyperinfection syndrome, especially in immunocompromised individuals.
    • Transmission: Larvae penetrate the skin from contact with contaminated soil.
    • Geographical distribution: Tropical and subtropical regions, but also occurs in temperate areas.

  5. Enterobiasis (Pinworm Infection)
    • Causative agent: Enterobius vermicularis
    • Symptoms: Perianal itching, irritability, sleep disturbances, and sometimes abdominal pain.
    • Transmission: Ingestion of eggs from contaminated hands, surfaces, or food.
    • Geographical distribution: Worldwide, particularly in temperate regions; commonly affects children.

  6. Lymphatic Filariasis (Elephantiasis)
    • Causative agents: Wuchereria bancrofti, Brugia malayi, Brugia timori
    • Symptoms: Lymphedema (swelling of limbs), elephantiasis (thickening of the skin and underlying tissues), and hydrocele (swelling of the scrotum).
    • Transmission: Mosquito bites (primarily Culex, Anopheles, and Aedes species).
    • Geographical distribution: Sub-Saharan Africa, Southeast Asia, the Pacific, and parts of the Americas.

  7. Onchocerciasis (River Blindness)
    • Causative agent: Onchocerca volvulus
    • Symptoms: Severe itching, skin rash, depigmentation, and nodules under the skin. Can lead to visual impairment or blindness if the eyes are affected.
    • Transmission: Blackfly bites (genus Simulium).
    • Geographical distribution: Sub-Saharan Africa, with some cases in Latin America and Yemen.

  8. Dracunculiasis (Guinea Worm Disease)
    • Causative agent: Dracunculus medinensis
    • Symptoms: Painful blister and ulcer, often on the lower limbs. The emerging worm can cause secondary infections.
    • Transmission: Ingestion of water contaminated with infected copepods (small crustaceans) that harbor larvae.
    • Geographical distribution: Historically widespread in Africa and Asia, now largely confined to a few countries due to eradication efforts.

  9. Toxocariasis
    • Causative agents: Toxocara canis and Toxocara cati
    • Symptoms: In visceral larva migrans (VLM), symptoms may include fever, cough, abdominal pain, and eosinophilia; in ocular larva migrans (OLM), it may cause visual impairment or blindness.
    • Transmission: Ingestion of eggs from contaminated soil or food, or from contact with infected animal feces.
    • Geographical distribution: Worldwide, especially in areas where pets are not regularly dewormed.

Diagnosis and Treatment

Diagnosis of parasitic nematode infections typically involves stool examinations for eggs or larvae, blood tests for antibodies or microfilariae, or skin snips in the case of onchocerciasis. Advanced imaging or biopsies may be required for some infections.

Treatment often involves anti-parasitic medications such as albendazole, mebendazole, ivermectin, diethylcarbamazine, and praziquantel, depending on the type of nematode and the severity of the infection.

Prevention and Control
  • Improving sanitation: Proper disposal of human feces and access to clean water.
  • Personal hygiene: Handwashing, wearing shoes, and using protective clothing.
  • Mass drug administration (MDA): In endemic areas to reduce transmission, especially for lymphatic filariasis and onchocerciasis.
  • Vector control: Reducing the population of mosquitoes and blackflies.
  • Public health education: Raising awareness about transmission and prevention methods.

Would you like more information on any specific nematode or disease?
Newly discovered viruses in parasitic nematodes could change our understanding of how they cause disease
New research shows that parasitic nematodes, responsible for infecting more than a billion people globally, carry viruses that may solve the puzzle of why some cause serious diseases.
A study led by Liverpool School of Tropical Medicine (LSTM) used cutting-edge bioinformatic data mining techniques to identify 91 RNA viruses in 28 species of parasitic nematodes, representing 70% of those that infect people and animals. Often these are symptomless or not serious, but some can lead to severe, life-changing disease.

Nematode worms are the most abundant animals on the planet, prevalent in all continents worldwide, with several species infecting humans as well as agriculturally and economically important animals and crops. And yet in several cases, scientists do not know how some nematodes cause certain diseases.

The new research, published in Nature Microbiology(link is external)(opens in a new tab), opens the door to further study of whether these newly discovered viruses – only five of which were previously known to science – could contribute to many chronic, debilitating conditions. If a connection can be proven, it could pave the way for more effective treatments in the future.

This is a truly exciting discovery and could change our understanding of the millions of infections caused by parasitic nematodes. Finding an RNA virus in any organism is significant, because these types of viruses are well-known agents of disease. When these worms that live inside of us release these viruses, they spread throughout the blood and tissues and provoke an immune response. This raises the question of whether any of the diseases that these parasites are responsible for could be driven by the virus rather than directly by the parasitic nematode.

Professor Mark J. Taylor, co-corresponding author
Professor of Parasitology
Centre for Neglected Tropical Diseases
Department of Tropical Disease Biology
Liverpool School of Tropical Medicine, Liverpool, UK.


Parasitic nematodes including hookworms and whipworms can cause severe abdominal problems and bloody diarrhoea, stunted development and anaemia. Infection with filarial worms can lead to disfiguring conditions such as lymphoedema or ‘elephantiasis’, and onchocerciasis, or ‘river blindness’, that leads to blindness and skin disease.

This is a truly exciting discovery and could change our understanding of the millions of infections caused by parasitic nematodes.

The study authors propose that these newly identified viruses may play a role in some of these conditions. For example, Onchocerciasis-Associated Epilepsy (OAE) that occurs in children and adolescents in Sub-Saharan Africa has recently been associated with onchocerciasis, but it is not known why this causes neurological symptoms such as uncontrollable repeated head nodding, as well as severe stunting, delayed puberty and impaired mental health.

One of the viruses in the parasites that cause onchocerciasis identified in the new study is a rhabdovirus – the type that causes rabies. The authors of the study suggest that if this virus is infecting or damaging human nerve or brain tissue, that could explain the symptoms of OAE.

The full extent and diversity of the viruses living in parasitic nematodes, how they impact nematode biology and whether they act as drivers of disease in people and animals now requires further study.

The illuminating discovery of these widespread yet previously hidden viruses was first made by Dr Shannon Quek, a Postdoctoral Research Associate at LSTM and lead author of the new study, who had initially been using the same data mining method to screen for viruses within mosquitoes that spread disease, before deciding to investigate nematodes.

