Wednesday 29 March 2023

AI = the death of art?

File under "well said." XCIII

"We always plan too much and think too little.We resent a call to and hate unfamiliar argument that does not tally with what we already believe or would like to believe."

Joseph Schumpeter.

Just smarter apes?

But, But, But … We’re 98% Similar to the Chimp!

Cornelius G Hunter

Transposable elements just don’t make sense. These so-called “jumping genes” are segments of junk DNA that insert themselves at random in our genomes. That is the evolutionary interpretation of these genetic units, but how and why do they move about, and why don’t they wreak havoc on the genome? The answers to these questions, which have been emerging in recent years, is that transposable elements are exquisite, finely-tuned, highly-functional molecular machines that contradict evolutionary expectations. Evolutionists have a long, failed history of presumed disutility—after all, the world arose by chance, surely it doesn’t work very well—and transposable elements are just one more example of this failed prediction. But the junk-to-hero story is only one of three ways that transposable elements utterly demolish evolutionary theory. The other two prongs in this Darwin-destroying triad are serendipity and pattern.

By serendipity, I am referring to the rather awkward findings, which are undeniable at this point, that if evolution is true, then it must have come about by highly complex, non adaptive, mechanisms. From diploid genetics to horizontal gene transfer, alternate gene splicing, genetic regulation, epigenetics, mechanisms that cause adaptive mutations, and transposable elements, evolution must have bumbled along by luckily constructing fantastically complex mechanisms. Those mechanisms would provide no immediate adaptive value, yet somehow would persist and become vital agents in evolutionary history. Simply put, evolution must have created evolution in a most unlikely (astronomically unlikely) set of circumstances. That’s serendipity, not science, and transposable elements heaps more fuel onto the fire.

By pattern, I am referring to another set of awkward findings, again undeniable, that the pattern of structures observed across the species consistently contradicts evolution’s predictions. One of those contradictions are the enormous differences found in otherwise allied species.

All three of these contradictions—disutility, serendipity, and pattern—are on display this week in new, systematic study of transposable elements out of Didier Trono’s lab in Switzerland. The study details the interactions between transposable elements and a class of proteins. The findings indicate the complexity and interdependency of these molecular mechanisms. As the press release admits:

Long considered as junk DNA, transposable elements are now recognized as influencing the expression of genes. … the extent of this regulation and how it is harnessed were so far unknown. EPFL scientists have now taken the first extensive look at a family of ~350 human proteins, showing that they establish a complex interplay with transposable elements … KZFPs can convert transposable elements in exquisitely fine-tuned regulatory platforms that influence the expression of genes, which likely takes place at all stages of development and in all human tissues. … It is a highly combinatorial and versatile system … As a field, epigenetics has come into prominence in recent years, revealing a previously unimagined complexity and elegance in genetics.

Not exactly junk DNA. And of course all of this would require large amounts of serendipity. For evolutionists are now forced to say that transposable elements would have to have played a, err, key role in evolution itself. Evolution would have had to have constructed this highly specific, detailed, system including hundreds of proteins and genetic elements, with hundreds of specific interactions, providing no immediate benefit. As Trono explains:

The vast majority of KZFPs binds to specific motifs in transposable elements. For each KZFP we were able to assign one subset of transposable elements, and also found that one transposable element can often interact with several KZFPs.

Finally, all of this contradicts the expected common descent pattern. This failure has become so common we now have non evolutionary terminology, such as “species-specific” and “lineage-specific.” The paper uses the term “species-restricted”:

KZFPs partner with transposable elements to build a largely species-restricted layer of epigenetic regulation

Species-restricted? In other words, the designs we are discovering in biology are unique to particular species. This is precisely the opposite of what evolution expects. Note also the teleological language (which as usual is evident in the infinitive form): The proteins “partner” with the transposable elements “to build” a largely “species-restricted” layer of epigenetic regulation. This is a classic example of evolution’s absurd creation story language.

The contradictory pattern was, of course, unsuspected. As Trono explains:

KZFPs contribute to make human biology unique. Together with their genomic targets, they likely influence every single event in human physiology and pathology, and do so by being largely species-specific -- the general system exists in many vertebrates, but most of its components are different in each case. … This paper lifts the lid off something that had been largely unsuspected: the tremendous species-specific dimension of human gene regulation.

Yes, it was largely unsuspected. For what these findings reveal is a tremendous species-specific dimension of human gene regulation. In other words, we would need proteins and genetic elements to evolve, via independent and yet interdependent, random mutations, to construct an entirely new set of genetic regulation instructions. This is astronomically unlikely, no matter how many millions of years are available. From a scientific perspective, these findings demolish evolution.

Tuesday 28 March 2023

The salt of the earth

On the father of the bomb.

The pale horse on the rampage.

AI's moral deficit?

Robert J. Mark on AI’s Glaring Errors

Evolution News

Robert J. Marks contributed a piece at The Daily Caller this week on artificial intelligence, ChatGPT, and the manifold problems of new AI systems like Google’s Bard and older ones such as Amazon’s Alexa. Dr. Marks directs Discovery Institute’s Bradley Center and is author of the recent DI Press Book Non-Computable You. Despite the confidence in new AI coming from Big Tech executives, it makes quite glaring mistakes, although Marks believes AI has its genuine uses and benefits. Snapchat’s chatbot “My AI” gave advice about how to hide the smell of pot and alcohol to someone posing as a disgruntled teenager. Microsoft’s Bing bot professed its love for a tech journalist. A Google app made egregiously racist errors. ChatGPT is also politically biased despite claiming neutrality.

Marks writes,

Many warn of the future dangers of artificial intelligence. Many envision AI becoming conscious and, like SkyNet in theTerminator franchise, taking over the world (This, by the way, will never happen). But make no mistake. LLMs are incredible for what they do right. I have used ChatGPT many times. But user beware. Don’t trust what an LLM says, be aware of its biases and be ready for the occasional outlandish response.

ROBERT MARKS, MARKS: FROM POLITICAL BIAS TO OUTLANDISH DARES, HERE’S WHY ROBOTS CANNOT REPLACE US | THE DAILY CALLER

Marks encourages readers to try out ChatGPT and come to their own conclusions. Be sure to read the rest of his article Here

And yet even more primeval tech Vs Darwinism.

