Darwinists can't show their work because the caterpillar ate it?

 Fossil Friday: How the Caterpillar Got Its Legs, or Not

Gunter Bechly

This Fossil Friday features a caterpillar trapped in 45-million-year-old tree resin of Eocene Baltic amber. A caterpillar of course looks very much different from the butterfly into which it eventually develops. The wonderful metamorphosis of caterpillars into butterflies was first discovered by the British physician William Harvey (1651) and Dutch biologist Jan Swammerdam (1669), and famously featured in paintings by the pioneer entomologist Maria Sybilla Merian in her book Metamorphosis insectorum Surinamensium (Merian 1705).

The more primitive groups of insects like roaches, locusts, cicadas, and bugs have a so-called hemimetabolous development, where the nymph is similar in body plan to the adult insect, and with each molting grows in size and especially in length of the wing sheaths. However, most insect species, and indeed most animals on our planet, belong to Holometabola, the clade of insects with complete metamorphosis, which includes lace wings, beetles, bees and wasps, mosquitoes and flies, scorpionflies and fleas, as well as caddisflies and butterflies. In these insects the larva has a very different body plan from the adult insect. After the final larval stage there is a resting stage called pupa or chrysalis, in which the larval body is mostly dissolved into a kind of cell soup and rearranged into the adult body plan. This miraculous development was featured in the Illustra Media documentary Metamorphosis (Illustra Media 2011, Klinghoffer 2011) and poses a considerable conundrum for evolutionary biologists.

The Nature of the Conundrum

Only three hypotheses for the evolution of metamorphosis in insects have been presented: one, which suggests that the holometabolan larva is equivalent to the hemimetabolan nymph, fell out of favor decades ago. Another hypothesis suggested that the holometabolan caterpillar originated from a weird hybridization event of an insect with a velvet worm (Williamson 2009), which is generally considered as preposterous nonsense (Giribet 2009; also see Evolution News 2011). The currently preferred hypothesis is based on very old ideas of Harvey (1651) and Berlese (1913), which were further developed and elaborated by Truman & Riddiford (1999, 2002, 2019, 2022). Their so-called pronymph hypothesis suggests that the juvenile stages of hemimetabolous and holometabolous insects are not homologous, but that only the hemimetabolan pronymph is equivalent to the caterpillar larva, and the multiple nymphal instars are all equivalent to the pupal stage (also see Grimaldi & Engel 2005). However this hypothesis faces two formidable challenges:

The proymph is a non-feeding final embryonic stage, lacking functional mouth parts, which hatches from the egg and immediately molts into the first nymphal instar. The caterpillar larva is a pure feeding stage, basically a gut with legs. How could one evolve into the other with functional and advantageous intermediate forms?

Likewise, how could a single pupal stage, in which the complete body plan is dissolved and rearranged (including even the brain, see Truman et al. 2023 and Saplakoglu 2023), evolve via viable transitional forms from a normal series of nymphal instars that gradually transform into the adult with each molting? This appears to be not just unlikely but inconceivable and virtually impossible. Therefore, this hypothesis is controversial even among mainstream biologists, who have raised many objections to the interpretation of the pupa as only nymphal stage (e.g., DuPorte 1958). All that evolutionists have to offer are vague speculations such as this: “Perhaps 280 million years ago, through a chance mutation, some pro-nymphs failed to absorb all the yolk in their eggs, leaving a precious resource unused. In response to this unfavorable situation, some pro-nymphs gained a new talent: the ability to actively feed” (Jabr 2012). Easy peasy.

Anyway, we should expect that such a marvellous mode of development evolved from normal nymphal stages, if at all, after hundreds of millions of years of gradual change. However, that is not at all what the fossil record shows.

Actually, the first holometabolan insects are recorded from the same Pennsylvanian period as the first flying insects. Molecular clock data even suggest that Holometabola are at least as ancient (about 328-318 mya) as the earliest fossil record of flying insects (Labandeira 2011), or place “the origin of Holometabola in the Carboniferous (355 Ma), a date significantly older than previous paleontological and morphological phylogenetic reconstructions” (Wiegmann et al. 2009a, 2009b, Misof et al. 2014). My dear colleague and frequent co-author André Nel (2019) recently commented that “the late Carboniferous was also the time of the oldest known holometabolous insects, with complete metamorphosis (wasps, beetles, scorpionflies).” Indeed, fossils from larval and adult holometabolous insects of different orders have been found in late Carboniferous layers (see Kukalová-Peck 1997, Nel et al. 2007, 2013, Béthoux 2009, Kirejtshuk & Nel 2013, Kirejtshuk et al. 2014).

Early and Abrupt Appearance

This very early and abrupt appearance of the highly complex holometabolan metamorphosis represents one of the many examples of the waiting time problem, because it certainly required many coordinated mutations, which again required orders of magnitude more time to originate and spread than was available.

But any theory for the origin of the caterpillar larva needs to explain a lot more than that. While hemimetabolan nymphs and all adult winged insects have only three pairs of thoracic legs, the caterpillar larvae of butterflies and plant wasps additionally possess several pairs of chubby abdominal leglets called prolegs. “These prolegs pose an evolutionary mystery, and scientists have long grappled over how and why they got them” (Pallardy 2023). Where did those prolegs come from? There are three alternative hypotheses on the table:

Prolegs are serially homologous with thoracic legs, and thus derived from reactivated abdominal legs of crustaceans. This alternative was challenged and arguably refuted by previous evo-devo studies like Yue & Hua (2010) and Oka et al. (2010).

Prolegs are novel adaptations without immediate precursor structures.

Prolegs are derived from endites, internally facing structures of the crustacean limbs (e.g., Oka et al. 2010).

Now, a new study by Matsuoka et al. (2023) tested these three hypotheses with evo-devo data. The authors suggest that prolegs are novel traits, but based on the re-activation of pre-existing endite genes. The press release makes it very clear: prolegs “seem to be modified endites. As crustaceans evolved into insects, endites were largely lost. But in butterflies and moths, the gene for them got reactivated, providing caterpillars with their prolegs.” (Pallardy 2023).

To evaluate the feasibility of this hypothesis we first have to look at the distribution of prolegs within holometabolan insects, because this character is not hierarchically distributed as would be predicted by Darwinism, but instead is very incongruent (homoplastic): prolegs occur in the larvae of plant wasps, scorpionflies and fleas, caddisflies and butterflies, and some families of flies, but are absent in all other holometabolan groups. This incongruent pattern implies that prolegs were either reduced multiple times, or instead originated independently as a convergence, which is also suggested by developmental data (Suzuki & Palopoli 2001). Actually, Hinton (1955) proposed an independent origin of prolegs 27 times within Diptera. This alone is a grandiose empirical failure of Darwinian theory, because the unique anatomical similarity does not seem to be plausibly based on inheritance from a common ancestor. For the sake of the argument we will let this pass and just look at the new study.

Assessing the new study

As we have seen above, Darwinists now explain the origin of caterpillar leglets with the reactivation of a crustacean gene, that was dormant for maybe 100 million years. Seriously? After such a long period without function and without adaptive pressure to eliminate deleterious mutations, this gene should still have remained functional instead of been degraded by random genetic noise? This would be akin to a genuine miracle and arguably would violate an assumed law of evolution known as Dollo’s Law, which is based on the simple fact that history does not repeat itself (Gould 1970). Could this law be broken on some realistic time scale?