As a child [in Indonesian], I saw a lot of people infected with these diseases and I suffered from the dengue virus on three occasions. That got me interested in tropical diseases. Diseases caused by parasitic nematodes are very long-term, life-long illnesses that persistently affect people. It has a significant impact on people's quality of life, their economic outputs and mental health.

There are a lot of studies about the microbiomes of mosquitoes, and how the bacteria that lives inside can block the spread of viruses, which might stop vector-borne diseases like dengue. This interplay between organisms in the same host led me to think - what else might be inside parasitic nematodes as well? Which after my discovery will now be the focus of our research.

Dr Shannon Quek, lead author
Centre for Neglected Tropical Diseases
Department of Tropical Disease Biology
Liverpool School of Tropical Medicine, Liverpool, UK.


The study also involved researchers from University of Antwerp and KU Leuven, Belgium, Brock University, Canada, University of Queensland, Australia, University of Buea, Cameroon and the University of Energy and Natural Resources, Ghana.
Abstract
Parasitic nematodes have an intimate, chronic and lifelong exposure to vertebrate tissues. Here we mined 41 published parasitic nematode transcriptomes from vertebrate hosts and identified 91 RNA viruses across 13 virus orders from 24 families in ~70% (28 out of 41) of parasitic nematode species, which include only 5 previously reported viruses. We observe widespread distribution of virus–nematode associations across multiple continents, suggesting an ancestral acquisition event and host–virus co-evolution. Characterization of viruses of Brugia malayi (BMRV1) and Onchocerca volvulus (OVRV1) shows that these viruses are abundant in reproductive tissues of adult parasites. Importantly, the presence of BMRV1 RNA in B. malayi parasites mounts an RNA interference response against BMRV1 suggesting active viral replication. Finally, BMRV1 and OVRV1 were found to elicit antibody responses in serum samples from infected jirds and infected or exposed humans, indicating direct exposure to the immune system.

Main
Humans and animals are frequently infected with multiple species of parasitic nematodes1,2,3 and suffer from chronic, lifelong infections and exposure to continuous reinfection4. Such infections impose a substantial health burden on billions of people, impacting their health, quality of life and economic productivity. Medically important parasitic nematodes infect over one billion people, resulting in up to 7.53 million disability-adjusted life years globally5. Prominent examples include intestinal species such as Ascaris lumbricoides and Trichuris trichiura4, which infect an estimated 511 and 412 million people, respectively5, as well as the hookworms Necator americanus, Ancylostoma duodenale and Ancylostoma ceylanicum, which collectively infect up to 186 million people globally5. Infected individuals can suffer from severe abdominal discomfort, bloody diarrhoea, stunted development and anaemia. Other examples include the filarial nematodes Wuchereria bancrofti and Brugia malayi, the causative agents of lymphatic filariasis that infect up to 96 million people globally5,6, and Onchocerca volvulus, which infects up to 21 million people5. In the case of O. volvulus, recent estimates indicate that 14.6 million are afflicted with skin disease and 1.15 million with blindness7. Furthermore, there has been increasing recognition of a disease known as onchocerciasis-associated epilepsy (OAE), occurring in children and adolescents in onchocerciasis meso- and hyperendemic foci across sub-Saharan Africa8. This condition manifests as a variety of epileptic seizures, including uncontrollable repeated head nodding (‘nodding syndrome’), as well as severe stunting, delayed puberty and impaired mental health (Nakalanga syndrome)9. OAE has been epidemiologically linked to infection with O. volvulus10, but the pathogenesis has yet to be identified8.

A variety of viruses can be found infecting several human parasitic protozoa, including Plasmodium vivax, Trichomonas vaginalis and Cryptosporidium parvum11,12. Viruses infecting Leishmania sp. have been studied in great detail13 and can increase disease severity, parasite prevalence and potentially the incidence rates of both drug resistance and mucocutaneous leishmaniasis14,15. RNA virus infections have been identified in plant-parasitic nematodes16, parasitic flatworms17,18 and free-living nematodes17,19,20, although the impact of viral infections on the biology of the worms is largely unknown.

Here we analysed the transcriptomes of 41 parasitic nematode species infecting humans and animals and discovered 91 virus or virus-like genomic sequences across 28 species. We further characterize the viruses infecting B. malayi and O. volvulus, describing their genomic diversity, geographic spread, phylogeny, abundance throughout different developmental stages, tissue tropism, localization and vertebrate host serology. Finally, we show that an RNA interference (RNAi) response is induced in B. malayi against BMRV1, providing evidence for active viral replication.

[…]

Discussion
We reveal an abundant and diverse RNA virome spanning 14 different viral orders and 24 families within parasitic nematodes. Of the 91 viruses discovered, only 5 have been previously reported, including 3 from A. suum and A. lumbricoides23,25. Our survey is probably an under-representation of the true extent and diversity of the parasitic nematode RNA virome owing to a variety of factors including variations in sample preparation resulting in discarded viral reads and the restricted number, or lack, of transcriptomes for several important parasites. Nevertheless, our analysis supports a conserved global spread of virus–nematode associations across multiple continents in the case of the viruses of A. suum and A. lumbricoides, and O. volvulus, suggesting an ancient and stable co-evolution. This is perhaps best exemplified by members of the Trichinellidae (Supplementary Fig. 1), which show a close evolutionary relationship, as well as phylogenetic clustering of diverse virus sequences from different species and orders of parasitic nematodes.

The parasitic nematodes identified with viruses include several important human parasitic nematodes, A. lumbricoides, T. trichiura, O. volvulus, B. malayi, A. ceylanicum and Trichinella spiralis, which cause substantial public health issues, with over 1.5 billion people infected with one or more such parasites4,5,6,44,45. Several other species cause an even greater global burden in the livestock industry46, with 15 economically important parasites (A. suum, Dictyocaulus viviparous, Haemonchus contortus, Ostertagia ostertagi, Oesophagostomum dentatum, Teladorsagia circumcinta, Trichuris suis plus 8 Trichinella spp.) of cattle, sheep and pigs, harbouring 37 previously unreported viruses.