A Power Grid in Muscle Cells Has Profound Design Implications

David Coppedge

A finding announced in Nature represents a blockbuster for intelligent design. We knew about ATP synthase — that rotary engine that uses proton flow to create “batteries” of energy-packed ATP molecules. Those motors in the mitochondria are arranged along folds (cristae) in the mitochondrial membranes to maximize their output.

But researchers have learned that the mitochondria themselves are connected by electrical wires in a vast intracellular network. This allows us to see another level in the hierarchy of design in the cell.

The findings are of revolutionary significance. Skeletal muscle cells were known to have many mitochondria, but it was not clear how the products of ATP production, called metabolites, became distributed throughout the cell. Many assumed it was by diffusion, or simple spreading out of molecules from regions of high concentration to areas of low concentration. The truth is far more exciting. Research News from the National Institutes of Health explains:

A new study overturns longstanding scientific ideas regarding how energy is distributed within muscles for powering movement. Scientists are reporting the first clear evidence that muscle cells distribute energy primarily by the rapid conduction of electrical charges through a vast, interconnected network of mitochondria — the cell’s “powerhouse” — in a way that resembles the wire grid that distributes power throughout a city. The study offers an unprecedented, detailed look at the distribution system that rapidly provides energy throughout the cell where it is needed for muscle contraction.

Introducing the “Mitochondrial Reticulum”

Diffusion is too slow for a fast-acting muscle cell. Electricity, though, is fast. The same proton-motive force that powers ATP synthase is conducted along cellular wires, the researchers found. You’ve heard of the endoplasmic reticulum. They’re calling this one the “mitochondrial reticulum” — a conductive pathway for energy distribution. The Editor’s Summary of the paper puts it this way:

How is energy distributed within the cell? In the skeletal muscle, energy distribution has been proposed to occur through metabolite-facilitated diffusion, although genetic evidence has raised questions about the importance of this mode of distribution. Using various forms of high-resolution microscopy, Robert Balaban and colleagues explore whether the mitochondria themselves — as well as actually generating the energy — also have a role in its distribution. They find that they do, by forming a conductive pathway throughout the cell in the form of a proton-motive force. Throughout this network, the mitochondrial protein localization seems to be varied, allowing optimized generation and utilization of the mitochondrial membrane potential. This energy distribution network, which depends on conduction rather than diffusion, is potentially extremely rapid, thereby enabling muscle to respond almost instantaneously to new energy demands.

Not only is the system extremely fast, it is well organized. The Abstract states:

Within this reticulum, we find proteins associated with mitochondrial proton-motive force production preferentially in the cell periphery and proteins that use the proton-motive force for ATP production in the cell interior near contractile and transport ATPases. Furthermore, we show a rapid, coordinated depolarization of the membrane potential component of the proton-motive force throughout the cell in response to spatially controlled uncoupling of the cell interior. We propose that membrane potential conduction via the mitochondrial reticulum is the dominant pathway for skeletal muscle energy distribution.

The mitochondrial reticulum was known before, but scientists had not previously seen that it conducts electricity. The potential of this discovery to shed light on muscular dystrophy, heart disease, and other disorders is apparent.

The images in the paper even look like a power grid. More:

For the current experiments, the NIH scientists collaborated in a detailed study of the mitochondria structure, biochemical composition, and function in mouse skeletal muscle cells. The researchers used 3D electron microscopy as well as super-resolution optical imaging techniques to show that most of the mitochondria form highly connected networks in a way that resembles electrical transmission lines in a municipal power grid.

A Case of Design Prediction

It’s clear why this is a superior design to diffusion. Strenuous exercise can raise the power demands of a muscle cell by 100-fold. “Researchers have suspected that a faster, more efficient energy pathway might exist but have found little proof of its

existence — until now,” we read. That’s a case of design prediction!

Robert Balaban of the National Heart, Lung, and Blood Institute (NHLBI), a co-leader of the team, tells more about how well-optimized the organization of this power grid is.

The study provides unprecedented images of how these mitochondria are arranged in muscle. “Structurally, the mitochondria are arranged in such a way that permits the flow of potential energy in the form of the mitochondrial membrane voltage throughout the cell to power ATP production and subsequent muscle contraction, or movement,” Dr. Balaban explained. Mitochondria located on the edges of the muscle cell near blood vessels and oxygen supply are optimized for generating the mitochondrial membrane voltage, while the interconnected mitochondria deep in the muscle are optimized for using the voltage to produce ATP, Balaban added.

This implies another level in the design hierarchy: not only is the power grid well organized inside the cell, but the cells are organized in the muscle tissues for the optimum utilization of the power where it is needed most.

Implications for Intelligent Design

The implications of this spectacular discovery for intelligent design are profound. To see why, we must remember that muscles first appear in the Cambrian explosion. Many of the Cambrian phyla that burst on the scene had muscles for contraction (jellyfish), crawling (worms), fin movement (Anomalocaris and Metaspriggina, the vertebrate fish), and coordinated action of jointed appendages (trilobites and other arthropods). Most of the Cambrian animals used muscles in various ways. Muscles are but one of many new cell types that appear suddenly, fully functional, across multiple phyla in the early Cambrian.

As Stephen Meyer emphasizes in Darwin’s Doubt, these new cell types are arranged in a hierarchy: tissues, organs, systems — and ultimately, integrated body plans. This hierarchical arrangement of complex parts for unified function challenges all undirected mechanisms such as natural selection. It takes foresight — a plan for a functional goal and the means to achieve it — to bring parts together into a hierarchical arrangement that works. The film Darwin’s Dilemma illustrates this point as well. In our uniform experience, Meyer argues, the only cause capable of doing that is intelligence.

Now we can extend this hierarchical thinking into the arrangement inside one new cell type in a Cambrian animal: a muscle cell. That optimal hierarchical arrangement, furthermore, extends downward into the intracellular environment and upward into the tissue in which the cell resides. It’s hierarchy all the way down.

Secular humanism's Homer?