As shown by Rana (2017), there were several studies that evaluated the time frame in which the function of a gene is degraded and lost, so that it cannot be reactivated:

The study by Marshall et al. (1994) suggested that reactivation is reasonable over time scales of 0.5-6 million years. The authors concluded that “the reactivation of long (>10 million years)-unexpressed genes and dormant developmental pathways is not possible unless function is maintained by other selective constraints.”

Lynch & Conery (2000) showed that duplicated genes lose function by stochastic silencing within a few million years. Rana (2017) mentions that such duplicated genes can serve as proxy for dormant genes, because they are no longer under the influence of selection. Lynch and Conery found a half-life of 4 million years, which implies that function is lost after 16-24 million years.

Protas et al. (2007) showed that such a loss of function happens much more quickly, in about 1 million years, if it is advantageous and thus influenced by selection.

Horne (2010) studied the reactivation of eye sight in blind ostracods and commented that “there appear to be several well-documented examples of the reactivation of dormant genes, allowing the reappearance of ‘lost’ characters, in some cases after several [my emphasis] million years.” 

So, we have a realistic time frame of roughly 1-24 million years for the reactivation of a dormant gene. Indeed, short term reversals can be observed in lab experiments, e.g., concerning drug resistance among germs (Gouda et al. 2019). Anything longer than the mentioned time constraint is prohibited by Dollo’s Law of irreversibility (Gould 1970, Bull & Charnov 1985). Any apparent reactivation on longer time frames (see examples mentioned by Fryer 1999, Dingle 2003, Cruickshank & Paterson 2006, Horne 2010, and Rana 2017) cannot be reasonably explained with Darwinian processes, but requires intelligent design as more plausible and causally adequate explanation. Rana (2017) correctly emphasized that “it is not unusual for engineers to reuse the same design or to revisit a previously used design feature in a new prototype.”

But There Might Be a Loophole

Lynch (2022) recently found that “the long half‐life of enhancers, transcription factor binding sites, and protein−protein interaction motifs suggest that evolutionary reversals are possible after much longer periods of loss than previously suspected.” He concluded that “these data indicate that reactivation of these smaller functional units is possible after many millions of years and suggest that re-evolution of complex traits may occur through their loss and regain. Thus these data suggest that organisms need not surmount “the sheer statistical improbability … of evolution ever arriving at the same complex genic end‐result twice” (Müller in Gould 1970), rather “organisms might only need to retrace a single step such as the reacquisition of a transcription factor binding site in a cis‐regulatory element of a protein−protein interaction motif.”

However, there is a caveat, because the longer half-life does not apply to silenced protein coding genes, which would degrade much faster. Lynch (2022) explicitly admitted that “it seems unlikely that the genetic information for the development and function of the character can be maintained for long periods of time in the absence of the character (Bull & Charnov, 1985).” This could only be avoided in cases of serially homologous characters, when at least one instance of expression of this character would remain, so that selection could work against the deterioration of function by random copy errors. Therefore, Lynch (2022) suggested as a loophole for the violation of Dollo’s law “that the developmental programs required for the establishment of serially homologous characters may never really be lost so long as a single instance of the character remains.”

How Would Darwinists Argue?

So, let’s have a look at the possibility that this loophole could allow for the reactivation of the endite gene in caterpillars as suggested in the new study by Matsuoka et al. (2023). Probably, Darwinists would argue as follows: putative homologs of abdominal leg endites are present as pairs of eversible vesicles on the abdomen in some primitive wingless insects (apterygotes) like diplurans, bristletails, and silverfish that are known from (controversial) Devonian and Carboniferous fossils. Such vesicles are absent in all known winged insects and thus were reduced in the stem species of crown group pterygotes, which lived at least 323 million years ago in the earliest Pennsylvanian (Namurian) period according to the oldest fossil record (Brauckmann et al. 1994, Brauckmann & Schneider 1996, Prokop et al. 2005, Prokop & Hörnschemeyer 2016, Wolfe et al. 2016), and 410 million years ago in the Late Devonian period according to molecular clock estimates (Wiegmann et al. 2009b, Misof et al. 2014). This is 10 million years prior to the oldest fossil record of holometabolans (313.7 mya, Wolfe et al. 2016) and 60 million years prior to molecular clock estimates of their origin (350 mya, Wiegmann et al. 2009a, 2009b, Misof et al. 2014 / 328-318 mya according to Labandeira 2011). Therefore, the transformation would have occurred after 60-10 million years of gene suppression if the prolegs would belong to the ground plan of holometabolan insects. This would still reach or exceed the above mentioned limits imposed by Dollo’s law.

But it gets much worse for the evolutionist hypothesis. As we have seen above, larval prolegs do not belong to the ground plan of holometabolan insects (Peters et al. 2014), but developed independently multiple times in several crown groups among them. Therefore, we have to look at the age of those crown groups and not the age of Holometabola as a whole to evaluate the available window of time. Let’s be maximally generous and assume that larval prolegs are at least homologous in caddisflies (Trichoptera) and butterflies (Lepidoptera), so that they could belong to the ground plan of their common amphiesmenopteran ancestor. According to The Timetree of Life (Wiegmann et al. 2009a, 2009b) the relevant crown groups originated in Permian and Triassic periods: Lepidoptera, for example, about 230 million years ago and Amphiesmenoptera (the clade of Trichoptera+Lepidoptera) 282 million years ago. This molecular dating roughly agrees with the early fossil record of these groups. This implies that the reactivation of the dormant gene would have occurred after 128-41 million years (410/323-282 mya) of absence of any instantiated serially homologous character, which is simply impossible according to the limits proposed by mainstream evolutionary biology itself.

Is This Hard Science? Really?

Of course, such inconvenient facts do not bother evolutionary biologists at all, because the law obviously must have been broken, because we know it happened. Apparently laws do not mean much in evolutionary biology and can be suspended whenever a just-so story requires it. Sounds like hard science — not!

Why is it that you cannot find such simple calculations as we just made above anywhere in the mainstream scientific literature, to check if a scenario is plausible and compatible with other claims of evolutionary theory? Are the scientists really interested in testing their hypotheses and eventually finding out that they don’t hold water? It certainly doesn’t look like that to me. In spite of all the scientific efforts by Darwinists, the origin of complete metamorphosis in holometabolan insects remains an unsolved mystery, which is much better and causally more adequately explained by intelligent design.

As crooked as it gets?

 

Design is wrong by definition?

 

It's complicated? IV

 

The third horseman picks up his pace?

 

North America's last king?

 

File under "Well said" CII

 "In war, truth is the first casualty."

       Aeschylus

It's complicated? III

 

It's complicated? II

 

It's complicated?

 

Psalms chapter 9 American Standard Version

 I will give thanks unto JEHOVAH with my whole heart; I will show forth all thy marvellous works.

2I will be glad and exult in thee; I will sing praise to thy name, O thou Most High.

3When mine enemies turn back, They stumble and perish at thy presence.

4For thou hast maintained my right and my cause; Thou sittest in the throne judging righteously.

5Thou hast rebuked the nations, thou hast destroyed the wicked; Thou hast blotted out their name for ever and ever.

6The enemy are come to an end, they are desolate for ever; And the cities which thou hast overthrown, The very remembrance of them is perished.

7But JEHOVAH sitteth as king for ever: He hath prepared his throne for judgment;

8And he will judge the world in righteousness, He will minister judgment to the peoples in uprightness.

9JEHOVAH also will be a high tower for the oppressed, A high tower in times of trouble;

10And they that know thy name will put their trust in thee; For thou, JEHOVAH, hast not forsaken them that seek thee.

11Sing praises to JEHOVAH, who dwelleth in Zion: Declare among the people his doings.