The full extent and diversity of the parasitic nematode RNA virome, how it impacts nematode biology and whether they act as drivers or modulators of disease pathogenesis remain critical knowledge gaps. Indeed, in the parasite Toxocara canis, which causes neurotoxocariasis, components of the TCLA virus have been reported to be highly expressed in infective larvae (18% of expressed sequence tags) before entry into a vertebrate host (for example, humans and dogs)29, with human infections eliciting antibody responses against several TCLA virus proteins29, indicating potential roles in transmission and infectivity. Alternatively, extrapolation from the most well-characterized RNA viruses of Leishmania sp. protozoan parasites suggests potential roles of nematode viruses in disease pathology and progression. Both Leishmania virus 1 (LRV1) and T. vaginalis virus induce hyperinflammatory immunity, which drives disease pathogenesis and subverts host immunity to the parasites’ advantage14,15,47. We show that BMRV1 and OVRV1 elicit antibody responses from the host showing direct exposure to the immune system, and we speculate that this suggests the potential to modulate host immunity to the parasite and cross-reactive immunity to other RNA viruses.
[…]

Fig. 4: Representative FISH microscopy images of B. malayi showing localization of virus RNA within nematode tissues, alongside the Wolbachia endosymbiont as a technical control.
Virus RNA stained red; Wolbachia stained green; DAPI nuclear stain blue. a–e, Note the different levels of viral infection in microfilariae (a), localization of the viral stain in male testes (b) and the hypodermal cells near the male spicule (c). Virus signal within adult female reproductive tracts appears between developing eggs within the paired uteri of adult females, with early embrys in the left uteri and ‘pretzel-stage’ microfilariae in the right (d), with the developing eggs casting a ‘shadow’ in between virus staining, visible in 3D images of female uteri (e). f–j, In older adults (>12 months), we observed ‘epicuticular inflations’ often with an intense viral signal (f), typically occurring near the head (g) or tail regions of the nematodes. They can appear as single separate inflations at different nematode orientations, either next to internal organs (h) or the hypodermal chords (i), or as a continuous inflation along the nematode flank (j). Scale bars measure 20 µm (a,b,h,i) or 50 µm (d,g). Gridlines in three-dimensional 𝓏-stack figures (c,e,f,j) measure 40 µm by 40 µm. A total of 15 adult male and female parasites were processed in separate experiments. Parasites with epicuticular inflations were typically between 12 and 19 months at the time of sampling, with jird animal hosts being 15–22 months of age, respectively. Parasites without were typically 3–6 months of age, with the jird animal hosts being 6–9 months of age.

Fig. 5: Validation of OVRV1 using RT-PCR, western blot and representative IFA staining of O. volvulus nodules with anti-OVRV1 glycoprotein antibodies.
Anti-OVRV1 glycoprotein antibodies stained green; DAPI nuclear stain blue. a, RT-PCR experiments show that OVRV1 can be amplified only from reverse-transcribed RNA, from both O. volvulus (lane 1, n = 1) and O. ochengi (lanes 2–4, n = 3). b, Western blots against the OVRV1 glycoprotein show different molecular weight bands occurring depending on the life cycle stage of O. volvulus (n = 3). All IFA images include the DAPI nuclear stain (blue). c,d, Images of the paired uteri from adult O. volvulus females show virus stains surrounding and entering developing embryos within the uteri (solid arrow), while surrounding but not within the early embryos (hollow arrow). Developing embryos can show either complete infection rates (c) or a much smaller proportion (d). e, Mature microfilariae released from the female, located within surrounding nodule tissues, stain heavily for OVRV1 glycoprotein. f,g, Intense antibody staining is observed surrounding the nematode rachis, where eggs are first formed (solid arrows). The heavily stained rachis is either surrounded by early-stage eggs with green staining surrounding them (f) or without surrounding eggs (g). h,i, Cellular inflations containing intense antibody staining are observed on the external face of the adult female uterine walls (solid arrows). j,k, Male O. volvulus are frequently observed to be infected, with viral stains occurring in different tissues (j), as well as surrounding and entering the male testes (k). Parasites were obtained from sections of fixed O. volvulus nodules from human patients (n = 8 nodules).


So, if you reject the evolutionary explanation of these viruses-nematode associations in favour of a creationist 'intelligent [sic] design' explanation you must assume the designer intended the consequences of its design since it is axiomatic of the creationist cult that the designer is a perfect, omniscient god for whom the consequences of its design must have been known in advance and so were designed with that function in mind.

And of course we can dismiss the childish nonsense about 'genetic entropy; causing 'devolution' [sic] because these viruses are clearly gaining an advantage in infecting the nematodes because that gives them easy access to their vertebrate hosts, and anything which conveys an advantage is evolution, not 'devolution'. Only someone ignorant of evolution would fall for such biologically nonsensical excuse for parasites, as any biologist worthy of the term would have known before he came up with it.

So, the question remains unanswered by creationists - is this an example of malevolent design, or of evolution?

Tuesday, 3 September 2024

Refuting Creationism - How Butterflies Evolved Dark Wing Patterns Millions of Years Before 'Creation Week'


Genomic dark matter solves butterfly evolutionary riddle | Media Relations | The George Washington University
Heliconius erato with one wing (right) altered by CRISPR gene. Dorsal view

Luca Livraghi.
Heliconius erato with one wing (right) altered by CRISPR gene. Ventral view

Luca Livraghi.
This is one of those research papers that creationists traditionally misrepresent as 'proving' that something biologists have long known about is wrong, and so it somehow discredits the entire body of science, and, in this specific case, that the existence of RNA that is non-coding but functional, somehow proves there is no such thing as 'junk' DNA.

In reality, of course, it simply shows us that sometimes, evolution happens in unexpected ways.

The assumption, which is almost always valid and based on sound scientific evidence, is that DNA is transcribed into messenger RNA (mRNA) that mRNA is transcribed by ribosomes into proteins. Proteins then serve functions such as structural proteins or as enzymes catalysing chemical processes in the cell. In the special case of so-called homeobox genes (hox genes) these have a regulatory function in a developing embryo, stimulating groups of cells to organise into specific tissues such as limbs, eyes and other specialised tissues, by switching other genes off and on at certain times.

