To chance and necessity be the glory? III

Hummingbird Tongue Design Gets an Upgrade
Evolution News & Views September 11, 2015 3:54 AM

One of the memorable moments in Illustra Media's documentary Flight: The Genius of Birds is the hummingbird tongue animation (see it on YouTube). The unique nectar-trapping mechanism of unfurling flaps (lamellae) on supporting rods that automatically fold over to seal in the nectar was discovered by two biologists at the University of Connecticut in 2011 (see the paper in PNAS). This was cutting-edge science at the time the film was made, because most biologists previously had assumed the tongue worked by simple capillary action.

The two biologists have continued their work since then, spending five years filming hummingbirds in the wild. Now, along with a mechanical engineer who is an expert in fluid mechanics, they have published a new paper in the Proceedings B of the Royal Society that should increase our admiration for the design of this structure. It's not only a nectar trap; the hummingbird tongue is a micropump!

News from UConn Today includes a video clip of the tongue in action (see it by clicking image above; nice soundtrack too). The new findings debunk the notion that capillary action called "wicking" draws nectar up the tongue.

Rico-Guevara explains that a hummingbird's tongue, which can be stuck out about the same length as its beak, is tipped with two long skinny tubes, or grooves. Rather than wicking, he says, the nectar is drawn into the tongue by the elastic expansion of the grooves after they are squeezed flat by the beak.
The tongue structure is collapsed during the time it crosses the space between the bill tip and the nectar pool, but once the tip contacts the nectar surface, the supply of fluid allows the collapsed groove to gradually recover to a relaxed cylindrical shape as the nectar fills it.

When the hummingbird squeezes nectar off its tongue during protrusion, it is collapsing the grooves and loading elastic energy into the groove walls. That energy subsequently facilitates the pumping of more nectar. [Emphasis added.]

This pumping action apparently works in concert with the lamellae (flaps) shown in the Illustra film. What's new is that the cylinders are in a flattened shape when they enter the nectar. Having been compressed by the beak, they store elastic energy that makes them rapidly expand in the fluid as they unfurl. This expansion helps to pump the fluid into the cylindrical cavity upward from the lamellae. That way, more nectar can be delivered into the bird's mouth.

Figure 1 shows the beak in cross-section from a CT scan. It looks beautifully designed to squeeze the tongue's cylinders during protrusion, with the lower bill fitting into spaces in the upper bill that spread laterally to flatten the tongue as it exits the bill tip. This design probably also squeezes the previous load of nectar into the mouth at the same time. "After complete loading, the grooves filled with nectar were brought back inside the bill and squeezed for the next cycle, all in less than a tenth of a second," they observed. The caption for Figure 1 explains how these two mechanisms (pumping and trapping) work together:

The hummingbird tongue fills with nectar even when only the tip is immersed. (a) Hummingbirds can drink from flowers with corollas longer than their bills by extending their bifurcated, longitudinally grooved tongues to reach the nectar. During protrusion, the tongue is compressed as it passes through the bill tip, which results in a collapsed configuration of the grooves (cross-section). (b) Upon reaching the nectar, the tongue tips fringed with lamellae roll open and spread apart, but some of the grooved portions of the tongue will never contact the nectar pool. For the grooves to fill with nectar, they must return to their uncompressed, cylindrical configuration.
Why doesn't the collapsed tongue rebound immediately after it leaves the beak and enters the air? That would result in open tubes that would need to fill by capillary action when they enter the nectar. But capillary action is much slower than the observed filling. Apparently the tongue material is designed to expand upon contact with the nectar. "After contacting the surface, the grooves expanded and filled completely with nectar," they found.

All hummingbirds have this mechanism. They filmed 32 wild birds, representing18 species (in 7 of the 9 main hummingbird clades), with a high-speed camera in natural wild habitats, undergoing hundreds of feeding cycles -- all with the same results. This allowed them to falsify the "century-old paradigm" of the capillary hypothesis and shed new light on this rapid, dynamic process.