12For he that maketh inquisition for blood remembereth them; He forgetteth not the cry of the poor.

13Have mercy upon me, O JEHOVAH; Behold my affliction which I suffer of them that hate me, Thou that liftest me up from the gates of death;

14That I may show forth all thy praise. In the gates of the daughter of Zion I will rejoice in thy salvation.

15The nations are sunk down in the pit that they made: In the net which they hid is their own foot taken.

16Jehovah hath made himself known, he hath executed judgment: The wicked is snared in the work of his own hands. Higgaion. Selah

17The wicked shall be turned back unto Sheol, Even all the nations that forget God.

18For the needy shall not alway be forgotten, Nor the expectation of the poor perish for ever.

19Arise, O JEHOVAH; let not man prevail: Let the nations be judged in thy sight.

20Put them in fear, O JEHOVAH: Let the nations know themselves to be but men. Selah

There is no preDarwinian Darwinism?

 

On the primeval AI of earth's Flora

 The Superior Programming that Makes Plants Look Smart

David Coppedge

Wesley Smith has warned more than once against anthropomorphizing plants and ascribing intelligence — even personhood — to flowers and trees. But like responsive robots, plants can have smarts programmed into them. “So sure, investigate how plants interact with their environment,” he advises. “But use proper, non-personal language. They are plants.” Let’s do that, and look at some of the superior programming that makes plants look smart because their design is smart

Leaf Recycling

Science Magazine notes that “leaf recycling is a two-step process.” Leaves don’t just curl up and die on a cold day. That algorithm would be too simplistic, and potentially harmful to the tree if warm sunny days follow. Actually, two signaling molecules — strigolactone and ethylene — can work independently to begin the process of leaf senescence (pictured above), but together, they work in synergy. “This multistep process probably preserves leaves when possible, only carrying through to leaf senescence when the stress becomes too much

Nitrogen Fixing

Separating molecular nitrogen’s triple bond requires a lot of energy and pressure when humans do it, but some plants do it with ease, utilizing the capabilities of nitrogen-fixing bacteria. These bacteria have an enzyme called nitrogenase that so far has defied our attempts to understand it or duplicate it. Even though legumes outsource the work, they regulate their symbiotic partners’ activity depending on nitrogen availability in the soil, according to researchers at Chapman University. This does not require plants to be sentient. We are all familiar with machines like thermostats, rheostats, and governors that can adjust their work depending on environmental conditions

Climbing

Some plants and animals produce tentacles (in plants, tendrils) that can grab things. At Iowa State University, scientists are attempting to create (so far with only partial success) artificial tentacles that can wrap around delicate objects. The tendrils in ivy and other climbing plants are touch-sensitive. Contact changes the concentration of hormones in the tendril so that growth is accelerated on the far side, producing curvature. As a result, the tendril wraps around the object so that the plant can anchor itself to something firm. Time-lapse photos of ivy growing up a wall might look like the action of an intelligent agent. We see from Iowa State’s biomimetic experiments, though, that the intelligence is imposed by the agent. It’s a matter of programming with the right materials.

Watching the Clock

Every living thing keeps time, and plants are no exception. In fact, they have two clocks, says Duke University:

Time management isn’t just important for busy people — it’s critical for plants, too. A Duke University study shows how two biological clocks work together to help plants deal with intermittent demands such as fungal infections, while maintaining an already-packed daily schedule of activities like growth.

The anthropomorphic language might make it seem that plants are like people, but time management regulation can be programmed, as we know from our own machines that contain timers or sun sensors. Researchers at Duke showed this by chemically altering the circadian rhythms in Arabidopsis plants to see how the “morning” clock and the “evening” clock interacted. In the process, they identified a regulating gene named NPR1 that links the two clocks. Their work is published in Nature:

Mathematical modelling and subsequent experiments show that NPR1 reinforces the circadian clock without changing the period by regulating both the morning and the evening clock genes. This balanced network architecture helps plants gate their immune responses towards the morning and minimize costs on growth at night. Our study demonstrates how a sensitive redox rhythm interacts with a robust circadian clock to ensure proper responsiveness to environmental stimuli without compromising fitness of the organism.

Separating Behavior from Intelligence

Intelligent agents can exhibit behavior, but not all behaving entities are intelligent agents. For example, the Curiosity rover on Mars might look to an alien visitor like a sentient being acting autonomously. Its behavior, however, has been programmed into it. Some of that behavior runs from embedded instructions in its software; some of its actions are controlled by sentient beings millions of miles away. It would be fallacious to call Curiosity “intelligent” or a “person.”

This is the fallacy Adrian Barnett toyed with in his book review for New Scientist that Wesley Smith wrote about. Barnett stated that “plants are smart” as if they conjured up their intelligence by themselves; it’s only our “serious parochialism” that makes us unable to appreciate “intelligence not as we know it.”

Another reviewer in Nature, Ian T. Baldwin commits the same fallacy, though in a more nuanced way. A plant scientist, Baldwin reviewed three new books on plant behavior, including the one by Richard Karban that Barnett reviewed in New Scientist. 

The food writer Michael Pollan, author of The Omnivore’s Dilemma (Penguin, 2006) among others, wrote an article in The New Yorker in 2013 exploring why terms such as intelligence, memory and even behaviour have been contentious for plant scientists.His thesis boils down to a divide in biology that allows zoologists to use anthropomorphic terms, but denies the privilege to plant scientists. Pollan allies himself with a small band of intrepid researchers crusading against the “cerebrocentric” view that permits behaviour only to organisms with brains. He tells of collateral damage from sensationalist treatments that exaggerate plant-science findings, and of glimmers of a new sensitivity towards all life.

Pollan identifies an interesting story about the development of an emerging scientific field, and the baggage that scientists bring to their work. The idea that plants are ‘smarter’ than their immobility suggests is now supported by rigorous experimentation and fieldwork that are uncovering the genes and chemicals that mediate plants’ environmental intelligence. We know now that much of a plant’s rich behavioural repertoire is hard to observe because it is played out in a chemical arena. Plants overcome the constraints of immobility mainly by harnessing their prowess as synthetic organic chemists. For instance, floral scents contain compounds that attract pollinating animals and repel flower-eating ones. Nectar is a brew of nutrients and toxins that optimize the behaviour of pollinators. Much of the relevant literature is now synthesized in three books by leading researchers in the field: Edward Farmer’s Leaf Defence, Anthony Trewavas’s Plant Behaviour and Intelligence and Richard Karban’s Plant Sensing and Communication.

The fallacy is obvious when you imagine him writing a similar exaltation of “rover intelligence” after observing Curiosity’s behavior. Would it make any sense to praise Curiosity’s “prowess as a synthetic organic chemist”? 

Baldwin gave the three books varying degrees of commendation. Excited as he is by the resurgence of interest in plant behavior, he understands that these “phytomorphic” activities must be understood mechanistically and biochemically.

The root of the fallacy, though, is Darwinian thinking. It allows no room for human exceptionalism. To the evolutionist, humans differ not in kind but in degree. Animal and plant intelligence is just as self-generated as that “emerging” from our physical brains. While they can partially see how anthropomorphism is misleading, they cannot draw a divide between us and them. That’s why Baldwin praises Trewavas for thinking like a plant and avoiding animal envy:

Trewavas, by contrast, moves effortlessly from mechanistic research to invigorating insights into real-world plant behaviour. Plant Behaviour and Intelligence is a wild ride, covering ground from the origins of life to intelligent nutrient-foraging behaviour in the roots of higher plants. Trewavas’s five decades of research into plants’ molecular biology and physiology, and their evolution as self-organizing systems, make him fully ‘phytomorphized’. He thinks like a plant, effortlessly calling on specific traits to look at how plants solve problems in similar ways to social insects — from siphonogamy (in which pollen tubes carry sperm cells to egg cells) to highly dispersed sensory systems. He celebrates behaviour in plants while avoiding “animal envy”.