Fine-Tuned Fallacy Exposed - How Earth's Ecosystems Caused Multiple Mass Extinctions Between 185 And 85 Million Years Before 'Creation Week'


Fossils of Crinoids that were probably killed in an Oceanic Anoxic Event

Credit: Professor Tom Gernon
Land-sea tag-team devastated ocean life millions of years ago reveal scientists | University of Southampton

It can only be by remaining wilfully ignorant of the history of life on Earth and how it has been affected by catastrohic changes, that creationists are able to maintain the childish delusion that Earth is somehow fine-tuned for life, and especially their life.

The fact that very much of the surface of Earth, such as oceans, deserts and high mountain ranges is lethal without special equipment, and without cloths, shelter and fire , most of the northern and southern latitudes are not survivable in an average winter should be a clue to the fallacy of the claim, but then, from the safety of small town, Bible Belt America, where the rest of the world might as well not exist, such places can be safely ignored.

But the fact remains, whether ignored or not, that there have been several periods in the history of life on Earth that the planet has become a very hostile place, resulting in mass extinctions wheree life looked as though someone had hit the reset button. The primary cause of these fluctuations is almost certinly plate techtonics which, through mid-ocean ridge activity, release sulphates and phosphates which produce blooms of plankton which then die, locking up carbon and producing anoxic sediments on the ocean bed, and by releasing CO2 into the atmosphere where if causes a rise in ocean temperature.

Volcanic activity also produces basalt which, when eroded and washed into the sea adds to the phosphates which produce planktonic blooms and subsequent deoxygenation.

How these terrestrial and marine sources act together to produce the frequent OAEs has now been explained.

Monday, 2 September 2024

Refuting Creationism - Why The Gaps In The Fossil Record Are Not A Problem For Darwin's Theory Of Evolution


Darwin’s fear was unjustified: writing evolutionary history by bridging the gaps - News - Utrecht University

Creationists have been fooled by their cult into believe several absurdities concerning Charles Darwin and the Theory of Evolution.

The first is that the study of evolution consists of learning what Charles Darwin wrote in 1859, as though he was some sort of infallible prophet, in much the same way that religious people learn their religion by studying copies of ancient manuscripts and the writings of venerated early theologians.

The second is that the Theory of Evolution (TEO) is all about the fossil record.

The third is that Darwin claimed a whole series of intermediate fossils would be found for every evolved species, so it follows that any 'missing' fossils are failures of the Theory of Evolution and are fatal to the theory.

Charles Darwin of course was primarily a biologist, not a geologist so his understanding of the fossil record was based on observation, not necessarily on an understanding of the processes of fossilisation and why they are rare. No-one in their right mind would imagine there is some fundamental law at work which requires every generation of every evolving species to deposit a fossil where it can easily be found, and Darwin never made any claim about such unbroken series existing, only that fossils would conform to the theory that species have evolved over time.

But the gaps in the fossil record are largely irrelevant today anyway, since the fossil record is mere confirmation of the TOE, just as Darwin predicted, while the major supporting evidence comes from genetic evidence of which Darwin knew nothing, the nested hierarchies of cladistics which is the morphological evidence, biogeography which shows distribution patterns as the TOE predicts, embryology which 'reruns' evolution such as the beginnings of gills in mammalian embryos and the same sequences of cell specialisations in distantly related species.
What is the main evidence for the Theory of Evolution? The Theory of Evolution is supported by a wide range of evidence from various scientific disciplines. The main categories of evidence for evolution include:
  1. Fossil Record
    • The fossil record provides a chronological catalog of life on Earth. Fossils show a gradual change in species over time, including the appearance of transitional forms that bridge gaps between major groups of organisms. For example, the transition from fish to amphibians is well-documented by fossils such as Tiktaalik, which shows features of both fish and tetrapods.
    • Fossils also show patterns of extinction and the emergence of new species, supporting the idea of descent with modification over millions of years.

  2. Comparative Anatomy
    • The study of anatomical structures reveals similarities between different species that suggest a common ancestry. For example, the forelimbs of humans, whales, birds, and bats have different functions (grasping, swimming, flying), but they share a common skeletal structure, known as homologous structures, indicating they evolved from a common ancestor.
    • Vestigial structures, like the human appendix or the pelvic bones in whales, are remnants of features that were functional in an ancestor but are now reduced or repurposed, further supporting evolutionary change over time.

  3. Genetics and Molecular Biology
    • DNA and molecular evidence provide some of the most compelling evidence for evolution. All living organisms use DNA as the hereditary material, and many genes are conserved across species. For instance, humans share about 98-99% of their DNA with chimpanzees, suggesting a recent common ancestor.
    • Molecular clocks, which measure the rate of genetic mutations over time, help trace the evolutionary timeline and relationships between species.
    • The presence of "junk" DNA and shared genetic sequences (such as pseudogenes) among related species suggests a common origin.

  4. Biogeography
    • The geographic distribution of species provides evidence for evolution. Similar species are often found in regions that were once connected or are separated by barriers that limit gene flow, such as oceans or mountain ranges.
    • The distinct species found on islands, such as the finches on the Galápagos Islands studied by Charles Darwin, evolved from a common ancestor and adapted to different environments, illustrating adaptive radiation.

  5. Embryology
    • The study of embryos shows that related species often go through similar stages of development. For example, vertebrate embryos (fish, amphibians, reptiles, birds, mammals) all have pharyngeal pouches and tails at some stage, which reflects their common ancestry.
    • Differences that arise later in development correspond to the adaptations of each species, supporting the idea of descent with modification.

  6. Direct Observation of Evolutionary Processes
    • Evolution can be observed directly in nature and laboratories. Examples include the development of antibiotic resistance in bacteria, pesticide resistance in insects, and changes in beak shapes of finches in response to environmental changes.
    • Artificial selection, such as the breeding of dogs or crops, also demonstrates how selection pressures can lead to rapid changes in species over relatively short periods.

  7. Radiometric Dating
    • Radiometric dating methods, such as carbon dating and uranium-lead dating, provide estimates of the age of fossils and geological formations. These methods help place fossils within a timeframe consistent with the evolutionary timeline, confirming that older fossils belong to simpler organisms, while younger fossils show more complex life forms.