Rescuing Evolutionary Theory from Darwinian Mythology

Evolution News

On a new episode of ID the Future, historian of science Michael Keas begins a two-part conversation with Robert Shedinger, the Wilford A. Johnson Chair of Biblical Studies and Professor of Religion at Luther College and author most recently of The Mystery of Evolutionary Mechanisms: Darwinian Biology’s Grand Narrative of Triumph and the Subversion of Religion. Shedinger reports on the contrast between Darwin’s private view of his theory of natural selection and the public view as detailed in his published work. Shedinger also notes the deficiency in evidence for Darwin’s proposal, despite claims to the contrary from his followers and evangelizers today. Download the podcast or listen to it Here

Monday 27 March 2023

The science acknowledges the thumb print of JEHOVAH?

Scientific Paper Argues Antarctic Icefish “Designed to Utilize Hemoglobinless Blood”

Casey Luskin

As Emily Reeves has Mentioned, a peer-reviewed paper in BIO-Complexity published tackles the question of the origin of how certain fish species live in extremely cold Antarctic waters. Titled “The Cardiovascular System of Antarctic Icefish Appears to Have Been Designed to Utilize Hemoglobinless Blood,” and authored by medical researcher Gregory Sloop, the paper argues that, “The circulatory system of Antarctic icefish may have been Designed to prevent high blood viscosity at low temperatures by taking advantage of the increased solubility of oxygen at low temperatures, allowing use of hemoglobin-free blood.” He argues that this complex system “could not have evolved via a series of gradual steps” because:

The hemoglobinless phenotype requires simultaneous customization of the heart, vasculature, and blood, including its viscosity. Simultaneous, coordinated acquisition of multiple unique features, as required by the absence of hemoglobin, is inconsistent with Darwinian evolution, which postulates that species develop by small, incremental changes over time.

More Cold, More Viscous

When liquids become cold they tend to become more viscous. Sloop observes, however, that “the viscosity of icefish blood at its native temperature, approximately 0°C, is very similar to that of human blood at 37°C.” Fish that lives in very cold waters, such as Antarctic icefish, must therefore solve a problem: How are they able to pump blood through their bodies at such low temperatures?

One way Antarctic icefish solve the problem is by having no erythrocytes (red blood cells) in their blood. So how do they deliver oxygen throughout their bodies? Some believe it’s due to nitrous oxide (NO) dissolved in the bloodstream, which actually causes hypoxia in icefish tissues. But Sloop maintains that it is thanks to “a customized cardiovascular system [rather] than a conventional one that was pressed into service when a mutation caused the loss of hemoglobin expression.” Some of these “cardiovascular customizations” include:

Solubility of O2 increases with lower temperature, allowing the blood to carry more O2 at such a low temperature.

Increased cardiac output.

A special “high-output, low resistance circulation” where “trunk skeletal muscle capillaries are two to three times greater in diameter than those of typical teleosts, reducing vascular resistance” and “Icefish retinas are more densely vascularized than those of red-blooded notothenioids, increasing O2 delivery to this metabolically active tissue.”

This larger cardiac output and special vasculature require “a blood volume two to four times greater than that of red-blooded fish” which “in turn requires a customized heart that is heavier and has a larger stroke volume than that of red-blooded notothenioids.” As a result “stroke volume of the icefish heart is 6 to 15 times greater than in other teleosts.”

To sustain this larger heart, special heart contractile cells called “cardiomyocytes” are in the icefish “relatively large and contain a relatively large number of mitochondria.” Indeed, in one icefish species the percent of cardiomyocytes devoted to mitochondria are “the highest in any teleost and higher than in any vertebrate except for the Etruscan shrew.”

Special kidneys to accommodate the low-pressure blood circulation.

Special “corpuscle” blood cells unique to icefish which convert carbon dioxide and water into carbonic acid.

An “Example of Teleology in Biology”

The effect of all of these special features is to allow Antarctic icefish to have lower hematocrits (the percent volume used by red cells in the blood), which lowers blood viscosity, making it easier for the fish’s heart to pump blood under such cold conditions. Sloop concludes:

The customized icefish heart, vasculature, and blood form a system with mutually dependent parts. … The hemoglobinless phenotype requires simultaneous, coordinated acquisition of multiple unique features. This is difficult to explain with Darwinian evolution, which postulates that species develop by small, incremental changes over long periods. … Multiple customized components are necessary to utilize hemoglobinless blood. Actualizing the design for the icefish cardiovascular system requires each customized component to be in place simultaneously. This is more innovation than can be accomplished by random mutation as postulated in Darwinian evolution.

Sloop offers this potent observation: “Proponents of intelligent design see customizations to decrease blood viscosity as examples of teleology in biology.”

Sunday 26 March 2023

On the danger of science as master rather than servant.

Aeschliman on Three Great Authors Critiquing Scientism

Evolution News

On a classic episode of ID the Future, Andrew McDiarmid concludes a two-part conversation with Michael D. Aeschliman, author of the revised and expanded The restoration of man: C. S. Lewis and the Continuing Case Against Scientism. Here Aeschliman places Lewis among a strong line of thinkers critiquing scientism. These include the philosopher and mathematician Blaise Pascal, who showed that scientific knowledge on its own could never be sufficient for being fully human, as well as the theologian and physicist Stanley L. Jaki, who brilliantly integrated science and theology. Aeschliman’s list also includes the great English author Jonathan Swift, whose satirical work skewered the illusions of scientific reductionism. Download the podcast or listen to it Here

Unsanctionable?

more on the struggle for the empire of God.

On the crisis in the 51st American state?

Chemistry Vs. OoL science.

Journalism has fallen?

Saturday 25 March 2023

Commonsense on the rebound?

Feminism's civil war?

Friday 24 March 2023

Waco revisited.

Ask not what your country should do for you?

the science concludes that that JEHOVAH may know a thing or two about engineering after all.

Peer-Reviewed Paper Answers Claims of “Bad Design” of the Human Foot/Ankle

Casey Luskin

In a peer-reviewed paper published in BIO-Complexity, Bristol University engineering professor Stuart Burgess explains “Why the Ankle-Foot Complex Is a Masterpiece of Engineering and a Rebuttal of ‘Bad Design’ Arguments.” Brian Miller has

previously Covered Professor Burgess’s arguments in a lecture, but those are framed as a response to arguments from ID-critics such as Jeremy DeSilva and Nathan Lents. Those critics claim that the human foot-ankle complex is sub-optimal because it reflects an unguided process where evolution attempted to convert a skeletal structure adapted for quadrupedal

locomotion to bipedalism. Burgess argues in response that the ankle-foot complex “show a very high degree of complexity and fine-tuning” and “masterful engineering.” Moreover, “Engineering insight reveals a close relationship between form and function in the ankle, a relationship seen in its multiple bones and the layout of those bones” and the “five midfoot bones are needed to form the optimal kinematic and structural interface between the hindfoot and forefoot.”