Darwinian thinking unravels, though, when you see it cannot be sustained logically. For one thing, Baldwin and Barnett use their own sentience, including conscious purposeful choice, to ascribe it to plants and animals. This would be like Curiosity coming into contact with Opportunity and deciding it was an independent, autonomous, intelligent being that emerged from the Martian soil like itself. 

For another logical short-circuit, Darwinians routinely ascribe motives and goals to plants and animals, even when they deny this is possible. The unguided neo-Darwinian mechanism cannot see a distant target and move toward it. Baldwin says that plant defenses “evolved primarily to thwart herbivores.” He says “leaves evolved to have particular traits.” Nothing in Darwinism allows the phrase “evolve to” in foresight or in hindsight. Such language is just as misleading as anthropomorphism.

The only logically self-consistent position is to see plants and animals as possessing design impressed on them by an outside intelligent cause. In this way, we can appreciate and study the rational design in plants that makes their behaviors so interesting (and often worth imitating). Our physical bodies and brains also carry the imprint of design, but we humans have the additional gift of conscious self-awareness that allows us to choose our behaviors. This sets us apart from the rest of the living world. It’s the reason we use reason to study plants, but plants do not study us.

Homology=Common Ancestry?

 

In the beginning there was information?

 

Phillipians chapter 3 verses 1 through 9 New international Version.

 1Further, my brothers and sisters, rejoice in the Lord! It is no trouble for me to write the same things to you again, and it is a safeguard for you. 2Watch out for those dogs, those evildoers, those mutilators of the flesh. 3For it is we who are the circumcision, we who serve GOD by his Spirit, who boast in Christ Jesus, and who put no confidence in the flesh— 4though I myself have reasons for such confidence.

If someone else thinks they have reasons to put confidence in the flesh, I have more: 5circumcised on the eighth day, of the people of Israel, of the tribe of Benjamin, a Hebrew of Hebrews; in regard to the law, a Pharisee; 6as for zeal, persecuting the church; as for righteousness based on the law, faultless.

7But whatever were gains to me I now consider loss for the sake of Christ. 8What is more, I consider everything a loss because of the surpassing worth of knowing Christ Jesus my Lord, for whose sake I have lost all things. I consider them garbage, that I may gain Christ 9and be found in him, not having a righteousness of my own that comes from the law, but that which is through faith in a Christ—the righteousness that comes from GOD on the basis of faith. 

The idolising of necessity and chance is the real science stopper?

 The Best and Worst Heuristics for Biological Discovery

Paul Nelson

The bad news first. What’s the worst possible heuristic for making biological discoveries?

We don’t know what this structure does, so it probably does nothing. Remember, evolution produces a lot of non-functional debris.

What’s the best heuristic?

We don’t know what this does. Let’s find out.

Here’s a case in point at Cell. It’s open access and incredibly cool and interesting:

“Mammalian oocytes store proteins for the early embryo on cytoplasmic lattices”

According to the Summary section:

Mammalian oocytes are filled with poorly understood structures called cytoplasmic lattices. First discovered in the 1960s and speculated to correspond to mammalian yolk, ribosomal arrays, or intermediate filaments, their function has remained enigmatic to date. Here, we show that cytoplasmic lattices are sites where oocytes store essential proteins for early embryonic development. Using super-resolution light microscopy and cryoelectron tomography, we show that cytoplasmic lattices are composed of filaments with a high surface area, which contain PADI6 and subcortical maternal complex proteins. The lattices associate with many proteins critical for embryonic development, including proteins that control epigenetic reprogramming of the preimplantation embryo. Loss of cytoplasmic lattices by knocking out PADI6 or the subcortical maternal complex prevents the accumulation of these proteins and results in early embryonic arrest. Our work suggests that cytoplasmic lattices enrich maternally provided proteins to prevent their premature degradation and cellular activity, thereby enabling early mammalian development.

Kraken released?

 Fossil Friday: Triassic Kraken Hypothesis Provoked Scornful Darwinist Revenge

Gunter Bechly

Professor Mark McMenamin is a maverick paleontologist and critic of neo-Darwinism, who is known for very interesting but controversial hypotheses like Hypersea (McMenamin & Schulte McMenamin 1993, 1994, Zimmer 1995), The Garden of Ediacara (McMenamin 1986, 1998), Paleotorus (McMenamin 2009), and the Triassic Kraken (McMenamin & Schulte McMenamin 2011, 2013, McMenamin 2023). The latter hypothesis has met with particularly scornful skepticism from his peers (Simpson 2011, Switek 2011, Than 2011, DNews 2013, Pappas 2013, Viegas 2016, HourDark 2020), and of course from the usual suspects, i.e., activists of the Darwinian thought police like P. Z. Myers (2011) and Donald Prothero (2011, 2013). It has even been called a “dangerous speculation” (Dresow 2022).

An Admittedly Bold Hypothesis

McMenamin’s kraken hypothesis has never been published in a peer-reviewed journal but was only proposed in two congress abstracts (McMenamin & Schulte McMenamin 2011, 2013), a magazine article (McMenamin 2012), and a book chapter (McMenamin 2016). It was also covered by numerous sensationalist press releases and media reports (Bryner 2011, Flatow 2011, GSA 2011, Herald Sun 2011, IB Times 2011, Leach 2011, Praetorius 2011, Wang 2011). The admittedly bold hypothesis claims that a gigantic 100-foot Triassic cephalopod killed large ichthyosaurs and arranged their bones in a self-portrait-like pattern. The main evidence is a curious biserial pattern of ichthyosaur vertebrae at the Berlin-Ichthyosaur State Park in Nevada, which mimics the pattern of suckers on a cephalopod tentacle. Meanwhile, a second locality with this pattern was discovered in Switzerland (Sander et al. 2022). Just this year, McMenamin described a large cephalopod beak from the same Triassic layers in Nevada, which could directly confirm the actual existence of the postulated “kraken” (McMenamin 2023, also see Pappas 2013).

Nevertheless, instead of a reasonable and fair scientific debate, McMenamin’s hypothesis has been ridiculed by other scientists and science journalists. Of course, this was totally unrelated (irony warning) to the fact that McMenamin is an outspoken critic of neo-Darwinism and has dared to write a positive review for an ID documentary based on Stephen Meyer’s book Darwin’s Doubt at Amazon (McMenamin 2010), just a year before the publication of his kraken hypothesis. He was even accused by vicious activists in the skeptic movement (Prothero 2013) of being a “creationist” himself, even though a fair reading of his review clearly shows that he is not. Others were not beneath abusing McMenamin with the insulting nick name McMinimal (Simpson 2011).

An Inconvenient Thinker

To be clear: There are some good scientific arguments against McMenamin’s interpretation (e.g., the fact that basal fossil coleoids from the Mesozoic all had uniserial suckers; see Anonymous 2020, Greenfield 2021), and his kraken hypothesis may very well be wrong. However, the way he and his hypothesis were treated by the scientific community is far from impartial. It is clearly driven by the desire to marginalize and ostracize an inconvenient thinker — who made the big mistake of showing sympathy for the ID movement — as a foolish crackpot who should be ignored. McMenamin is lucky to have a tenured position as college professor, because his opponents would not shy away from destroying his career as they tried or successfully did with other dissidents who think outside the box. I can tell you a thing or two about that myself. So much for objective science and academic freedom.