All observed licks followed the same pattern: tongue thickness was stable during protrusion of the tongue, and rapidly increased after the tongue tips contacted the nectar... After complete loading, the grooves filled with nectar were brought back inside the bill and squeezed for the next cycle, all in less than a tenth of a second.
Capillary action could not have filled the cylinders this rapidly. In addition, no meniscus (diagnostic of capillarity) was observed to form in any of the 96 video sessions. The pumping action, by contrast, fills the entire tongue in just 14 milliseconds. Here's how it works, according to their new model:

We suggest that while squeezing nectar off the tongue during protrusion, the bird is collapsing the grooves and loading elastic energy into the groove walls that will be subsequently used to pump nectar into the grooves. The collapsed configuration is conserved during the trip of the tongue across the space between the bill tip to the nectar pool. Once the tongue tips contact the nectar surface, the supply of fluid allows the collapsed groove to gradually recover to a relaxed cylindrical shape until the nectar has filled it completely; hereafter, we refer to this previously undocumented mechanism as 'expansive filling'.
The tongue stays flattened and sealed, in short, until it hits the nectar pool. Then, inside the fluid, the tongue's twin cylinders rapidly expand, pumping nectar up into the tongue as it darts into the flower at speeds of a meter per second. As the tongue is withdrawn, the lamellae then seal the cylinder tightly shut for delivery into the bird's mouth, as shown in the Illustra animation (fluid trapping). This is a wonderful dual mechanism that results in much more efficient food capture in far less time.

Fluid trapping is the predominant process by which hummingbirds achieve nectar collection at small bill tip-to-nectar distances, wherein tongue grooves are wholly immersed in nectar, or when the nectar is found in very thin layers. Expansive filling accounts for nectar uptake by the portions of a hummingbird's tongue that remain outside the nectar pool. The relative contributions of the two synergistic mechanisms (fluid trapping and expansive filling) to the rate and volume of nectar ultimately ingested are determined by the distance from the bill tip to the nectar surface during the licking process.
In other words, these two "synergistic mechanisms" give the hummingbird the biggest possible nectar bang for the buck, regardless of how deep the nectar pool is. The new model explains how the tongue can fill up even in a short flower. Since hummingbirds already "have remarkably high metabolic rates, amazing speed and superb aeronautic control," it is essential they get the optimum return on investment of feeding energy.

All these traits result from the ability of hummingbirds to feed on nectar efficiently enough to fuel an extreme lifestyle out of a sparse, but energetically dense, resource. Therefore, the way in which they feed on nectar determines the peaks and span of their performance, and thus their behaviour (and evolutionary trajectory), across a range of environmental axes.
But did evolutionary theory contribute anything to this study? The authors speculate briefly about "co-evolution" of flowers and their pollinators, but do not offer any "trajectory" by which a bird could evolve either of these mechanisms from ancestors lacking them. How useful is it to offer up evidence-free promissory notes like this?

The new explanation of the mechanics of nectar uptake we provide here suggests that physical constraints are the main determinants of the relationship between pollinator type and nectar concentration, and can guide us through alternative hypotheses of hummingbird-flower coevolution.
By contrast, they save their best lines for what might be termed (though not by the authors) intelligent design. The paper begins:

Pumping is a vital natural process, imitated by humans for thousands of years. We demonstrate that a hitherto undocumented mechanism of fluid transport pumps nectar onto the hummingbird tongue.
This implies a seamless connection between human design and biological design. They conclude on the design theme:

Our discovery of this elastic tongue micropump could inspire applications, and the study of flow, in elastic-walled (flexible) tubes in both biological and artificial systems.

You see, not only does a design focus inspire study of biological systems, it leads to better designed applications. Everyone can agree on this: hummingbirds are inspiring!

Has Richard Darwkins stopped evolving?

awkins's Contributions as a Scientist Are Already Past Their Sell-By Date, Says Nature Reviewer

David Klinghoffer September 10, 2015 12:33 PM

In the journal Nature, Nathaniel Comfort delivers a softly devastating review of Richard Dawkins's memoir, part two, Brief Candle in the Dark: My Life in Science. Or let me rephrase that -- it's a devastating review of Dawkins himself as a scientist, including his enchantment with computer simulations. The problem with computers is that they're only as effective as the assumptions you bring to them. Garbage in, garbage out:

Much of Dawkins's research has been in silico, writing programs for evolutionary simulations. In his simulations, life is utterly determined by genes, which specify developmental rules and fixed traits such as colour. The more lifelike his digital animals ("biomorphs") become, the more persuaded he is that real genes work in roughly the same way. Dawkins's critics accuse him of genetic determinism. This synopsis of his work shows that his life virtually depends on it.

A curious stasis underlies Dawkins's thought. His biomorphs are grounded in 1970s assumptions. Back then, with rare exceptions, each gene specified a protein and each protein was specified by a gene. The genome was a linear text -- a parts list or computer program for making an organism --insulated from the environment, with the coding regions interspersed with "junk".

Today's genome is much more than a script: it is a dynamic, three-dimensional structure, highly responsive to its environment and almost fractally modular. Genes may be fragmentary, with far-flung chunks of DNA sequence mixed and matched in bewildering combinatorial arrays. A universe of regulatory and modulatory elements hides in the erstwhile junk. Genes cooperate, evolving together as units to produce traits. Many researchers continue to find selfish DNA a productive idea, but taking the longer view, the selfish gene per se is looking increasingly like a twentieth-century construct.