Burgess observes that many who have studied the foot without a preconceived bias have recognized its “excellent design.” He quotes Leonardo da Vinci who called the human foot “a masterpiece of engineering and a work of art,” and more modern researchers who observe the “nearly effortless human gait” or who note that various foot structures “work in perfect synchronisation” because it is “superbly constructed for ambulation.”

A Contrast with “Bad Design

In contrast, “bad design” proponents believe that most of the seven anklebones are pointless, poorly coordinated, and fundamentally a bad design because a “fused structure” would work better than “a joint with so many separate parts.” Burgess answers arguments that the ankle-foot performs poorly for bipedalism because it was originally evolved for quadrupedal locomotion by observing that such arguments “are based on circular reasoning and assumptions about what evolution could or could not do in the past.” He believes that “A better scientific approach to assessing the quality of design is to study the actual biomechanics and functions of the foot.”

Burgess observes that “The requirements for agile bipedal movement are extremely demanding.” After all, the foot must be “a compact multifunctioning precision device” which has to fulfill multiple requirements which are sometimes contradictory:

Act as a strong and stiff lever to propel the body forwards in walking and running. Joint movement is plantarflexion.

2. Act as a flexible platform to absorb shocks and adapt to uneven ground. Joint movements include dorsi-flexion, pronation, and supination.

3. Provide 3-point contact with the ground to allow standing on one or two legs and to enable controlled push-off from the ball of the feet. The control must involve fine adjustment of direction as well as power.

Difficult and Contradictory Demands

Yet Burgess further notes that “The requirements of a stiff lever and flexible platform are difficult to achieve because they are contradictory. To achieve these two requirements the foot must have stiffness and flexibility in just the right places. In addition, the foot must have the ability to adjust stiffness through precise control of muscles.” The foot is able to accomplish this because it “has three interconnecting flexible arches that perform multiple functions in particular three-point contact with the ground, stiff lever for take-off and flexibility for shock absorption.” Burgess notes how well-designed these arches are:

There are several features that maintain the integrity of the arches: (i) foot arches segmented like a Roman arch, which induces compressive forces, particularly the bone that forms the keystone to the arch; (ii) short ligaments that tie adjacent bones together; (iii) longer ligaments (like the spring ligament) that tie the arch across multiple bones; (iv) muscle-tendon groups that act like a sling, pulling the arches upwards; and (v) muscles that stiffen the arch.

He further notes that the bones of the midfoot allow it to perform five main sub-functions, including providing a “flexible transverse arch,” “Load bearing structure during pronation,” “Kinematic interfaces for pronation-supination,” “Structural interface for longitudinal loads,” and “Stiffening of the medial arch.”

Burgess also finds that “Another specialised design feature in the ankle-foot complex is the elastic hinge joints,” as some 17 of such joints allow “significant flexibility” in the foot and also aid in shock absorption. In fact, Burgess reports that these elastic hinge joints have at least five sub-functions, including “(i) flexibility; (ii) load-bearing; (iii) energy storage; (iv) failsafe design; and (v) ultra-low friction.”

Bad-design proponents have asked why there are paired bones at the bottom of the leg above the ankle instead of a single bone. Burgess notes there are good reasons for this as fibula is “well known to provide stability to the ankle joint” via “a type of linkage system with multiple bars.” He cites two specific advantages to having a fibula bone:

One advantage of the fibula is that it increases the moment arm (mechanical advantage) of muscles acting on the ankle-foot complex. A second advantage is that the fibula increases the attachment area for muscles and therefore allows more muscle to act on the joint.

Answering Bad Design

After providing this review of the engineering functions of the ankle-foot complex, Burgess is able to address claims that many foot and angle bones are functionless. In reality, “this paper has shown that all the bones of the ankle-foot complex have very important roles in the specialized design features. In particular, the five bones of the midfoot have multiple functions.” He also definitively shows that the fibula bone is necessary because it “provides essential stability to the ankle joint during pronation by forming a multi-bar linkage mechanism.” Burgess shows that a fused ankle structure would not function better because “It is well known in the medical field that ankle fusions lead to a degradation of ankle performance” and relative movement of ankle bones affords various functions, including shock absorption.

A major anti-design argument is that ankles are prone to sprains or other injuries, but Burgess notes that this confuses misuse with bad design:

The importance of this differentiation can be illustrated by analogy with a modern car. Most modern cars are well designed and very reliable when in good condition and used properly. However, despite the high quality of design, a modern car will fail if overloaded or neglected, or if it is simply very old. Therefore, when considering malfunctions in joints it is important to check why there was a malfunction. If the ankle-foot complex malfunctions due to overload, neglect, or health issues, this does not mean the design can be judged as bad.

Burgess ends with four conclusions:

There are four highly specialised design features in the ankle-foot complex

2. The ankle-foot complex is superior to human-engineered joints

3. Lents’s bad design arguments are contrary to scientific evidence

4. Engineering insight explains form and function

This last point is crucial because it shows that the very design and structure of the ankle-foot complex must exist to for it to perform its functions. According to Burgess, the system exhibits “very sophisticated engineering design.”

Pre-human powered flight v. Darwin.

Fossil Friday: The Abrupt Origin of Winged Insects

Gunter Bechly

This Fossil Friday features Lithomantis varius, a large fossil insect from the Carboniferous (Namurian) brickwork quarry of Hagen-Vorhalle in Germany, which is one of the most ancient fossil localities for winged insects and dates to about 318 million years ago. Lithomantis belongs to the winged insect order Paleodictyoptera, which only existed in the Palaeozoic era.

Insect wings are extremely complex structures that are highly adapted to their function Delitzschalan as flight organs. They have a fan-like plicated structure to give the wing surface stability; additionally they are enforced by a complex wing venation; the wing is also supplied with sensory hairs; and the wing base has a highly complex arrangement of articulatory plates to allow for sophisticated movement, enabled by an associated muscular and neural system.