An interlude IX

 

No laughing matter?

 

The bitter fruit of the imperium?

 

File under "Well said" CI

 "He will guard the feet of his faithful servants,

but the wicked will be silenced in the place of darkness.

“It is not by strength that one prevails;"

1Samuel chapter 2 verse 9 New International Version.

High noon for OOL Science's gatekeepers.

 On Origin of Life, Chemist James Tour Has Successfully Called These Researchers’ Bluff

Brian Miller

David Klinghoffer and Tova Forman previously wrote about Rice University chemist James Tour’s 60-day challenge to leading origin-of-life researchers to demonstrate that the field had substantively advanced in the past seventy years (here,here). Tour offered to remove all his videos on the topic if three leading experts agreed that any of five fundamental problems had been solved:

Linking of amino acids into chains (aka polypeptides)

Linking of nucleotides into RNA molecules

Linking of simple sugars (aka monosaccharides) into chains known as polysaccharides 

Origin of biological information

Assembly of components into a cell

Tour issued this challenge in response to the many false claims made by YouTubers, such as Dave Farina, about how these hurdles to life’s origin had been fully addressed. The deadline has expired, and no one has presented solutions to any of the problems. 

The Rules

For the first three problems, Tour allowed origin-of-life researchers to assume a chemical mixture started with amino acids, nucleotides, or sugars with the same handedness (aka enantiomerically pure). For instance, all the amino acids were left-handed as required in modern proteins. For the first problem, participants needed to detail how chains of just two amino acids — aspartic acid and lysine — could have formed with the correct bonds. For the second problem, proposed solutions needed to describe how nucleotides could have linked into chains with less than 2 percent of the wrong linkages. And for the third, proposals needed to explain how molecules of the simple sugar glucose could have properly joined in high yields. 

For the fourth problem, researchers could assume that the first three challenges had been solved. They only needed to explain how amino acids, nucleotides, or simple sugars could have linked together in the correct order to contain the required functional information to perform some biologically relevant task. For the fifth problem, researchers could assume that all cellular components were available in abundance. They only needed to explain how the biological building blocks could have assembled into a functional cell. Proposed solutions for all the problems had to rely only on chemistry that could have occurred on the early Earth. 

The implications of failure

The failure of any origin-of-life expert to propose a solution to even one of the five problems has dire implications for the field. Tour allowed origins researchers to assume unrealistically favorable starting conditions. The hurdles are collosal for life’s constituent molecules to form in sufficiently high concentrations and purities to allow for even the slightest possibility of their linking into proteins, RNA, or complex polysaccharides (here, here). In addition, any cellular component that formed on the early Earth would have decomposed long before finding its way to the staging ground for an aspiring cell. Consequently, even if every problem were fully solved, life’s genesis would still face the insurmountable hurdle of transporting the components of life to the same microscopic environment. 

YouTubers and other defenders of the secular faith of scientific materialism have confidently asserted that scientists are steadily unraveling the mystery of life’s origin. Yet Tour called on leading experts to demonstrate whether they had achieved any real progress in answering any of the most fundamental questions. None could rise to the challenge. 

At some point, both the scientific community and the public will need to recognize that the lack of progress cannot be explained by a lack of serious effort by highly competent scientists but by the philosophical assumptions blinding them from seeing the truth staring them in the face. The answer to life’s origin does not reside in the fields of physics and chemistry but in the mind behind our universe. 

Time for the OOL Establishment to throw down?

 

Against Calvin again.

 

Following the science re: the God hypothesis.

 

Isaiah ch.58 New International Version

 “Shout it aloud, do not hold back.

Raise your voice like a trumpet.

Declare to my people their rebellion

and to the descendants of Jacob their sins.

2For day after day they seek me out;

they seem eager to know my ways,

as if they were a nation that does what is right

and has not forsaken the commands of its God.

They ask me for just decisions

and seem eager for God to come near them.

3‘Why have we fasted,’ they say,

‘and you have not seen it?

Why have we humbled ourselves,

and you have not noticed?’

“Yet on the day of your fasting, you do as you please

and exploit all your workers.

4Your fasting ends in quarreling and strife,

and in striking each other with wicked fists.

You cannot fast as you do today

and expect your voice to be heard on high.

5Is this the kind of fast I have chosen,

only a day for people to humble themselves?

Is it only for bowing one’s head like a reed

and for lying in sackcloth and ashes?

Is that what you call a fast,

a day acceptable to the LORD?

6“Is not this the kind of fasting I have chosen:

to loose the chains of injustice

and untie the cords of the yoke,

to set the oppressed free

and break every yoke?

7Is it not to share your food with the hungry

and to provide the poor wanderer with shelter—

when you see the naked, to clothe them,

and not to turn away from your own flesh and blood?

8Then your light will break forth like the dawn,

and your healing will quickly appear;

then your righteousness a will go before you,

and the glory of the LORD will be your rear guard.

9Then you will call, and the LORD will answer;

you will cry for help, and he will say: Here am I.

“If you do away with the yoke of oppression,

with the pointing finger and malicious talk,

10and if you spend yourselves in behalf of the hungry

and satisfy the needs of the oppressed,

then your light will rise in the darkness,

and your night will become like the noonday.

11The LORD will guide you always;

he will satisfy your needs in a sun-scorched land

and will strengthen your frame.

You will be like a well-watered garden,

like a spring whose waters never fail.

12Your people will rebuild the ancient ruins

and will raise up the age-old foundations;

you will be called Repairer of Broken Walls,

Restorer of Streets with Dwellings.

13“If you keep your feet from breaking the Sabbath

and from doing as you please on my holy day,

if you call the Sabbath a delight

and the LORD'S holy day honorable,

and if you honor it by not going your own way

and not doing as you please or speaking idle words,

14then you will find your joy in the LORD,

and I will cause you to ride in triumph on the heights of the land

and to feast on the inheritance of your father Jacob.”

The mouth of the LORD has spoken.

Necessity and chance can't bring us truth,beauty and goodness?

 Why Scientific Materialism Is No Match for Truth, Beauty, and Goodness

Andrew McDiarmid

Is the world a good place? Is truth relative? Can beauty be defined? On a classic episode of ID the Future, host David Klinghoffer speaks with biologist Dr. Ann Gauger, a Senior Fellow with Discovery Institute’s Center for Science and Culture, about her article “The Transcendental Treasury of Truth, Beauty, and Goodness” for Evolution News. 

These abstract concepts don’t derive from the material world, yet we feel impoverished without them; they’re foundations of a life worth living. Truth, says Klinghoffer, has fallen on hard times these days. Gauger calls truth a correspondence with reality and says we must have it to thrive. “Truth is essential for our lives,” says Gauger. “We can’t function in a society that isn’t based on truths. It’s destructive to families, it’s destructive to the culture, it’s destructive to political action.” Materialistic evolutionary explanations for truth, beauty, and goodness are out there, but they fall flat upon closer inspection. Some of them even reduce these qualities to mere illusion. Gauger holds that truth, beauty, and goodness are hallmarks of a designed world. Meditating on them can promote a spirit of gratitude, an important part of a healthy, happy life. Download the podcast or listen to it here.

No one is safe.

 BREAKING NEWS | Explosion at Convention in India

JW.org

On Sunday, October 29, 2023, at least two bombs exploded at the regional convention held in Kerala, India. The incident occurred just after the opening prayer.