Dawkins's synopsis shows that he has not adapted to this view. He nods at cooperation among genes, but assimilates it as a kind of selfishness. The microbiome and the 3D genome go unnoticed. Epigenetics is an "interesting, if rather rare, phenomenon" enjoying its "fifteen minutes of pop science voguery", which it has been doing since at least 2009, when Dawkins made the same claim in The Greatest Show on Earth(Transworld). Dawkins adheres to a deterministic language of "genes for" traits. As I and other historians have shown, such hereditarianism plays into the hands of the self-styled race realists (N. Comfort Nature 513, 306-307; 2014).

Note the reference to "erstwhile" junk DNA, the acknowledgement by Comfort that epigenetics and its impact on evolutionary thinking are no flash in the pan, and the recognition that gene determinism plays into the hands of racialists -- and, one might add, genuine racists. Also see biologist Ann Gauger's comments here this morning on the design implications of "dynamic genomes."

Comfort, a science historian at Johns Hopkins, isn't impressed by Dawkins's atheist evangelizing, but he passes over that briefly. At Why Evolution Is True, Jerry Coyne complains that Comfort doesn't try to argue against Dawkins on the God question. But he doesn't need to. The aggressive atheist stance shared by Dawkins and Coyne is supposed to be an inference from the science. If the science is already outdated, "curiously static" while science passes it by in the scientist's own lifetime, what more is there to say?

Everyone agrees that Dawkins is a terrific writer -- his "greatest gift has been as a lyricist," says Comfort. In that respect, we in the intelligent design community could profit by taking notes from him.

But a scientist whose legacy amounts to little more than his sparkling prose style is not going to go down in the history books, at least not prominently. Nor should anyone be concerned that his acid musings on faith will have much impact in the long run.

Yet more on life's antidarwinian bias.III

Dynamic Genomes in Bacteria Argue for Design

Ann Gauger September 10, 2015 3:02 AM

Recent research described in a review article in the Journal of Biochemistry & Analytical Biochemistry ("Rethinking the Bacterial Genetic Regulation") indicates there is more to bacterial genetics than was previously suspected.

Bacterial geneticists have had tidy maps of genomes, with promoters and transcription units and operons neatly outlined -- all components that make sure that genes that work together are expressed at the same time. Those things are all still true. But nobody knew until recently about the existence of higher-level dynamics involved in genome regulation.

Using techniques analogous to those of the famous ENCODE project, which opened our eyes to the human genome's complex expression and interaction patterns, scientists have discovered that just like in our genome, much of a bacterium's genome is transcribed in both directions. This opens up the possibility of new forms of gene regulation. In addition, researchers have found the genome is organized into large-scale domains where long stretches of DNA are brought together so that genes involved in related functions can work together.

The way that the DNA supercoils seems to be involved in these dynamic domains. Some genes are preferentially expressed when the DNA is supercoiled, others when it is relaxed. There is also evidence to suggest "rapid movements (snaps) of the chromosomal loci and fast longitudinal density waves fluxing forth and back" along the nucleoid, the region of the cell where the bacterial cell's DNA is located. The DNA is active and moving.

Such dynamic structural change is a remarkable thing.

It may potentially provide global levels of organization that can change in response to the environment in which the cell finds itself. The authors describe one way it may happen in a plant bacterial pathogen, and they suggest that similar modes of environmental response could be involved in other pathogens as well.

Codes within codes within codes -- highly efficient and highly intelligent systems -- don't happen by accident and/or selection. The cell might begin with one code, which is incredible in itself. To layer another code in the opposite direction is far and away beyond that. Then to add a third layer of structural dynamics is simply awe-inspiring.

Darwinism vs. The real world XI

nderstanding Cardiovascular Function: Evolutionary Biologists Face a Catch-22

Howard Glicksman September 11, 2015 11:16 AM

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News & Views is delighted to present this series, "The Designed Body." Dr. Glicksman practices palliative medicine for a hospice organization.

The last several articles in this series have looked at the heart: its structure, how it works, how it is controlled, and how it helps the body meet its metabolic needs, given the laws of nature. We also reviewed the four main conditions that cause the heart to malfunction resulting in significant debility: coronary artery disease, valvular heart disease, heart failure, and some of the arrhythmias.