  8. Phylogenetics
    • The study of evolutionary relationships through phylogenetic trees, constructed based on genetic, morphological, and biochemical data, helps map the evolutionary history of species. These trees show how species diverged from common ancestors and how closely or distantly related they are.

Conclusion

These lines of evidence, taken together, provide a comprehensive framework that supports the Theory of Evolution. Each category of evidence converges to confirm that all species are related through common descent and have evolved over time through natural processes like mutation, natural selection, genetic drift, and gene flow.

Creationists claim there is no evidence for 'macro-evolution'. Is this claim valid?

The claim by creationists that there is "no evidence for macro-evolution" is not valid according to the scientific consensus. Scientists define "macro-evolution" as large-scale evolutionary changes that occur over long periods, leading to the emergence of new species, genera, families, and higher taxonomic groups. This process involves the accumulation of genetic changes that eventually result in speciation — the splitting of one species into two or more distinct species.

Here is why the claim that there is no evidence for macro-evolution is not supported:
  1. Fossil Record
    • Transitional Fossils: The fossil record contains numerous examples of transitional forms that demonstrate macro-evolutionary changes. These fossils show intermediate characteristics between different groups of organisms. Notable examples include:
    • Tiktaalik: A transitional form between fish and early amphibians, showing both fish-like features (fins, scales) and tetrapod-like features (a neck, wrist bones).
    • Bird Evolution: Fossils like Archaeopteryx and Microraptor show traits of both non-avian dinosaurs and birds, documenting the evolution of birds from theropod dinosaurs.
    • Mammalian Evolution: The transition from reptiles to mammals is well-documented with fossils such as Cynognathus and Morganucodon, showing the gradual evolution of mammalian features such as a differentiated jaw and specialized teeth.
    • Human Evolution: Fossils such as Australopithecus afarensis ("Lucy") and Homo habilis demonstrate the gradual transition from early primates to modern humans, showing changes in brain size, bipedalism, and tool use.

  2. Genetics and Molecular Evidence
    • Genomic Data: DNA evidence strongly supports macro-evolution. For example, comparisons of genomes between different species show patterns of genetic similarity that correspond with evolutionary relationships. Humans share a significant percentage of their DNA with other primates, such as chimpanzees (98-99%), suggesting a common ancestor.
    • Endogenous Retroviruses (ERVs): Certain retroviruses integrate into the host genome, and these viral sequences can be inherited. ERVs are found in the same locations across the genomes of related species, which would be highly unlikely unless they shared a common ancestor.
    • Gene Duplication and Diversification: Macroevolution is supported by observations of gene duplication, where new genes can evolve new functions, leading to the development of novel traits and the divergence of species over time.

  3. Observed Speciation Events
    • Speciation in Real-Time: There are numerous documented cases of speciation (the formation of new species) occurring in nature, especially in organisms with short generation times. Examples include:
    • Cichlid Fish in African Lakes: These fish have diversified into hundreds of species with distinct characteristics in a relatively short period.
    • Polyploidy in Plants: Many new plant species have arisen through polyploidy, where an organism gains extra sets of chromosomes, creating reproductive barriers with the parent species.
    • Apple Maggot Flies (Rhagoletis pomonella): This insect species has been observed to split into distinct populations based on host plant preference, a process that could lead to speciation.

  4. Comparative Anatomy and Embryology
    • Homologous Structures: Similarities in bone structures, like the limbs of vertebrates, indicate common ancestry. The differences between these structures have accumulated over time, leading to macro-evolutionary changes.
    • Developmental Biology: Embryonic development patterns often reveal similarities across species that are not apparent in adult forms. For instance, the presence of gill-like structures in the embryos of vertebrates (including humans) suggests a common origin with fish.

  5. Phylogenetic Evidence
    • Evolutionary Trees: Phylogenetic trees constructed using genetic, morphological, and biochemical data consistently show that species have diverged from common ancestors. These trees reflect branching patterns predicted by macro-evolutionary theory.

  6. Mechanisms for Large-Scale Evolutionary Change
    • The mechanisms that drive microevolution (small-scale changes within species) — such as mutation, natural selection, genetic drift, and gene flow — are the same processes that, over extended periods, result in macro-evolutionary changes. There is no scientific barrier that separates microevolution from macroevolution; rather, macroevolution is the accumulation of many microevolutionary changes.

Conclusion

The claim that there is "no evidence for macro-evolution" reflects a misunderstanding or rejection of the broad range of scientific evidence supporting the process. The fossil record, genetic data, observed speciation events, comparative anatomy, and phylogenetic studies all provide robust evidence for macro-evolution. In science, macroevolution is a well-established process, substantiated by multiple independent lines of evidence from different fields.

In actual fact, Chares Darwin accepted that the fossil record was at best gappy with:

One other consideration is worth notice: with animals and plants that can propagate rapidly and are not highly locomotive, there is reason to suspect, as we have formerly seen, that their varieties are generally at first local; and that such local varieties do not spread widely and supplant their parent-forms until they have been modified and perfected in some considerable degree. According to this view, the chance of discovering in a formation in any one country all the early stages of transition between any two forms, is small, for the successive changes are supposed to have been local or confined to some one spot. Most marine animals have a wide range; and we have seen that with plants it is those which have the widest range, that oftenest present varieties; so that with shells and other marine animals, it is probably those which have had the widest range, far exceeding the limits of the known geological formations of Europe, which have oftenest given rise, first to local varieties and ultimately to new species; and this again would greatly lessen the chance of our being able to trace the stages of transition in any one geological formation.

It should not be forgotten, that at the present day, with perfect specimens for examination, two forms can seldom be connected by intermediate varieties and thus proved to be the same species, until many specimens have been collected from many places; and in the case of fossil species this could rarely be effected by palaeontologists.

We shall, perhaps, best perceive the improbability of our being enabled to connect species by numerous, fine, intermediate, fossil links, by asking ourselves whether, for instance, geologists at some future period will be able to prove, that our different breeds of cattle, sheep, horses, and dogs have descended from a single stock or from several aboriginal stocks; or, again, whether certain sea-shells inhabiting the shores of North America, which are ranked by some conchologists as distinct species from their European representatives, and by other conchologists as only varieties, are really varieties or are, as it is called, specifically distinct. This could be effected only by the future geologist discovering in a fossil state numerous intermediate gradations; and such success seems to me improbable in the highest degree.