According to initial reports, two of our sisters were killed. At least 55 individuals were injured. There were over 2,200 people in attendance. The police are currently investigating the situation. Our thoughts and prayers are with all those affected by this tragedy.—Psalm 9:9.

Ps. Luke ch.9:24NIV"For whoever wants to save their life will lose it, but whoever loses their life for me will save it."

It's ID all the way up?

 Intelligent Design at High Altitudes

David Coppedge

Jay Storz at the University of Nebraska was hiking with colleagues on one of the most godforsaken habitats on the planet: windswept, low-oxygen volcanic peaks in Argentina. It was like exploring Mars. That was until they found carcasses of mummified mice beside a rock pile. How did they get there? It’s freezing. There’s no food. There’s no water. Everywhere one looks there is only bare rock. Phys.org quotes Dr. Storz:

Well-trained mountain climbers can tolerate such extreme elevations during a one-day summit attempt, but the fact that mice are actually living at such elevations demonstrates that we have underestimated the physiological tolerances of small mammals.” 

Once they knew what to look for, they found over a dozen other mice remains on 18 summits above 6,000 meters (19,500 feet). Radiocarbon dating showed they had died within the last few hundred years.

The evidence indicated that the mice were not one-day visitors scampering up for the view but were members of populations thriving at that elevation.

“The discovery of the mouse mummies on the summits of these freezing, wind-scoured volcano summits was a huge surprise,” Storz says. “In combination with our live-capture records of mice on the summits and flanks of other high elevation Andean volcanoes, we are amassing more and more evidence that there are long-term resident populations of mice living at extreme elevations.”

A Personal Experience

It reminded me of a personal experience (pictured above) at a lower elevation that was near my limit: the 14,500-foot summit of California’s Mount Whitney, highest peak in the contiguous 48 states. I can only imagine the difficulty hiking up another 5,000 feet in the Andes. Gasping for air every 20 steps or so as I forced myself to the top of my unimpressive peak-bagging record, I was greeted by eager marmots and birds looking for handouts like they were on a picnic. 

The finding now raises important questions, including how mammals can live in a barren world of rock, ice, and snow where the temperatures are never above freezing, and there is roughly half the oxygen available at sea level. It’s not clear why the mice would have climbed to such heights.

The paper by Storz and colleagues in Current Biology doesn’t mention evolution or natural selection. Genetic tests on the mice, identified as members of Phyllotis vaccarum, did not indicate any noteworthy differences from the populations that live at lower elevations. 

Average genome-wide pairwise nucleotide diversity for the total sample of mice was typical for natural populations of rodents (π = 0.42%). After filtering our dataset to 42 mice, excluding two closely related individuals, we confirmed that the summit mice exhibited close affinities to the Phyllotis vaccarum reference genome and other live-trapped specimens of P. vaccarum from lower elevations on the flanks of the same volcanoes and in the surrounding Altiplano (Figure 1B,C). Results of a model-based clustering analysis revealed very low population structure in the total sample, as proportional assignments of ancestry to genetically defined clusters were similar for mice from all localities (Figure 1B). A principal component analysis of genomic variation also revealed low levels of population structure across the surveyed region, as PC1 and PC2 explained only 6.94% and 2.36% of total variation, respectively, and the patterning of variation did not distinguish the set of summit mice from mice collected at less extreme elevations in the surrounding region

Conclusion: scientists had underestimated the adaptability of small mammals to extreme elevations. “Such extreme elevations were previously assumed to be completely uninhabitable by mammals,” they said. The results “challenge assumptions about the environmental limits of vertebrate life and the physiological tolerances of small mammals.”

High-Altitude Humans

A large team of 22 mostly Italian researchers, publishing by the bioRxiv preprint server, discusses their opinions on how “Convergent evolution of complex adaptive traits enabled human life at high altitudes.” As a side anecdote, one of the authors, a member of the Mount Everest Summiters Club in Nepal, has the listed surname “Sherpa” — the word indicating those noble but underappreciated guides who help flatlanders carry their packs up the highest mountains on Earth. They trot around on those trails like it’s a walk in the park.

This team does invoke evolutionary theory. They looked for genetic clues of adaptation by natural selection for people groups who live at high elevations. 

Convergent adaptations represent paradigmatic examples of the capacity of natural selection to influence organisms’ biology. However, the possibility to investigate genetic determinants underpinning convergent complex adaptive traits has been offered only recently by methods for inferring polygenic adaptations from genomic data. Relying on this approach, we demonstrate how high-altitude Andean human groups experienced pervasive selective events at angiogenic pathways, which resemble those previously attested for Himalayan populations despite partial convergence at the single-gene level was observed. This provides unprecedented evidence for the drivers of convergent evolution of enhanced blood perfusion in populations exposed to hypobaric hypoxia for thousands of years.

Note to the Authors

The people groups in the study are all members of Homo sapiens. They are fully human, interfertile members of humankind. 

In conclusion, the obtained results highlighted polygenic mechanisms mediated by adaptive evolution of several focal adhesion genes as the possible drivers of enhanced angiogenesis and oxygen transport in Andean human groups similarly to what previously observed in Tibetan/Sherpa populations, thus providing unprecedented evidence for the molecular bases of their convergent adaptation to hypobaric hypoxia.

While it may be interesting to compare genomes between mountaineers and flatlanders, nothing in the data requires a Darwinian interpretation. They could only say that certain genes were “possible drivers” of angiogenesis and oxygen transport in the mountaineers. Note the level of speculation in their previous paragraph:

Interestingly, LAMA1/2/3, COL1A2/2A1/4A2, and ITGA2/4/8/11 have been previously found to participate to gene networks targeted by natural selection in Tibetan and Sherpa populations. Such an incomplete genetic convergence between Andean and Himalayan high-altitude peoples is not unexpected within the framework of an evolutionary scenario largely characterized by polygenic adaptive events, in which single loci play a negligible role with respect to their overall synergic interactions. Nevertheless, we provided evidence for the same biological functions/pathways (i.e., those related to angiogenetic processes) having adaptively evolved in both the considered populations, plausibly in response to the selective pressure imposed by hypobaric hypoxia. The identified genetic signatures might indeed contribute to the increase in the density of blood vessels that results in an improved blood flow and oxygen delivery to tissues despite the hypoxic stress, which is an adaptive trait qualitatively (but not quantitatively) similar between Andean and Himalayan groups (Gnecchi-Ruscone et al., 2018; Sharma et al., 2022; Wu et al., 2022). In fact, such a trait appears to be more enhanced and generalized in Tibetan/Sherpa populations with respect to Andean ones, being especially limited to improved uterine artery blood flow during pregnancy in the latter groups (Beall, 2007; Julian & Moore, 2019). The fact that several of the adaptive loci identified in the present study (e.g., PTK2, VEGFA, PDGFA, and PDGFD) play a pivotal role in the development of vascular tissue specifically in placenta and embryo, and thus in the establishment of efficient maternal-fetal circulation (Shen et al., 2005; Adams & Alitalo, 2007; Khankin & Karumanchi, 2010; Russell et al., 2019), seems to support such an observation. Moreover, it might suggest that natural selection succeeded in optimizing angiogenesis in Andean individuals mainly in early life and/or at the reproductive stage, thus leading to improved fetal development during intrauterine life (e.g., in terms of maturation of the respiratory system), which represents a key aspect to reduce neonatal mortality at high altitudes where efficiency of respiratory functions is crucial to ensure the individual’s survival.