But what exactly happens to make the heart suffer cardiac arrest? It's important to realize that although the conditions mentioned in the last several articles can predispose a person to die from cardiac arrest, they are not the final event that actually causes it. Understanding how life came into being requires understanding how the body dies of cardiac arrest as well. It's like knowing all the different ways a car can "die" and then working backwards to figure out how to prevent them from happening. If you think about it, that's exactly how the control systems in the body are set up: to prevent not only respiratory but also cardiac arrest.

Cardiac arrest is the sudden stoppage of effective cardiac output, where the heart is no longer able to provide enough blood flow to sustain life. Clinical assessment will show that the person is unconscious and unresponsive to tactile stimulation and not breathing because the brain does not have enough blood flow for it to work properly. In addition, a pulse will not be palpable and no heart sounds will be heard because the heart is not pumping blood effectively enough.

There are basically three different conditions that can cause cardiac arrest. One is called asystole, (flat-line) where there is no electrical activity and no ventricular contraction. This results in no systolic function and therefore no cardiac output and blood flow within the circulatory system. Another is called pulseless with electrical activity(formerly called electromechanical dissociation), where there is electrical activity but no mechanical response from the ventricles. This is effectively like asystole in that there is no systolic function and therefore zero cardiac output and blood flow within the circulation.

The third are the malignant and life-threatening ventricular arrhythmias such as ventricular tachycardia, ventricular flutter, and ventricular fibrillation. Ventricular tachycardia (100-250 bpm) and ventricular flutter (150-300 bpm) are very rapid and regular rhythms that can severely limit cardiac output and blood flow within the circulation. If prolonged, these tachyarrhythmias usually degenerate into ventricular fibrillation. Ventricular fibrillation is an extremely rapid ventricular arrhythmia (400-600 bpm) in which there is electrical disorganization and an absence of coordinated ventricular contraction. Essentially, the ventricle quivers and is unable to effectively pump blood, leading to minimal, if any, cardiac output and blood flow within the circulatory system.

The malignant and life-threatening ventricular arrhythmias take place due to electrical irritability within the heart muscle and are most often associated with coronary artery disease and/or left ventricular failure. If a person dies unexpectedly from a cardiac arrest, it is called sudden cardiac death and is most often due to one of these arrhythmias. In fact, it is unfortunate that the first symptom for 25 percent of people with coronary artery disease is sudden cardiac death.

There are many different conditions that can lead to the other two causes of cardiac arrest, which effectively results in no systolic function and zero cardiac output. Both of these conditions require a massive failure in cardiac function. Although it is the sinus node that naturally paces the heart (usually at about 60-100 bpm), there exists a hierarchy of other cells below it that can also automatically depolarize and pace the heart, albeit at lower rates.

So, if the sinus node malfunctions, the AV node takes over with what is called a junctional rhythm, usually at a rate of 40-60 bpm. And if the AV node malfunctions, the specialized conduction tissue below it automatically paces the heart at even a lower rate of 20-40 bpm. People who experience this usually feel very tired and weak and have problems even walking slowly. However, when there is no systolic function, whether there is electrical activity or not, something catastrophic must have happened. Here are a few of the usual culprits.

It is important to remember that all of the parts of the heart are made up of cells, each of which must control its volume and chemical content and require certain chemicals to work properly. So, either a major blood flow problem to the heart or the lungs or a generalized metabolic problem in the body can lead to a sudden loss of systolic function. If not reversed, ventricular fibrillation usually degenerates into asystole because there is limited, if any, blood flow going through the coronary arteries. This results in the death of most of the heart cells.

A sudden lack of sufficient coronary blood flow caused by the blockage of either a major vessel or several branches, due to a clot (thrombosis), can do the same thing. A major blockage of blood flow in the pulmonary arteries, due to clots coming from the leg or pelvic veins (pulmonary embolism), not only drastically reduces the blood level of oxygen, but also the return of blood to the left side of the heart and leads to asystole.

Severely low blood pressure (hypotension) often due to low blood volume (hypovolemia), from either excessive blood loss (hemorrhage) and/or excessive water loss (dehydration) results in limited blood flow to the heart cells, which leads to cell malfunction and death from asystole. Very low blood levels of oxygen (hypoxia) and/or glucose (hypoglycemia) prevents the cells from getting the energy they need to function properly and this is another cause of the total absence of heart function. High levels of hydrogen ion (acidosis) are toxic to cells and high or low blood levels of potassium (hyperkalemia or hypokalemia) can cause nerve and muscle cell malfunction, so these conditions can also result in cardiac arrest due to asystole. Also, the core temperature of the body affects its metabolism and how well the enzymes in the cells work, so when the body is extremely cold (hypothermia) this can result in a lack of heart function as well.