Geological research, though it has added numerous species to existing and extinct genera, and has made the intervals between some few groups less wide than they otherwise would have been, yet has done scarcely anything in breaking down the distinction between species, by connecting them together by numerous, fine, intermediate varieties; and this not having been effected, is probably the gravest and most obvious of all the many objections which may be urged against my views.

Darwin, Charles. On the Origin of Species By Means of Natural Selection, or, the Preservation of Favoured Races in the Struggle for Life (p. 159). Public Domain Books. Kindle Edition.


From that concluding paragraph, it is obvious that Darwin was less worried about the perceived gaps than about how they would be used to discredit his theory.

And now a team of researchers from Utrecht, Netherlands and Liverpool, UK, have shown that the gaps in the fossil records are not an unsurmountable problem for the TOE because they can easily be bridged with other evidence. Their findings are the subject of a recent paper in BMC Ecology and Evolution and a news release from Utrecht University:
Darwin’s fear was unjustified: writing evolutionary history by bridging the gaps
Fossils are used to reconstruct evolutionary history, but not all animals and plants become fossils and many fossils are destroyed before we can find them (e.g., the rocks that contain the fossils are destroyed by erosion). As a result, the fossil record has gaps and is incomplete, and we’re missing data that we need to reconstruct evolutionary history. Now, a team of sedimentologists and stratigraphers from the Netherlands and the UK examined how this incompleteness influences the reconstruction of evolutionary history. To their surprise, they found that the incompleteness itself is actually not such a big issue.

It’s as if you are missing half of a movie. If you are missing the second half, you can’t understand the story, but if you are missing every second frame, you can still follow the plot without problems.


The regularity of the gaps, rather than the incompleteness itself, is what determines the reconstruction of evolutionary history. If a lot of data is missing, but the gaps are regular, we could still reconstruct evolutionary history without major problems, but if the gaps get too long and irregular, results are strongly biased.

Niklas Hohmann, lead author
Faculty of Geosciences
Department of Earth Sciences
Utrecht University, Utrecht, The Netherlands.


Darwin
Since Charles Darwin published his theory of evolution, the incompleteness of the fossil record has been considered problematic for reconstructing evolutionary history from fossils. Darwin feared that the gradual change that his theory predicted would not be recognizable in the fossil record due to all the gaps.

Our results show that this fear is unjustified. We have a good understanding of where the gaps are, how long they are and what causes them. With this geological knowledge, we can reconstruct evolution hundreds of millions of years ago at an unprecedented temporal resolution.

Niklas Hohmann.


Simulations
Computer simulations of geological processes at timescales longer than any historical records can be used to examine the effects of the incompleteness. To that end, Hohmann and his team combined simulations of different modes of evolution with depositions of carbonate strata to examine how well the mode of evolution can be recovered from fossil time series, and how test results vary between different positions in the carbonate platform and multiple stratigraphic architectures generated by different sea level curves.

If Darwin could read the article, he would certainly be relieved: his theory has proven to be robust on the vagaries of the rock record. Deep-time fossil data – however incomplete – supports our understanding of the mode and tempo of evolution.

Niklas Hohmann.


Article
Hohmann, Niklas; Koelewijn, Joël R.; Burgess, Peter; Jarochowska, Emilia
Identification of the mode of evolution in incomplete carbonate successions BMC Ecology and Evolution 24, 113 (2024), https://doi.org/10.1186/s12862-024-02287-2
Abstract

Background

The fossil record provides the unique opportunity to observe evolution over millions of years, but is known to be incomplete. While incompleteness varies spatially and is hard to estimate for empirical sections, computer simulations of geological processes can be used to examine the effects of the incompleteness in silico.

We combine simulations of different modes of evolution (stasis, (un)biased random walks) with deposition of carbonate platforms strata to examine how well the mode of evolution can be recovered from fossil time series, and how test results vary between different positions in the carbonate platform and multiple stratigraphic architectures generated by different sea level curves.

Results
Stratigraphic architecture and position along an onshore-offshore gradient has only a small influence on the mode of evolution recovered by statistical tests. For simulations of random walks, support for the correct mode decreases with time series length.

Visual examination of trait evolution in lineages shows that rather than stratigraphic incompleteness, maximum hiatus duration determines how much fossil time series differ from the original evolutionary process. Gradual directional evolution is more susceptible to stratigraphic effects, turning it into punctuated evolution. In contrast, stasis remains unaffected.

Conclusions
  • Fossil time series favor the recognition of both stasis and complex, punctuated modes of evolution.
  • Not stratigraphic incompleteness, but the presence of rare, prolonged gaps has the largest effect on trait evolution. This suggests that incomplete sections with regular hiatus frequency and durations can potentially preserve evolutionary history without major biases. Understanding external controls on stratigraphic architectures such as sea level fluctuations is crucial for distinguishing between stratigraphic effects and genuine evolutionary process.


Introduction

The fossil record as source of information
Fossils provide a unique record of evolution on temporal and spatial scales not accessible to experimentation or direct human observation [23, 24]. Geological records have delivered fossil time series crucial in formulating and testing hypotheses on evolutionary dynamics and mechanisms of speciation spanning micro- to macroevolutionary scales (e.g., [3, 22, 87, 92]). Nevertheless, fossils remain underused in evolutionary biology. Their main application is still node and tip calibration of molecular clocks, which commonly relies on single occurrences or on assumptions about the probability of finding a fossil rather than stratigraphic data [17]. It is also subject to biases resulting from this small sample size [84]. The unique type of information contained in a fossil succession sampled over a long time interval is rarely exploited, likely due to the following barriers:
  1. The fossil record, being a part of the stratigraphic record, is patchy and distorted. At the time when Darwin [15] discussed this as a major limitation for the testing and development of the theory of evolution, little geological knowledge was present to elucidate the rules governing this incompleteness. Darwin’s concern widely persists (e.g., Patterson [73]), albeit mostly implicitly: most phylogenetic analyses published today do not use fossils which would have been relevant or use only a small fraction of them. Stratigraphy and sedimentology, which can provide relevant data on fossils and the constraints on their occurrence and sampling [46, 56], are jargon-laden, highly atomized disciplines whose utility for evolutionary biology is not obvious to biologists. Biostratigraphy, which uses fossils to establish the relative age of rocks and has amassed datasets that would be of high utility for evolutionary studies, employs taxonomic concepts that are often impractical for or incompatible with evolutionary questions [19, 20, 33, 75]. As a results, scientific communities studying evolution and the fossil record function in parallel, with limited exchange [30].
  2. There is a lack of methodological frameworks to incorporate fossils in their stratigraphic context in evolutionary studies. Historically, phylogenetic methods rarely incorporated geological information such as the relative order of appearance of taxa or specimens in the fossil record, which is the main subject of biostratigraphy [100]. This has led to radical discrepancies between the outcomes of phylogenetic and stratigraphic, or stratophenetic, approaches [26, 18, 22]. This barrier is gradually overcome by methodological advances, such as the Fossilized Birth-Death Model [85], which allows incorporation of parameters specific to the fossil record, such as fossilization rate, sampling probability and age uncertainties of fossil occurrences [5, 6, 95, 101].