According to Darwinism, the evolution of such a system would certainly have required a plethora of intermediate stages that brought this wonderful locomotory apparatus into being by an accumulation of many small changes over a long period of time. Since paleontologists have discovered thousands of fossil insects from the Paleozoic, we have certainly also found at least some of these transitional forms in the evolution of insect wings!? At least one? Nope, not a single one.

The oldest fossil winged insects belong the orders Palaeodictoptera (e.g., Delitzschala) and to the giant dragonfly order Meganisoptera, thus they were already equipped with the complete wing apparatus. There is not a single transitional form, so that the leading textbook on insect evolution, by Grimaldi & Engel (2005: 160), admitted: “An insect equivalent of an Archaeopteryx remains elusive but certainly existed.” Apparently, the engineering marvel of insect wings came into being abruptly rather than gradually, which is inexplicable with unguided evolution but quite expected with intelligent design.

Common sense has fallen?

Common sense re:Common ancestry?

Peer-Reviewed Paper Shows Vertebrate Embryonic Variation Contradicts Common Ancestry

Casey Luskin

Evolutionary biologists often argue that vertebrate embryos develop in highly similar manners, reflecting their common ancestry. But a peer-reviewed paper in BIO-Complexity, by David Swift (author of Evolution Under the Microscope), provides an insightful review on the subject. The Article is titled, “The Diverse Early Embryonic Development of Vertebrates and Implications Regarding Their Ancestry.” Swift shows that, despite common claims, vertebrates do not develop similarly, according to the predictions of evolution.

He opens by framing his thesis:

It is well known that the embryonic development of vertebrates from different classes (e.g., fish, reptiles, mammals) pass through a “phylotypic stage” when they look similar, and this apparent homology is widely seen as evidence of their common ancestry. However, despite their morphological similarities, and contrary to evolutionary expectations, the phylotypic stages of different vertebrate classes arise in radically diverse ways. This diversity clearly counters the superficial appearance of homology of the phylotypic stage, and the plain inference is that vertebrates have not evolved from a common vertebrate ancestor. The diversity extends through all stages of early development — including cleavage and formation of the blastula, gastrulation, neurulation, and formation of the gut and extraembryonic membranes.

Now intelligent design does not require common ancestry to be false, but even a guided form of common ancestry might lead to different predictions from strictly unguided descent with modification. Thus, Darwin and subsequent evolutionists such as Ernst Haeckel found embryology to be a crucial line of evidence supporting Darwin’s thesis. According to Swift, common ancestry predicts that vertebrate development should exhibit striking homologies. But more than that, “If common ancestry is the explanation for homologies, not only should homologous organs be derived from equivalent embryonic tissues (the cardinal criterion for homology) but they should also develop by comparable processes.”

Very Different Pathways

The crux of Swift’s thesis is that although vertebrate embryos do pass through a similar “phylotypic stage,” the pathways of development are very different:

[D]espite their morphological similarities and contrary to evolutionary expectations, the striking fact is that the “phylotypic stages” of different groups of vertebrates arise in remarkably diverse ways, even with key tissues such as the germ layers (see below) deriving from completely different early embryonic sources. These observations clearly refute the presumed evolutionary homology of the vertebrate phylotypic stage, and hence undermine the inference of common ancestry based on that supposed homology.

He reprints the “hourglass model” of vertebrate development and points out that this is merely an “observation” about development — not an explanation of how it arose:

From: Irie N, Satoh N, Kuratani S (2018) The phylum Vertebrata: A case for zoological recognition. Zoological Lett. 4(32):1–20. doi:10.1186/s40851-018-0114-y, under Creative Commons License

One of the key stages of development that leads to this similar “phylotypic stage” is gastrulation, which Swift notes is crucial because it establishes the basic body plan and “leads to the establishment of the germ layers — ectoderm, mesoderm and endoderm — from which all of the body’s tissues are derived.”

Differences in Vertebrate Development

Swift cites various specific differences in vertebrate development to make his case, especially in gastrulation. He predicts that “from an evolutionary perspective we would surely expect gastrulation to be ‘conserved’” but finds that “for almost all of the major classes of vertebrates” there are key differences in gastrulation, including “the mechanism of gastrulation is significantly different from any of the others,” and “the source tissues of the germ layers are different.”

After reviewing mechanisms of gastrulation in various vertebrate classes, Swift notes that “the wide variety of structures of the blastulas of different classes of vertebrate challenges the view that the resultant embryonic tissues can be considered equivalent or homologous.” Specifically, in different types of vertebrates different parts of the blastula ultimately become the embryo itself. He describes these differences as follows:

Chondrichthyans (lancelets): “It is a one-cell thick epithelial layer, forming the upper surface of the blastula.”

Teleosts (bony fish, e.g., zebrafish): “It is a multiple-cell layer, beneath the overlying enveloping layer.”

Amphibians: “It is the whole of the blastula, comprising the multilayered dome of the upper hemisphere and the mass of cells in the lower hemisphere.”

Reptiles and birds: “It is the upper surface of the blastula, comprising a single-cell thick epithelial layer, overlying the hypoblast.”

Placental mammals (e.g., primates): “It is part of the inner cell mass, within the outer trophoblast.”

He cites further differences between which cells become the endoderm and which become the mesoderm, noting:

in amniotes (reptiles, birds, mammals) cells that are internalized arise from a central area of the epiblast, i.e., the presumptive endoderm and mesoderm are surrounded by presumptive ectoderm; whereas

in anamniotes (chondrichthyans, teleosts, amphibians) the cells that internalize are from the edge of the epiblast, i.e., the presumptive endoderm and mesoderm surround the presumptive ectoderm.

Swift summarizes major differences in the mechanisms of gastrulation as follows:

Chondrichthyans: by cells rolling over a posterior overhang of the epiblast.

Teleosts: by involution around the edges of the epiblast as it spreads around the yolk.

Amphibians: by involution through an annular blastopore.

Reptiles: by involution through a canal-like blastopore.

Birds: by cells ingressing through a primitive streak, formation of the primitive streak being accompanied by growth of an underlying endoblast.

Placental mammals: by cells ingressing through a primitive streak.

Three Substantial Distinctions”

Swift thus finds that these diverse modes of development cannot be considered homologous:

In the light of these three substantial distinctions — the different overall structure of the blastulas, the different parts of the blastula that become the embryo, and the different relative positions of the presumptive ectoderm and mesoderm/endoderm in amniotes and anamniotes — there is no doubt that the tissues that become the embryo are not equivalent, and hence are far from being homologous across the various vertebrate classes.