In seeking to understand how human life came into being, we need to consider whether an explanation is within the credibility zone. In trying to explain how the heart is able to provide the blood flow the body needs, evolutionary biologists are faced with a Catch-22. Not only is the heart made up of cells, but so are all the organs and tissues involved in providing the control mechanisms needed to allow the heart to function in the first place. In other words, the heart is dependent on its own function for survival because all of the systems in the body that control chemicals like oxygen, glucose, water, potassium, hydrogen ion, and things like clotting, blood pressure, and temperature, are also made up of cells that are dependent on the heart providing enough blood flow.

The universal human desire to know the truth requires us to go beyond just describing how life looks, as evolutionary biology does. We must dig deeper. Seeing what is required for the body to maintain proper heart function, and how easily that can fail, you wonder how anyone could believe that such an intricate system, co-dependent on so many other controls in the body, could have come about without intelligent agency.

As our exploration of heart function has shown, the body must take control to follow the rules imposed on it by the laws of nature. That is because real numbers are a matter of life and death. So far in this series I have shown how the body controls its blood volume and heart function. But that is still not enough to explain how the body is able to do what it needs to do to live. As I noted above, the blood pressure is another factor that needs to be addressed.

Even if the heart is working properly and there is enough blood volume, debility and death can still take place if the blood pressure isn't just right. What is the blood pressure, how is it controlled, and what can make it drop too low or rise too high? That's what we'll begin to consider next time.

Psalms1-7 New Jerusalem Bible.

1.1 How blessed is anyone who rejects the advice of the wicked and does not take a stand in the path that sinners tread, nor a seat in company with cynics,

2 but who delights in the law of Yahweh and murmurs his law day and night.

3 Such a one is like a tree planted near streams; it bears fruit in season and its leaves never wither, and every project succeeds.

4 How different the wicked, how different! Just like chaff blown around by the wind

5 the wicked will not stand firm at the Judgement nor sinners in the gathering of the upright.

6 For Yahweh watches over the path of the upright, but the path of the wicked is doomed.
2.1 Why this uproar among the nations, this impotent muttering of the peoples?

2 Kings of the earth take up position, princes plot together against Yahweh and his anointed,

3 'Now let us break their fetters! Now let us throw off their bonds!'

4 He who is enthroned in the heavens laughs, Yahweh makes a mockery of them,

5 then in his anger rebukes them, in his rage he strikes them with terror.

6 'I myself have anointed my king on Zion my holy mountain.'

7 I will proclaim the decree of Yahweh: He said to me, 'You are my son, today have I fathered you.

8 Ask of me, and I shall give you the nations as your birthright, the whole wide world as your possession.

9 With an iron sceptre you will break them, shatter them like so many pots.'

10 So now, you kings, come to your senses, you earthly rulers, learn your lesson!

11 In fear be submissive to Yahweh;

12 with trembling kiss his feet, lest he be angry and your way come to nothing, for his fury flares up in a moment. How blessed are all who take refuge in him!
3.1 [Psalm Of David When he was fleeing from his son Absalom] Yahweh, how countless are my enemies, how countless those who rise up against me,

2 how countless those who say of me, 'No salvation for him from his God!'Pause

3 But you, Yahweh, the shield at my side, my glory, you hold my head high.

4 I cry out to Yahweh; he answers from his holy mountain.Pause

5 As for me, if I lie down and sleep, I shall awake, for Yahweh sustains me.

6 I have no fear of people in their thousands upon thousands, who range themselves against me wherever I turn.

7 Arise, Yahweh, rescue me, my God! You strike all my foes across the face, you break the teeth of the wicked.

8 In Yahweh is salvation, on your people, your blessing!Pause.
4.1 [For the choirmaster For strings Psalm Of David] When I call, answer me, God, upholder of my right. In my distress you have set me at large; take pity on me and hear my prayer!

2 Children of men, how long will you be heavy of heart, why love what is vain and chase after illusions?Pause

3 Realise that Yahweh performs wonders for his faithful, Yahweh listens when I call to him.

4 Be careful not to sin, speak in your hearts, and on your beds keep silence.Pause

5 Loyally offer sacrifices, and trust in Yahweh.

6 Many keep saying, 'Who will put happiness before our eyes?' Let the light of your face shine on us. Yahweh,

7 to my heart you are a richer joy than all their corn and new wine.

8 In peace I lie down and at once fall asleep, for it is you and none other, Yahweh, who make me rest secure.
5.1 [For the choirmaster For flutes Psalm Of David] Give ear to my words, Yahweh, spare a thought for my sighing.