Might” Does Not Make Right

How many babies had to die in the womb before the essential genes to survive hypobaric hypoxia mutated in lucky zygotes to allow them to tolerate the thin air? How many mothers and fathers needed the same mutations? How many adults perished waiting for the beneficial mutations to become fixed in the population? (This is called “the cost of selection” in the literature.) 

To follow their example of “possibilities” and “suggestions” in scientific explanation, let’s suggest the possibility that early mountain climbers used their human reason to evaluate all the funerals in the high-altitude camp, concluding, “You know, this was a bad idea. Let’s go back to the coast.”

The engineering model of adaptation being developed by the design community looks at the observable genetic variations differently. Rather than depending on lucky cosmic rays to turn genes into super angiogenesis machines and oxygen transport systems, they identify built-in mechanisms that receive signals from the environment and switch on internal controls that respond to the conditions. Heritable adaptations by epigenetic processes could occur quickly, because they are driven not by random mutations but by foresight and intention in their engineered design. 

Moreover, design advocates are not surprised by seeing organisms that are over-engineered for survival, like the mountain mice and the Nepal sherpas. Darwinism has a problem with over-engineered things since it cannot see past the immediate present. We can make this prediction for design theory: fewer human mummies in the Himalayas with desperate expressions on their faces, waiting for the lucky mutations to arrive.

Further rants against exhaustive determinism.

 

Letting scripture interpret scripture..

 John ch.6:44NKJV"No one can come to Me unless the Father who sent Me draws him; and I will raise him up at the last day. "

Some claim to see in this text support for the doctrine of eternal exhaustive predeterminism . But why not let the scriptures speak for themselves though.

Luke ch.11:9,10NIV"“So I say to you: Ask and it will be given to you; seek and you will find; knock and the door will be opened to you. 10For EVERYONE who asks receives; the one who seeks finds; and to the one who knocks, the door will be opened."

Acts ch.17:27NKJV"so that they should seek the Lord, in the HOPE that they might grope for Him and find Him, though He is not far from each one of us;"

Of course if all outcomes are exhaustively predetermined from infinity there is no hope  for and God is far away from most of us having doomed us from infinity.

Why do some ask and not receive though?

James ch.4:3NIV"When you ask, you do not receive, because you ask with wrong motives, that you may spend what you get on your pleasures."

Are you seeking a knowledge of objective spiritual truth or vindication of pre-conceived biases?

                Is God a genie who grants desires? Or a wise instructor from which to receive needed correction and a compassionate Father who provides needed discipline?

Psalms Ch.141NKJV"Let the righteous strike me;

It shall be a kindness.

And let him rebuke me;

It shall be as excellent oil;

Let my head not refuse it.

For still my prayer is against the deeds of the wicked."

Determinism's apostle?

 

Yet another defence of free moral agency.

 

Genesis chapter four New International Version.

 Adam a made love to his wife Eve, and she became pregnant and gave birth to Cain. b She said, “With the help of the LORD I have brought forth c a man.” 2Later she gave birth to his brother Abel.

Now Abel kept flocks, and Cain worked the soil. 3In the course of time Cain brought some of the fruits of the soil as an offering to the LORD. 4And Abel also brought an offering—fat portions from some of the firstborn of his flock. The LORD looked with favor on Abel and his offering, 5but on Cain and his offering he did not look with favor. So Cain was very angry, and his face was downcast.

6Then the LORD said to Cain, “Why are you angry? Why is your face downcast? 7If you do what is right, will you not be accepted? But if you do not do what is right, sin is crouching at your door; it desires to have you, but you must rule over it.”

8Now Cain said to his brother Abel, “Let’s go out to the field.” d While they were in the field, Cain attacked his brother Abel and killed him.

9Then the LORD said to Cain, “Where is your brother Abel?”

“I don’t know,” he replied. “Am I my brother’s keeper?”

10The LORD said, “What have you done? Listen! Your brother’s blood cries out to me from the ground. 11Now you are under a curse and driven from the ground, which opened its mouth to receive your brother’s blood from your hand. 12When you work the ground, it will no longer yield its crops for you. You will be a restless wanderer on the earth.”

13Cain said to the LORD, “My punishment is more than I can bear. 14Today you are driving me from the land, and I will be hidden from your presence; I will be a restless wanderer on the earth, and whoever finds me will kill me.”

15But the LORD said to him, “Not so e ; anyone who kills Cain will suffer vengeance seven times over.” Then the LORD put a mark on Cain so that no one who found him would kill him. 16So Cain went out from the LORD'S presence and lived in the land of Nod, f east of Eden.

17Cain made love to his wife, and she became pregnant and gave birth to Enoch. Cain was then building a city, and he named it after his son Enoch. 18To Enoch was born Irad, and Irad was the father of Mehujael, and Mehujael was the father of Methushael, and Methushael was the father of Lamech.

19Lamech married two women, one named Adah and the other Zillah. 20Adah gave birth to Jabal; he was the father of those who live in tents and raise livestock. 21His brother’s name was Jubal; he was the father of all who play stringed instruments and pipes. 22Zillah also had a son, Tubal-Cain, who forged all kinds of tools out of g bronze and iron. Tubal-Cain’s sister was Naamah.

23Lamech said to his wives,

“Adah and Zillah, listen to me;

wives of Lamech, hear my words.

I have killed a man for wounding me,

a young man for injuring me.

24If Cain is avenged seven times,

then Lamech seventy-seven times.”

25Adam made love to his wife again, and she gave birth to a son and named him Seth, h saying, “GOD has granted me another child in place of Abel, since Cain killed him.” 26Seth also had a son, and he named him Enosh.

At that time people began to call on i the name of the LORD.

World atlas on the unChristian cross

  The Christian cross is regarded as the primary symbol of the Christian religion. The cross is a symbol of the instrument of the crucifixion of Jesus Christ. In Christianity, a crucifix is a cross with a three-dimensional representation of the body of Christ. The two most common forms of crosses present in the Christian religion are the Greek cross and the Latin cross.

The Pre-Christian Cross

A vast body of evidence shows that the cross was used centuries before the birth of Christianity. The cross is thought to have originated from the ancient Babylonians before its spread to other parts of the world such as Syria, Egypt, Greek, Latin, India, and Mexico. The pre-Christian cross was used as a religious symbol and as an ornament among the Egyptians, Syrians, Greeks, Persians, Europeans, and in some parts of Africa. There was, therefore, universal use of the pre-Christian cross. In many cases, its use was usually connected to some form of worship.

The pre-Christian cross existed in two forms; the tau cross and the svastika or fylfot cross. The tau cross resembles the Greek capital letter T. On the other hand, the fylfot cross resembles four Greek capital letter G's placed together. The tau cross was initially used among the pagans. It was later adopted by the Christians in Egypt where its use became common. For this reason, the tau cross is sometimes referred to as the Egyptian cross.

Evidence of the use of the cross centuries before the coming of Christ can be seen in British Museum on the effigy of King Samsi-Vul of Assyria. Besides, goddess Diana of the ancient Greeks is portrayed with a cross in a way that resembles how Virgin Mary is portrayed in statues by artists.

History Of The Christian Cross

The Christian cross as a Christian symbol has its roots in ancient paganism. The use of the Christian cross as a Christian symbol began after the time of the Constantine, which occurred three centuries after the coming of Christ. The crucifixion and death of Jesus on the cross conferred a new significance to the use of the cross in Christianity. Before the death of Jesus on the cross, the cross was used privately among Christians. Its purpose was restricted. After the Constantine, the use of the cross was acknowledged as a symbol of Christianity.