According to Swift, these fundamental differences in early vertebrate mechanisms of development during gastrulation suggest that vertebrates do not share a common ancestry:

The straightforward conclusion to draw from this radical diversity of their early embryonic development is that it shows the vertebrates have not evolved from a common vertebrate ancestor. This conclusion can be avoided only if there are credible explanations for how such diversity of early development might have arisen from the development prevailing in a common ancestor (whether or not similar to present-day cephalochordates) in an evolutionary way, via changes that (i) had a realistic probability of occurring, (ii) maintained viability, and (iii) offered, in most cases, significant advantage that could be favored by natural selection.

Meeting these evolutionary requirements poses a great challenge, however. Swift quotes a prominent developmental biologist, Rudolf Raff, who wrote: “One might reasonably expect mechanisms of early development to be especially resistant to modification because all subsequent development derives from early processes.” Swift calls this a “commonsense conclusion” because the complexity of vertebrate development demands that many coordinated modifications would be required to fundamentally change how development proceeds. He thus finds that “because of the interdependence of the mechanisms that are involved, constructive changes to embryonic development must entail coordinated production of and/or changes to several genes, e.g., for transcription factors and the DNA sequences on which they act, which is prohibitively improbable.”

This leads to a “waiting time” problem where multiple coordinated change would be required to transition from one developmental regime to another, posing “a formidable challenge to supposed evolutionary scenarios” as generating these changes would be “generally far in excess of the time available.”

Thursday 23 March 2023

An outbreak of journalism?

Darwinism's ministry of truth in action?

I Got Canceled by the National Science Teaching Association

Herman B Bouma

Cancel culture reigns supreme in mainstream science, as I can tell you from personal experience. A recent instance involves the National Science Teaching Association (NSTA) and its cancellation of my poster presentation, which had been scheduled for the NSTA annual conference going on right now in Atlanta, March 22-25.

In September 2022 I submitted a proposal to speak at the conference. My topic was “The Top 10 Scientific Arguments Against Darwin’s Theory — According to Darwin Himself.” Darwin took great care to reply thoughtfully to the scientific arguments against his theory and, by the time of the sixth edition of The Origin of Species in 1872, approximately one-third of his book consisted of his responses to 37 scientific arguments against his theory (all of which still have merit today). Based on Darwin’s discussion in The Origin of Species, I determined what Darwin likely would have considered to be the top ten scientific arguments against his theory. (For interested readers, see here for Dr. Casey Luskin’s own detailed take on the same Subject.)

On December 29, 2022, I received an email from the NSTA conference team inviting me instead to submit a proposal for a poster presentation. The email stated that my topic was “evaluated as one that is significant and of interest to your colleagues.” On January 9, 2023, I submitted a proposal for the poster presentation, which was then approved and, beginning in January, was listed in the online conference agenda. The listing presented the main takeaway of the poster presentation as follows: “Darwin acknowledged that there were ‘a crowd of difficulties’ with his theory and stated, ‘Some of them are so serious that to this day I can hardly reflect on them without being in some degree staggered; but, to the best of my judgment, [they] are not, I think, fatal to the theory.’”

Working on My Poster

In February I worked on my poster presentation and also prepared a handout for it. On February 22 I went to a local print shop and had 50 copies made of the handout. In the evening of the same day I attended “Atlanta 2023 — Poster Session Support Web Seminar,” a webinar sponsored by NSTA to help those preparing poster presentations.

However, on February 24 I received an email from Tricia Shelton, NSTA’s Chief Learning Officer, stating that “it has come to our attention that your session may be promoting creationism. … The purpose of this email is to inquire about your poster presentation to find out if it is focused on creationism or on modern evolutionary science ideas articulated in our national standards.” I responded on February 25, “My poster presentation is not focused at all on creationism. It is focused only on Darwin’s ideas and what he considered to be valid scientific arguments against his theory.”

Resolved by Modern Science?

I then received an email from her on February 28 in which she asked if I was seeking to challenge modern evolutionary theory by using intelligent design. She also said my poster would need to explain how each of the top ten scientific arguments against Darwin’s theory has been resolved by “modern scientific evidence.”

I replied that my poster presentation did not challenge evolution by using intelligent design. Rather, it only set forth what Darwin himself thought were the top ten scientific arguments against his theory, specifically, against his proposed mechanism for evolution, i.e., the application of natural selection to randomly produced variations. Thus, it sought to promote an objective evaluation of Darwin’s proposed mechanism.

I also stated that the scientific debate continues with respect to this mechanism and that I did not believe the top ten scientific arguments have been resolved using modern scientific evidence. I stated that if I was mistaken, I would appreciate her help and asked her to let me know what modern scientific evidence has resolved each of the ten arguments.

A Final Email

I received a third and final email from Ms. Shelton on March 7. In this email, instead of pointing out any modern scientific evidence resolving the ten arguments, she stated that my poster presentation focused only on Darwin’s words and did not “reference Framework-aligned teaching approaches.” However, the guidelines for poster presentations do not require that a poster presentation “reference Framework-aligned teaching approaches.” It seemed she was just looking for an excuse to cancel my poster presentation. She said my poster presentation could not be accepted “in its current state” and canceled it without giving me any opportunity to bring it into compliance.

It is bizarre that Ms. Shelton canceled my poster presentation when, as indicated earlier, the NSTA conference team found my topic to be “significant and of interest to your colleagues.” In her zeal to protect the established narrative about evolution, Ms. Shelton was determined to shut down any debate about Darwin’s theory, even if it was debate fostered by Darwin himself.

The “Censorship Industrial Complex”

At a Congressional hearing earlier this month, held by the House Select Subcommittee on the Weaponization of the Federal Government, one of the witnesses, Michael Shellenberger, warned the lawmakers of “the growth and power of a censorship industrial complex run by America’s scientific and technological elite,” a complex that has eroded Americans’ freedom of speech. This censorship industrial complex has been at work for quite some time now in attempting to shut down any debate about Darwin’s theory.