2 Listen to my cry for help, my King and my God! To you I pray,

3 Yahweh. At daybreak you hear my voice; at daybreak I lay my case before you and fix my eyes on you.

4 You are not a God who takes pleasure in evil, no sinner can be your guest.

5 Boasters cannot stand their ground under your gaze. You hate evil-doers,

6 liars you destroy; the violent and deceitful Yahweh detests.

7 But, so great is your faithful love, I may come into your house, and before your holy temple bow down in reverence of you.

8 In your saving justice, Yahweh, lead me, because of those who lie in wait for me; make your way plain before me.

9 Not a word from their lips can be trusted, through and through they are destruction, their throats are wide -- open graves, their tongues seductive.

10 Lay the guilt on them, God, make their intrigues their own downfall; for their countless offences, thrust them from you, since they have rebelled against you.

11 But joy for all who take refuge in you, endless songs of gladness! You shelter them, they rejoice in you, those who love your name.

12 It is you who bless the upright, Yahweh, you surround them with favour as with a shield.
6.1 [For the choirmaster For strings For the octachord Psalm Of David] Yahweh, let your rebuke to me not be in anger, your punishment not in the heat of wrath.

2 Have pity on me, Yahweh, for I am fading away. Heal me, Yahweh, my bones are shaken,

3 my spirit is shaken to its very depths. But you, Yahweh . . . how long?

4 Yahweh, relent and save my life rescue me because of your faithful love,

5 for in death there is no remembrance of you; who could sing your praises in Sheol?

6 I am worn out with groaning, every night I drench my pillow and soak my bed with tears.

7 My eyes waste away with vexation. Arrogance from all my foes!

8 Away from me, all evil-doers! For Yahweh has heard the sound of my weeping,

9 Yahweh has heard my pleading. Yahweh will accept my prayer.

10 Let all my enemies be put to confusion, shaken to their depths, let them retreat in sudden confusion.
7.1 [Lament Of David Which he sang to Yahweh about Cush the Benjaminite] Yahweh my God, I take refuge in you, save me from all my pursuers and rescue me,

2 or he will savage me like a lion, carry me off with no one to rescue me.

3 Yahweh my God, if I have done this: if injustice has stained my hands,

4 if I have repaid my ally with treachery or spared one who attacked me unprovoked,

5 may an enemy hunt me down and catch me, may he trample my life into the ground and crush my vital parts into the dust.Pause

6 Arise, Yahweh, in your anger, rise up against the arrogance of my foes. Awake, my God, you demand judgement.

7 Let the assembly of nations gather round you; return above it on high!

8 (Yahweh judges the nations.) Judge me, Yahweh, as my uprightness and my integrity deserve.

9 Put an end to the malice of the wicked, make the upright stand firm, you who discern hearts and minds, God the upright.

10 God is a shield that protects me, saving the honest of heart.

11 God is an upright judge, slow to anger, but a God at all times threatening

12 for those who will not repent. Let the enemy whet his sword, draw his bow and make ready;

13 but he is making ready instruments of death for himself and tipping his arrows with fire;

14 look at him: pregnant with malice, conceiving spite, he gives birth to treachery.

15 He digs a trap, scoops it out, but he falls into the snare he made himself.

16 His spite recoils on his own head, his brutality falls back on his own skull.

17 I thank Yahweh for his saving justice. I sing to the name of the Most High.

Darwinists continue to squabble over the family album.

As a Taxonomic Group, "Homo habilis" Is Challenged in the Journal Science
Casey Luskin September 9, 2015 3:40 PM

The limits of our genus Homo have long been controversial. One problem is that evolutionary biologists sometimes try to shoehorn un-human-like fossils into Homo in order to make it appear that ape-like and human-like creatures are kin. It's a classic case of scientists letting their evolutionary bias direct taxonomy.

What's less common is to see evolutionary paleoanthropologists admitting this has happened. Now in a recent article in Science, "Defining the genus Homo," Jeffrey H. Schwartz and Ian Tattersall explain that Homo habilis (literally, "handy man") was originally placed within Homo because researchers wanted an old species that apparently made tools:

In 1964, Leakey and colleagues attributed the newly discovered ~1.8-million-year-old partial mandible, skullcap and hand (OH7) and foot (OH8), plus other materials from Olduvai Gorge, to the new species Homo habilis. This species replaced the very roughly contemporaneous South African australopiths in Mayr's transformationist scenario, although there was scant morphological justification for including any of this very ancient material in Homo. Indeed, the main motivation appears to have been Leakey's desire to identify this hominid as the maker of the simple stone tools found in the lower layers of the Gorge, following the dictum of Man the Toolmaker. This association has subsequently proven highly dubious. The inclusion in Homo of the H. habilis fossils so broadened the morphology of the genus that further hominids from other sites could be shoehorned into it almost without regard to their physical appearance. As a result, the largely unexamined definition of Homo became even murkier.
As Schwartz and Tattersall explain, the link between "Homo habilis" and tools is dubious. Indeed, the link between "habilis" and "Homo" is dubious. A major review article by Wood and Collard in Science found that habilisis different from Homo in body size, body shape, mode of locomotion, jaws and teeth, developmental patterns, and brain size, and should be reclassified within Australopithecus.
Elsewhere Tattersall has critiqued the entire species Homo habilis by calling it "a wastebasket taxon, little more than a convenient recipient for a motley assortment of hominin fossils." He has called it "a rather heterogeneous assemblage, and it is probable that more than one hominid species is represented." Paleoanthropologists Daniel E. Lieberman, David R. Pilbeam, and Richard W. Wrangham likewise co-write that "fossils attributed to H. habilis are poorly associated with inadequate and fragmentary postcrania." In an article titled "Who Was Homo habilis -- and Was It Really Homo?" in Science, Ann Gibbons notes that "researchers labeled a number of diverse, fragmentary fossils from East Africa and South Africa 'H. habilis,' making the taxon a 'grab bag... a Homo waste bin,' says paleoanthropologist Chris Ruff of Johns Hopkins University in Baltimore, Maryland."

Penn State University paleoanthropologist Alan Walker explains the severity of disagreements over this species: "[T]his is not a matter of some fragmentary fossils that are difficult to agree on. Whole crania are placed by different people in different species or even genera." One reason for the disagreements is that the quality of the fossils is often poor. As Walker puts it, "[d]espite the number of words published on this species... there is not as much bony evidence as we would like."

In any case, Schwartz and Tattersall end their recent article by stating:

If we want to be objective, we shall almost certainly have to scrap the iconic list of names in which hominin fossil specimens have historically been trapped, and start from the beginning by hypothesizing morphs, building testable theories of relatedness, and rethinking genera and species.
Following this would mean we should not use the name "Homo habilis" because it's not like Homo, probably didn't use complex tools, and may not even be a true species. None of this bodes well for habilis which has, at times, been called a "link" between human-like members of Homo and the apelike australopithecines.

They conclude: "In contrast to Mayr's austere linearity, we may find that human evolution rivaled that of other mammals in its evolutionary experimentation and luxuriant diversity." I'll recast their ending in my own words: The hominid fossil record doesn't include a neat line of fossils leading to humans. In reality, there are so many diverse fossils that evolutionary relationships are extremely unclear.

Yet more on life's antidarwinian biasII

Life Continues to Ignore What Evolution Experts Say

Denyse O'Leary September 9, 2015 3:18 AM

ecently, philosopher James Barham published a series of articles called "Seeing Past Darwin," in which he looks at the recent growth and enormous implications of non-Darwinian biology and its approach to evolution. We've been discussing some of the specific issues in this series.

One motif recurs: Darwinian evolution -- which most lay hearers assume to be "evolution" period -- assumes that evolution is vertical: Organisms take their form from genes inherited with slight modifications from their ancestors through their parents. And these slight changes add up gradually over time to immense and profound changes.

Non-Darwinian biology studies mechanisms for evolution that don't really work that way, including horizontal gene transfer and epigenetic change.

Demonstrating these mechanisms doesn't "disprove" common ancestry. Rather, it shows that common ancestry drives far less evolution than current popular science media lead us to expect. Also we can no longer assume that when a change does occur, a satisfactory account must be Darwinian. It will take some time to unpack the controversial implications of our newfound knowledge of actual causes of evolution.

Some non-Darwinian mechanisms of evolution we haven't yet looked at play at least a small role in the history of life:

-- Genome doubling. Some plants can duplicate their chromosomes (polyploidy) to foster explosive growth without undergoing cell division. Thus, they can recover quickly from damage, such as being half eaten by grazing animals. The process, long considered a major force in plant evolution, immediately gives the cells much more DNA to work with, favoring adaptation to challenging new circumstances.

-- Jumping gene. We've looked at horizontal gene transfer between life forms. But some genes, transposons, can also move around within them. As Nature Education explains:

Some of the most profound genetic discoveries have been made with the help of various model organisms that are favored by scientists for their widespread availability and ease of maintenance and proliferation. One such model is Zea mays (maize), particularly those plants that produce variably colored kernels. Because each kernel is an embryo produced from an individual fertilization, hundreds of offspring can be scored on a single ear, making maize an ideal organism for genetic analysis. Indeed, maize proved to be the perfect organism for the study of transposable elements (TEs), also known as "jumping genes," which were discovered during the middle part of the twentieth century by American scientist Barbara McClintock. McClintock's work was revolutionary in that it suggested that an organism's genome is not a stationary entity, but rather is subject to alteration and rearrangement-a concept that was met with criticism from the scientific community at the time.