Modern Usage Of The Christian Cross

Today, the use of the cross as a Christian symbol in practiced universally. Churches, both Catholic and Protestant have crosses placed, carved, or drawn on the doors, windows, tops, and walls of their church buildings. Many Christians all over the world wear the cross on their necklaces, bracelets, rings, items of clothing, and key chains. Besides, many Christians, especially Catholics, make the sign of the cross during worship. When making the sign, the people touch their forehead, chest, and then each shoulder. Many believe that the sign of the cross is effective in protecting them from harm and driving away evil spirits.

The throne of the beast.

Luke ch.4:5,6NIV"The devil led him up to a high place and showed him in an instant all the kingdoms of the world. 6And he said to him, “I will give you all their authority and splendor; it has been given to me, and I can give it to anyone I want to. "

Of course if there was no truth to Satan's claims then this offer would be no test of the our Lord's loyalty to his Lord i.e JEHOVAH God.

This why the sincere truthseeker must make a clean break with politics and nationalism if he is serious about attaining an intimate relationship with the one true God.

Revelation ch.13:2-4NIV"The beast I saw resembled a leopard, but had feet like those of a bear and a mouth like that of a lion. The dragon gave the beast his power and his throne and great authority. 3One of the heads of the beast seemed to have had a fatal wound, but the fatal wound had been healed. The whole world was filled with wonder and followed the beast. 4People worshiped the dragon because he had given authority to the beast, and they also worshiped the beast and asked, “Who is like the beast? Who can wage war against it?”"

There is a reason why this visionary beast is an amalgam of the beasts in Daniel's prophecy see Daniel ch.7. It demonstrates that any first century fulfillments of Daniel's prophecy were merely tokens of larger more complete fulfillment to come. And also it alerts JEHOVAH'S People of JEHOVAH'S judgement against the bloodstained global political elite and its enablers and aspirants. Of course JEHOVAH Needs NO human help in dealing with his enemies thus any religiopolitical faction that teaches and behaves as if he does. Whether it claims to be Christian or not makes itself liable to the Judgement upon the "beast".

Revelation ch.13:8-10NKJV"All who dwell on the earth will worship him, whose names have not been written in the Book of Life of the Lamb slain from the foundation of the world.

9If anyone has an ear, let him hear. 10He who leads into captivity shall go into captivity; he who kills with the sword must be killed with the sword. Here is the [e]patience and the faith of the saints."

A robust case for design II.

 Understanding the Biochemistry — and Intelligent Design — of Muscle Contraction

Jonathan McLatchie

In an article yesterday, I gave a short overview of the arrangement and structure of muscles. Here, I will describe the biochemistry of muscle contraction. Readers may find it slightly easier to follow the discussion that follows by first viewing this short animation, which describes the sliding filament model of muscle contraction.

The Structure of a Muscle Fiber

previously noted that muscles contain thousands of cylindrical cells called muscle fibers, or myocytes. The motor neuron terminates at the muscle fiber’s neuromuscular junction. The tip of the motor neuron is known as the axon terminal, and it contains sacs of acetylcholine, an important neurotransmitter involved in muscle contraction. The muscle fiber also has a membrane called the sarcolemma, containing acetylcholine receptor sites, in addition to an inactivator called cholinesterase. The small space between the sarcolemma and axon terminal is called the synapse, or synaptic cleft.

The muscle fiber contains thousands of individual contracting units known as sarcomeres. These are organized end-to-end in cylinders known as myofibrils. In the center of the sarcomere are thick filaments comprised predominantly of the protein myosin, and thin filaments containing actin can be found at the ends, attached to the end boundaries of the sarcomere (known as the Z discs) by the protein titin. The structure of the muscle fiber is shown in the figure below:

Muscle contraction is driven by two contractile proteins — myosin and actin. Each myosin molecule consists of a long tail and a globular head. Myosin heads have ATPase activity, which allows them to hydrolyze ATP to generate energy for muscle contraction. Myosin heads also have binding sites for actin and ATP. Actin has binding sites for myosin heads. However, these binding sites are typically covered by two inhibitory proteins known as tropomyosin and troponin when the muscle is relaxed. These inhibitory proteins prevent the sliding of myosin and actin during relaxation of the muscle fiber.

The sarcomeres are surrounded by the sarcoplasmic reticulum (the muscular equivalent of the endoplasmic reticulum), which serves as a reservoir of calcium ions (Ca2+). As we shall see, Ca2+ ions are required for muscle contraction.

Polarization of the Sarcolemma

When a muscle fiber is in a state of relaxation, the sarcolemma has a resting potential, or is said to be polarized. This refers to the difference in electrical charges between the inside and outside. When the sarcolemma is polarized, there is a positive charge outside relative to the negatively charged inside. There is a greater concentration of sodium ions (Na+) outside the cell and a greater concentration of potassium ions (K+) and negative ions inside the cell.

Because of the concentration gradient, the Na+ ions tend to diffuse into the cell and the K+ ions tend to diffuse outside. These are actively transported back out and in respectively by the sodium and potassium pumps, which depend upon ATP to maintain polarization and muscle relaxation until a change is stimulated by a nerve impulse.

Depolarization of the Sarcolemma

The first step in muscle contraction is the arrival of a nerve impulse at the axon terminal, stimulating the release of the neurotransmitter acetylcholine. The acetylcholine diffuses across the synapse and binds to acetylcholine receptors on the sarcolemma. This renders the sarcolemma extremely permeable to Na+ ions, which rapidly enter the cell. This reverses the charges such that there is now a positive charge on the inside of the sarcolemma relative to the outside. This charge reversal is known as depolarization.

Inward folds on the sarcolemma known as transverse tubules (or, T tubules) carry this electrical impulse (referred to as an action potential) to the interior of the muscle cell. Depolarization triggers the release of Ca2+ ions from the sarcoplasmic reticulum. These bind to the troponin-tropomyosin complex, moving it away from the actin filaments.

The Sliding Filament

With the binding sites on actin now available, actin can be bound by the myosin heads, forming cross-bridges. Once the cross-bridges are formed, the myosin heads pivot, pulling the thin filaments towards the center of the sarcomere. This action is called the power stroke and is powered by the energy released when ATP is hydrolyzed. After the power stroke, the myosin heads require ATP to detach from actin. ATP is hydrolyzed into ADP and inorganic phosphate, which energizes the myosin head for the next cycle.

The cycle of cross-bridge formation, power stroke, ATP hydrolysis, and detachment repeats as long as calcium ions are present and ATP is available. This results in the shortening of the sarcomere and, collectively, the entire muscle fiber. This leads to muscle contraction. The force generated by many muscle fibers contracting in unison allows for body movement. The sliding filament model is graphically summarized in the figure below:

Repolarization

Muscle relaxation occurs when the electrical stimulation ceases — resulting in the ionic concentrations inside and outside the cell returning to their resting state. To restore the resting-membrane potential, the Na+ and K+ pumps actively transport sodium ions out of the cell while bringing potassium ions back into the cell. This returns the membrane potential to its polarized, negative resting state, typically around -90mV for muscle cells. Repolarization results in the myosin heads releasing their grip on actin, and calcium ions are actively transported back into the sarcoplasmic reticulum, causing muscle relaxation.

Evidence of Design

As should be apparent from the forgoing discussion, muscle contraction — which we so easily take for granted — is an incredibly complex and elegant process, involving incredible engineering and design. The process of muscle contraction and relaxation requires the coordinated action of actin, myosin, troponin, tropomyosin, acetyl choline, ion channels, and much more. To contend that the phenomenon of muscle contraction arose through a blind and undirected process, one tiny Darwinian step after the other, seems to me to strain credulity.