Recently, there is renewed appreciation for the importance of fossils in phylogenetic reconstructions [31, 70, 71, 80]. These studies focus on the role of the morphological information provided by extinct taxa, but less on what a modern understanding of the physical structure of the geological record contributes to reconstructing evolutionary processes from fossil-bearing stratigraphic successions.

Stratigraphic incompleteness and age-depth models
The incompleteness of the fossil record serves as an umbrella term for different effects that diminish the information content of the rock record, ranging from taphonomic effects and sampling biases to the role of gaps and erosion [56]. Here we focus on the role of gaps (hiatuses) in the rock record. Such gaps can arise due to sedimentation (including fossils) and subsequent erosion or lack of creation of rocks in the first place, e.g., when an environment remains barren of sediment formation or supply for a long time. Both processes result in gaps in the rock record and, as a result, in the fossil record. This type of incompleteness is termed stratigraphic (in)completeness, defined as the time (not) recorded in a section, divided by the total duration of the section [16, 88]. Stratigraphic completeness provides an upper limit on the proportion of evolutionary history that can be recovered from a specified section, even with unlimited resources and perfect preservation of fossils. Stratigraphic completeness is difficult to quantify in geological sections, and estimates range between 3 and 30% [98], suggesting that more than 70% of evolutionary history is either not recorded in the first place or destroyed at a later time.

Fossils older than a 1.5 million years cannot be dated directly, and their age has to be inferred from circumstantial evidence on the age of the strata in which they were found [56, 97]. This inference is formalized by age-depth models (ADMs), which serve as coordinate transformations between the stratigraphic domain, where the fossils were found (length dimension L, SI unit meter), and the time domain (time dimension T, SI unit seconds - we use the derived units years, kyrs, or Myrs) [37]. Age-depth models are always explicitly or implicitly used when fossil data is used for evolutionary inferences. Because they convey how positions of fossils relate to their age, ADMs are the basis for calculating evolutionary rates. As a result, revising ADMs commonly leads to a revision of evolutionary rates. For example, Malmgren, Berggren, and Lohmann [64] observed increased rates of morphological evolution in lineages of fossil foraminifera over a geologically short time interval of 0.6 Myr and proposed that this “punctuated gradualism” may be a “common norm for evolution”. MacLeod [63] revised the age-depth model and showed that the interval with increased rates of evolution coincides with a stratigraphically condensed interval, i.e., more change is recorded in a thinner rock unit. Re-evaluating the evolutionary history based on the revised age-depth model removed the apparent punctuation and showed that morphological evolution in that case had been gradual rather than punctuated.

Age-depth models contain information on both variations in sediment accumulation rate and gaps in the stratigraphic and - as a result – the fossil record. For example, stratigraphic completeness corresponds to the fraction of the time domain to which an age-depth model assigns a stratigraphic position. In the absence of an age-depth model, we can only make statements on the ordering of evolutionary events, but not on the temporal rates involved.

Forward models of stratigraphic architectures
Forward computer simulations of sedimentary strata provide a useful tool to study the effects of incompleteness and heterogeneous stratigraphic architectures. They have demonstrated that locations and frequency of gaps in the stratigraphic record are not random, but a predictable result of external controls, such as fluctuations in eustatic sea level [12, 67, 96].

Combined with biological models, forward models provide a powerful tool to test hypotheses on the effects of stratigraphic architectures on our interpretations of evolutionary history. For example, Hannisdal [32] combined simulations of a siliciclastic basin with models of taphonomy and phenotypic evolution. The results showed that when sample sizes are small, morphological evolution will appear as stasis regardless of the underlying mode. This might explain why stasis is the most common evolutionary pattern recovered from the fossil record [45].

Stratigraphic incompleteness and variations in sediment accumulation rates introduce multiple methodological challenges. Constructing complex ADMs requires sedimentological and stratigraphic expert knowledge, and they will potentially be associated with large uncertainties. Even in the “perfect knowledge” scenario where the age-depth model is fully known, evolutionary history in the time domain will inevitably be sampled irregularly: If two samples are separated by a hiatus, their age difference must be at least the duration of the hiatus, which might be millions of years. On the other hand, if sediment accumulation is rapid and no hiatuses are present, the age difference between samples might be only a few days.

Most studies “translate” fossil successions into time series using age-depth models based on simplified assumptions on the regularity of the stratigraphic record. These ADMs ignore stratigraphic incompleteness and often assume uninterrupted constant sediment accumulation (UCSA). This assumption implies that stratigraphic completeness is 100%, rock thickness is proportional to time passed, and linear interpolation between tie points of known age can be used to infer fossil ages from their positions. Such ADMs are usually used implicitly, without discussing their limitations. While the assumption of UCSA is sedimentologically and stratigraphically unrealistic, it brings strong methodological simplifications. For example, if distance between samples collected in a rock section is kept constant, UCSA implies that the underlying evolutionary history in the time domain is sampled at a constant frequency, the generated fossil time series are equidistant in time and can therefore be analyzed by standard methods of time series analysis [7, 45].

Objectives and hypotheses
We examine how commonly made simplified assumptions on stratigraphic architectures influence how the mode of evolution is recovered from fossil time series. We use tropical carbonate platforms as a case study, because they host large parts of the fossil record and are evolutionary hotspots [51].