Most people believe that when it comes to disagreements on policy and scientific theory, the best approach is to promote debate rather than censorship. Open and honest debate has always been the American way. However, in the case of Darwin’s theory, debate is rejected in favor of censorship. This is contrary to the hope of Charles Darwin himself, who wrote, “I look with confidence to the future, — to young and rising naturalists, who will be able to view both sides of the question with impartiality.” Those “young and rising naturalists” are out there, and I’ve learned much from them. But the National Science Teaching Association, for one, has no interest in doing so.

Headlong into that long sleep?

Euthanasia’s Cultural Collateral Damage: Less Respect for Human Life

Wesley J Smith

Euthanasia causes egregious cultural damage beyond the direct consequences of allowing the killing — or facilitating the suicides — of sick and disabled people. Eventually, the lives of the elderly, disabled, mentally ill, and seriously ill come to be seen as less valuable than the “healthy” and able-bodied — to the point that their homicides are often winked at by society. We saw this phenomenon during Jack Kevorkian’s mass assisted suicides in the ’90s, supported by much of the media and accompanied by the unwillingness of several juries to convict for nearly a decade.

A recent homicide case in Canada further illustrates the point. As regular readers of my work are well aware, Canada has fallen off the euthanasia moral cliff by allowing broad categories of people to be killed by doctors as a means of ending “suffering.” But that denigrating attitude toward people with serious health conditions is catching on, and now, a man, Francois Belzile, who killed his disabled wife has only had his wrist lightly slapped by a judge for the crime.

No Question About the Impact

From the Edmonton Journal story:

A retired accountant who killed his severely disabled wife will be allowed to serve his sentence on house arrest rather than in prison, with a judge ruling the accused’s “caregiver burnout” lessens his moral responsibility for the crime.

Belzile pleaded guilty last month to manslaughter for injecting Christiane Belzile — a 69-year-old, non-verbal stroke survivor for whom Francois Belzile had been sole caregiver for seven years — with a lethal dose of insulin after she was injured in a fall in 2018. Belzile then tried to end his own life.

Despite Francois’s refusal of state assistance — and a threat before the crime to end both their lives if they ceased to be able to live “independently” — he was deemed unable to form intent to murder and allowed to plead guilty to manslaughter. Good grief.

There is no question that euthanasia advocacy and legalization impacted the case:

[Defense attorney] Hurley added that Belzile saw his actions as “the compassionate shortening of the final step.” Hurley also noted societal attitudes toward assisted death are rapidly changing, noting, “The world has changed since Latimer, at least in Canada.”

(Canadian Robert Latimer murdered his daughter Traci, who was disabled by cerebral palsy, back in the ’90s. He served about ten years — but only because it was mandatory — and had the support of a majority of Canadian people according to polls.)

Out of His Misery

So, in essence, Francios put Christiane out of his misery and out of pride — i.e., his preferring death over dependency — and the judge winked at the crime by imposing such a light sentence for an egregious act.

What a frightening illustration of the lowered respect for “compromised” human life that euthanasia consciousness breeds. People with disabling conditions and those who love them should be terrified.

Wednesday 22 March 2023

Yet more evidence of technology all the way down.

A Biochemical Icon of Intelligent Design, ATP Synthase Does More than Spin

David Coppedge

The biochemical icon of rotary machines, ATP synthase, remains in the news with new discoveries. Now that cryo-electron microscopy is widely used, biophysicists are looking at the function of individual subunits of the engine and figuring out what they do. The fact that molecular machines exhibit more functional elegance the closer one looks indicates that intelligent design is the best explanation.

Automatic Brake

Animals and plants both contain these vital rotary engines that supply their energy needs in ATP. In animals, they are found in mitochondria. In plants and other photosynthetic organisms, they are found in chloroplasts. Photosynthesis, being dependent on light, has a problem: when it’s dark, their rotary engines might start running in reverse, risking “a wasteful ATP hydrolysis reaction.”

Working with the green alga Chlamydomonas reinhardtii (pictured above) as a “model organism,” a team of eight Japanese scientists took a closer look at the γ subunit in chloroplast ATP synthase (this is the “camshaft” part of the engine that drives the synthesis of ATP in the F1 domain). They found that two specific domains in the γ subunit act as an automatic brake in the dark. They wrote in PNAS in January,

Among the FoF1-ATP synthase complexes of all organisms, chloroplast FoF1 (CFoCF1) is a unique enzyme with a redox regulation mechanism; however, the underlying mechanism of redox regulation of the adenosine triphosphate (ATP) synthesis reaction in CFoCF1 has not been fully elucidated. By taking advantage of the powerful genetics of Chlamydomonas reinhardtii as a model organism for photosynthesis, we conducted a comprehensive biochemical analysis of the CFoCF1 molecule. Here we identify structural determinants for the kinetics of the intracellular redox response and demonstrate that the redox regulation of ATP synthesis is accomplished by the cooperative interaction of two γ subunit domains of CFoCF1 that are unique to photosynthetic organisms.

Figure 6 in the article (reproduced by Phys.org) shows how the two domains act like a

stopper:

The tight conformation weakens the interaction between the redox loop and the β-hairpin. Consequently, the β-hairpin remains stuck in the cavity between the α and β subunit, like a stopper, and inhibits the rotation of the central stalk (γεc-ring). In a reduced form, the redox loop recovers flexibility to interact with the β-hairpin. The redox loop interacts to pull out the β-hairpin from the cavity and thus accelerates the central stalk, like a cooperative regulator.

Watching the Snap

Another Japanese team, this one from the University of Tokyo, looked closer at the “catalytic dwell” in the F1 domain of the ATP synthase engine where ADP is converted to ATP with the addition of a phosphate. The F1 domain has 3 pairs of α, β subunits arranged like petals of a flower, each pair in a different phase of activity: insertion of ingredients, catalysis, and ejection of ATP. The γ subunit, like a camshaft, activates each α, β pair in turn as it rotates a full 360°. Dividing by three, each α, β pair feels the force of the camshaft during the catalysis stage (ADP + P yielding ATP) within 120° at each full turn of the crankshaft. At the other times, the pair is either receiving the ingredients or ejecting the finished ATP. When running in reverse, the F1 motor becomes an ATP cleaver, hydrolyzing ATP to yield ADP and P, ejecting protons in the process. In hydrolysis, then, ATP becomes the fuel to make the motor run in reverse.