Lee Spetner recounts in The Evolution Revolution:

McClintock pursued her research despite it being considered a backwater area, and eventually the importance of her work was recognized by the Nobel Prize committee in awarding her the Prize in Medicine in 1983. The transposable genetic elements she discovered have been subsequently revealed to be members of a class of genetic rearrangements that do not occur spontaneously by chance but are under strict cellular control.

One jumping gene in the model plant Arabadopsis was found to improvedisease resistance. But jumping genes are not always useful or welcome; they can cause harmful mutations. Some are even under investigation for promoting cancer:

Study author Dr Paul Edwards, at the Cancer Research UK Cambridge Institute, said: "These jumping genes play hopscotch across our genetic code in cancer cells more than in normal cells. When one of these mobile genetic sequences plants itself in the middle of a gene that controls the cell's growth it radically alters how the cell behaves, which can sometimes cause cancer.

-- Hybridization We've already seen that cross-breeding blind cavefish from different caves can restore devolved sight in at least some offspring (because the mutations that result in loss of sight differ from group to group, and some hybrids end up with all the necessary equipment). But natural hybridization can produce such changes too. Characteristics that are not evidenced in a given generation may remain as potentials.

Ferns separated 60 million years have interbred. The wolf and dog populations of North America are so heavily hybridized that it is a challenge to make sense of them at all in the face of "all the contradictory claims." Researchers have also identified at least three potential hybridization events (interspecific mating) in Eurasian mice. One scientist noted that other studies "may have missed evidence of hybridization because the researchers weren't specifically looking for it." That means we do not currently know how frequent it is. More strangely, common baker's yeast turns out to have two different versions of its genome, thought due to a hybridization event 100 million years ago.

As a mechanism, hybridization may have developed a taint due to implausible hypotheses such as the supposed pig-chimp hybrid that, according to one theory, produced humans. But, within the bounds of the plausible, it is a means of producing long-term changes in life forms over time.

-- Symbiosis. The theory of cell mergers (sometimes called endosymbiosis or symbiogenesis) was pioneered by University of Massachusetts biologist Lynn Margulis (1938-2011). She proposed that one organism might absorb another and that the second would continue to function as part of the first one, creating greater complexity. AsBritannica puts it, in 1970 " her theory was regarded as far-fetched, but it has since been widely accepted."

Sometimes it can seem like a series of nested dolls. For example, two species of bacteria live together, one inside the other, inside mealybugs. One researcher said, "The effort has revealed a level of molecular-level integration between bacterial species that scientists have never before seen," in that one bacterium has divested many key life functions, now taken care of by another. An animal (the bdelloid rotifer) avoids sex but escapes extinction by eating other life forms' DNA. One lichen turned out to have at least 126 species of fungi living symbiotically: "As the team notes in their paper published in Proceedings of the National Academy of Sciences, until very recently, the lichen was believed to have just one species of fungus." That's probably still in the textbooks.

Symbiosis can be "almost hilariously complicated," according to University of Montana microbiologist John McCutcheon. For example:

Mealybugs only eat plant sap, but sap doesn't contain all the essential amino acids the insects need to survive. Luckily, the bugs have a symbiotic relationship with two species of bacteria -- one living inside the other in a situation unique to known biology -- to manufacture the nutrients sap doesn't provide....

The researchers discovered the already complex three-way symbiosis actually depends on genes from six different organisms -- three more than the number of species that are currently found in the symbiosis.

Again, we don't know how common symbiosis (termed by one writer "slavery, but with benefits") is. While it is certainly a form of evolution, it does not typically originate new features. Rather, like horizontal gene transfer, it enables life forms to borrow each others' features, sometimes discarding some of their own, in return for more efficient operations overall. In that case, this mechanism of evolution can amount to an overall loss in complex machinery. But life goes on.

Readers may well wonder about the term "mechanism" of evolution, as used here. Consistent with Michael Behe's question, "How, exactly?", it means a process observed to account for inherited change. If a bacterium is observed to absorb antibiotic resistance genes from another bacterium and pass them on during cell division, we will term that a mechanism. It is not a theory about what "must have happened" over vast tracts of time; it is an event we have witnessed, produced by causes we can identify.

But what drives the process? That is, why do living cells attempt to protect themselves in ways that rocks and rotting wood do not? As we shall see, a number of non-Darwinian biologists now focus on the way that cells have changed and do change themselves to respond to challenges in their environment -- natural genetic engineering.