We test the following hypotheses:
  1. The mode of evolution identified in a fossil time series obtained under the assumption of uninterrupted constant sediment accumulation (UCSA) is the same as the mode of the original time series.
  2. Lower stratigraphic completeness reduces the chance of identifying the correct mode of evolution from fossil time series constructed based on the assumption of UCSA [41, 43]. The implication of this hypothesis is that different depositional environments have different chances of preserving the mode of evolution because of systematic differences in their completeness.


[…]

Conclusions
We tested the hypothesis that the commonly employed approach to identifying the mode of evolution in fossil succession, i.e., linear projection of stratigraphic positions of occurrences into the time domain without considering changes in sedimentation rate and gaps in the record, recovers the correct mode of evolution. We found that, although prolonged gaps distorted trait evolution record visually, tests for the mode of evolution were only weakly affected by gaps and irregular age-depth models. Our findings differ from those of Hannisdal [32], who found (using a different approach but asking the same question) that incomplete sampling in the stratigraphic record may result in all other modes of evolution being identified as stasis.

Our findings did not vary substantially between two stratigraphic architectures with varying gap distributions and degrees of stratigraphic completeness. The lack of influence of stratigraphic effects is counterintuitive, as deeper environments are often assumed to be more complete and therefore more suitable for sampling fossil series for evolutionary studies. In the case of undirected random walks, increasing the number of observations (i.e., sampling intensity, length of the fossil series) did not improve the identification of the mode of evolution, but rather worsened it.

Our study was motivated by improving the recovery of evolutionary information from highly resolved fossil successions, particularly at microevolutionary scales. We are convinced that such successions can aliment models and understanding that is not accessible to exclusively neontological methodologies, as illustrated by e.g. [44, 77, 90]. Our contribution is the use of stratigraphic forward modeling to ground-truth the methodologies serving this palaeobiological research program. Forward modeling allows rigorous testing of concerns that the fossil record is too distorted, or too incomplete, to answer (micro)evolutionary questions. They also offer the possibility to evaluate the robustness of identifications of the mode of evolution and estimates of its parameters under different simulated age-depth models. Finally, sedimentological information may aliment age-depth models [36, 52]. The proliferation of ever better stratigraphic forward models (e.g. CarboCAT [12, 67], SedFlux [50], strataR [42], CarboKitten.jl [34]) opens the possibility to validate these methods and improve our understanding of the fossil record.

Fig. 1
Study design for testing the mode of evolution in the stratigraphic domain. Computationally, first sampling positions are determined, then the age-depth model is used to determine the times that correspond to these positions. Last, the trait evolution at said times are simulated. The simulated mean trait values are the values observable at the sampled stratigraphic positions

Fig. 1
The outcome of simulating carbonate platforms in the stratigraphic domain. A Scenario A: deposition based on a fictional sea-level curve. B Scenario B: deposition based on the sea-level curve from Miller et al. [69] for the last 2.58 Myr. Graphs represent the position in the middle of the simulated grid along the strike


In summary, what this study shows is that when computer models are used to predict the course of evolution in a geological column in which what fossils there are show how environmental changes result in morphological changes, the computer prediction of and the fossil record match. This means that temporal gaps in the fossil record can be bridged and that assumptions about what happened in the gap are valid. In other words, the gaps are not a problem for the TOE.

Additionally, since most taxonomic relationships are deduced from multiple strands of evidence, of which the fossil record may or may not feature, the 'gaps' are irrelevant anyway.

So, not only are the 'gaps' not a problem for the TOE, let alone fatal for it, the assumptions we make based on logical deductions are as valid today as they were in Darwin's day. It's clear from his writing that Darwin was more concerned about how opponents of the TOE would misrepresent the gaps in the fossil record than he was about those gaps. From the way creationist frauds fool their dupes about them, it seem Darwin was right to be concerned.

Refuting Creationism - Merging Galaxies 12.8 Billion Years Before 'Creation Week'.


The interacting galaxies observed by the ALMA radio telescope at the Cosmic Dawn. This image shows the distribution of ionized carbon gas, which reflects the overall distribution and motion of interstellar matter. It is clearly visible that the two galaxies are interacting, and are connected by a structure between them. The two crosses in the image indicate the positions of the low-luminosity quasars discovered by the Subaru Telescope.
Dancing Galaxies Make a Monster at the Cosmic Dawn | NAOJ: National Astronomical Observatory of Japan - English

Creationists find the immensity of the Universe very difficult to force-fit into the creation myth in Genesis which describes it as a small flat planet with a dome over it, so they turn their putative creator god into an Almighty Liar by claiming it just made the Universe look old by placing all the photons to make it look like they started out tens of billions of years ago, when it created everything by magic just 10,000 years ago.

Strangely, they claim they can tell the Almighty Liar lied everywhere in the physical evidence that makes the Universe just look old, because they have a book in which it once told the truth!

Anyway, this is not the only contradictory belief they have to try to ignore, so they'll have no difficulty ignoring the evidence of a chaotic universe which they prefer to believe is perfectly ordered and designed with them in mind.

Sunday, 1 September 2024

Malevolent Designer - How Zebra Fish Can 'Heal' Blindness - And Humans Can't


Zebrafish photoreceptor cells stimulated with blue light show correct electrical activity. The picture was taken using the microscope that was custom-built for this study.
Seeing the Future: Zebrafish Regenerates Fully Functional Photoreceptor Cells and Restores Its Vision — Center for Regenerative Therapies Dresden (CRTD) — TU Dresden

Readers may remember my recent post about how researchers have discovered that zebra fish can heal a transected spinal cord, and why creationists need to explain why their putative omnibenevolent designer apparently chose not to give this ability to all vertebrates, including its supposedly favourite special vertebrate, humans
.
Was it because it prefers to watch paraplegics suffer or because it forgot how to?

Well, now we have more evidence, if you accept the childish creationist 'intelligent [sic] design, nonsense, of how the same fish, have apparently been given another ability that would have hugely benefitted humans and other animals - they can repair damage to their visual receptors in their eyes, in other words, they can heal blindness.

A believer in intelligent [sic] design, must accept that, since their designer god apparently knew how to give this ability to zebra fish, it knew how to give it to all vertebrates and made the conscious decision not to.

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