During normal operation, the motor catalyzes ATP. Biophysicists have long suspected that the camshaft (the γ subunit) exerts pressure on the incoming ADP and P to snap them together. If 0° represents the moment ATP is catalyzed, previous studies have found a short pause stage at 80° and a longer dwell at the subsequent 40° of rotation, representing the “chemomechanical coupling scheme,” as their Paper calls it.

In the reverse reaction, though, the angle for cleavage of ATP was unclarified. The team made a hybrid ATP synthase that ran extremely slowly so that they could observe “the world’s

smallest rotary biological molecule motor” running in reverse. Their hybrid allowed them to measure the angle at which ATP cleavage occurs.

As a result, the new hybrid F1 showed two pausing angles that are separated by 200°. They are attributable to two slowed reaction steps in the mutated β, thus providing the direct evidence that ATP cleavage occurs at 200° rather than 80° subsequent to ATP binding at 0°. This scenario resolves the long-standing unclarified issue in the chemomechanical coupling scheme and gives insights into the mechanism of driving unidirectional rotation.

See the “Graphical Abstract” in the paper that illustrates this “extremely long dwell” they measured. The finding reveals that in both directions, ATP synthase is finely tuned for its work. The reverse direction (hydrolysis) is not just like a motor leaking fuel. Its parts act with precision to cleave ATP in a specific way.

Insights into a Related Rotary Motor

There’s a cousin to ATP synthase. It’s a proton pump called V-ATPase (vacuolar-type adenosine triphosphatase), and its catalytic parts are labeled V1Vo instead of F1Fo. Like its counterpart, V-ATPase runs with a rotary action but spends ATP to pump protons into organelles. Its job is to acidify vacuoles and other organelles or intracellular compartments that need a lower pH to work. The Vo part pumps the protons (H+ ions) into the vacuole, increasing its acidity. A little thought shows that such a motor could be dangerous. Would you want an acid-generating motor running loose?

Scientists from a Toronto hospital, publishing in PNAS, were curious to figure out how these acid pumps get built without causing harm to the cell. The Vo complex is assembled in the endoplasmic reticulum (ER) and then transported to the Golgi apparatus to be combined with V1. What quality control mechanism keeps the domains inactivated until they are fully assembled and ready for action?

Using cryo-electron microscopy, the team imaged three proteins (Vma12p, Vma22p, and Vma21p) that must work together to achieve the quality control for safely handling the acid pumps during assembly. “The resulting structures,” they found, “show how a sequence of coordinated interactions and conformational changes ensures that only properly assembled Vo leaves the ER and proton pumping into the neutral ER is avoided.” Spilling acid into the ER could be bad! “Unsurprisingly,” they remark, “owing to their importance for Vo assembly, mutations in the human homologues of Vma12p, Vma22p, and Vma21p have been linked to disease.” So how do these three essential proteins perform quality control? Do you really want to know?

The structures described above suggest the sequence of events that occur during Vo assembly in the ER membrane and subsequent binding of V1 in the Golgi…. The c ring assembles around Voa1p, with binding of subunit d to the c8c′c″Voa1p ring masking the ER-retrieval motif of Voa1p. The Vo∆aef:Vma12-22p structure indicates that the Vma12-22p complex binds this fully assembled ring prior to interaction with subunits a, e, and f (Fig. 4A). Vma12-22p helps recruit and secure the interaction of subunit a with the c ring through interaction of Vma12p with subunits a and d….

Their Final Sentence

OK, OK. Suffice it to say that a complicated set of interactions takes place to ensure V-ATPase assembly is safe! Biochemists may wish to labor through the details. Fortunately, the authors provided diagrams and animations to illustrate the dynamics of all these working parts. Note their final sentence: “Importantly, the structures illustrate how Vma21p and Vma12-22p play central roles in both V-ATPase assembly and quality control.”

Quality control: it’s an engineering concept that permeates all three of these studies. Without quality control, these nanoscopic rotary engines, on which all life depends, would never last — indeed, would never emerge in the first place. Quality control belongs in the working vocabulary of intelligent design and engineering. It is not found in Darwin’s dictionary.

Junk DNA trope continues to be exposed as Junk science?

More Jobs for “Junk” DNA (Cont.)

Paul Nelson

If “junk” DNA goes toxic, does that suggest it had an original normal function? See the conclusion of this new paper, “Native functions of short tandem repeats”

Historically, repetitive elements within human genomes have been viewed as mostly unregulated ‘junk DNA’ that is not under selective evolutionary pressure. As such expansions of these repetitive elements are unfortunate accidents which become apparent and important only when they elicit highly penetrant and syndromic human diseases. Consistent with this line of reasoning, the field of REDs [Repetitive Element Diseases] has largely focused on emergent toxic mechanisms as drivers of disease only in the setting of large STR [Short Tandem Repeats] expansions rather than considering their pathology as alterations in the native functions played by these repeats in their normal genomic contexts. Here, we propose re-framing the discussion around repetitive elements in general — and STRs in particular — within human genomes. For each STR, we suggest first considering whether the STRs associated with a human disease have any native functions at their ‘normal’ size. If a native function exists, then expansion of these STRs can be viewed primarily as an aberrancy of that native function with coincident predictable impacts on gene expression dysregulation above certain repeat lengths. This reframing aligns with the approach typically taken in studying gain-of-function and loss-of-function mutations in disease associated single amino acid mutations and better ties the native functions of STRs to their pathology. It also suggests that shared regulatory rules will likely apply across REDs.

The article by Shannon E. Wright and Peter K. Todd is open access at eLife. Of course, lots of so-called “junk” has turned out to be functional. For another recent example, see Here

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Wednesday 29 March 2023

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Tuesday 28 March 2023

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Monday 27 March 2023

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Sunday 26 March 2023

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Saturday 25 March 2023

Friday 24 March 2023

Peer-Reviewed Paper Answers Claims of “Bad Design” of the Human Foot/Ankle

Fossil Friday: The Abrupt Origin of Winged Insects

Peer-Reviewed Paper Shows Vertebrate Embryonic Variation Contradicts Common Ancestry

Very Different Pathways

Thursday 23 March 2023

I Got Canceled by the National Science Teaching Association

Euthanasia’s Cultural Collateral Damage: Less Respect for Human Life

Wednesday 22 March 2023

A Biochemical Icon of Intelligent Design, ATP Synthase Does More than Spin

More Jobs for “Junk” DNA (Cont.)

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