Поставите питања везана за еволуциону биологију

[grigorije22]

http://creation.com/design-features-questions-and-answers

[Avocado]

Jeste ali to je samo siromasni kreacionisticki institut nemaju oni para i mogucnosti za istrazivanja

Jao, Grišo, imaju ogroman budžet... mani se besmislenih priča.

Pored svih primedbi na "nesvodljivu kompleksnost" najjednostavnije su empirijske. Kad god kreacionisti navedu kako neki organ ne bi mogao da funkcioniše bez nekog od sastavnih delova, naučnici pronađu primere upravo takvog organa, bez nekih sastavnih delova koji sasvim normalno funkcionišu (sa drugom funkcijom)... to se odavno desilo za flagellum... a ti i dalje furaš tu priču...

Najblesavija stvar kod klipa koji si postavio je što je on postavljan kao "odgovor" na klip koji ga potpuno i temeljno debankuje... po starom dobrom receptu...

[grigorije22]

http://creation.com/intelligent-design-a-war-on-science-says-the-bbc

[Avocado]

http://creation.com/...ce-says-the-bbc

Šta?

[grigorije22]

Michael Behe Hasn't Been Refuted on the Flagellum

http://www.evolutionnews.org/cover-image-flagellum.jpg

Those of us who have been reading the literature surrounding the ID/evolution controversy for any length of time will be quite acquainted with the standard Darwinian retort with regards the "Behean" argument for irreducible complexity as far as the bacterial flagellum is concerned. There seems to be this unanimity of opinion among Darwinian theorists that the claims of irreducible complexity with respect to the bacterial flagellum have been refuted, and that we ID proponents are constantly shifting the goal posts, burying our heads in the sand, and generally clutching at straws. Indeed, one person on Facebook recently remarked,

My main gripe with the ID proponents is that they never seem to give up. How many times do you need to be told that something is wrong before you'll admit it? How many times does ID need to be refuted in the peer reviewed media before you'll give it up as a lost cause? The bacterial flagellum irreducible complexity story is completely and utterly dead. It's wrong. Get over it.

I recently brought up the flagellum, as a documented instance of irreducible complexity, at a lunch bar Q&A session on the science/faith intersect, and received responses to much the same effect.

But is this claim actually true? Has this argument been refuted by critics? About a year ago, I read Why Intelligent Design Fails - A Scientific Critique of the New Creationism (edited by Matt Young and Taner Edis). Chapter 5 of that book was contributed by Ian Musgrave and is titled "Evolution of the Bacterial Flagellum." Targeted as a response to Michael Behe and William Dembski, Musgrave attempts to dispel of the notion of irreducible complexity once and for all. Reading his chapter, I recall being deeply unimpressed. On page 82 of the book, Musgrave offers us the following argument:

Here is a possible scenario for the evolution of the eubacterial flagellum: a secretory system arose first, based around the SMC rod and pore-forming complex, which was the common ancestor of the type-III secretory system and the flagellar system. Association of an ion pump (which later became the motor protein) to this structure improved secretion. Even today, the motor proteins, part of a family of secretion-driving proteins, can freely dissociate and reassociate with the flagellar structure. The rod- and pore-forming complex may even have rotated at this stage, as it does in some gliding-motility systems. The protoflagellar filament arose next as part of the protein-secretion structure (compare the Pseudomonas pilus, the Salmonella filamentous appendages, and the E. coli filamentous structures). Gliding-twitching motility arose at this stage or later and was then refined into swimming motility. Regulation and switching can be added later, because there are modern eubacteria that lack these attributes but function well in their environment.(Shah and Sockett 1995). At every stage there is a benefit to the changes in the structure.

Indeed, Mark Pallen and Nick Matzke make a very similar argument in their 2006 Nature Reviews article (a paper which was raised by an audience member during the recent UK Behe tour). Ken Miller is also reputed for routinely making similar claims regarding the flagellum's evolution from the Type III Secretion System based largely on considerations of protein sequence homologies.

So, do these points succeed in laying to rest that pesky business of intelligent design once and for all? Well, actually no; they don't. In fact, I submit that the arguments of all of the aforementioned gentlemen fundamentally trivialize several important issues.

First and foremost, it trivializes the sheer complexity and sophistication of the flagellar system -- both its assembly apparatus, and its state-of-the-art design motif. Actually, the process by which the bacterial flagellum is self-assembled within the cell is so sophisticated that I have long struggled to convey it in an accessible way to lay-persons. Its core concepts are notoriously difficult to grasp for those not accustomed to thinking about the system or for those encountering it for the first time. But, at the same time, the mechanistic basis of flagellar assembly is so breath-takingly elegant and mesmerizing that the sheer engineering brilliance of the flagellar motor -- and, indeed, the magnitude of the challenge it brings to Darwinism -- cannot be properly appreciated without at minimum a cursory knowledge of its underpinning operations. Let's take a peek.

The Self-Assembly of the Flagellar Apparatus

http://www.evolutionnews.org/flagellar%20assembly.jpg

The synthesis of the bacterial flagellum requires the orchestrated expression of more than 60 gene products. Its biosynthesis within the cell is orchestrated by genes which are organised into a tightly ordered cascade in which expression of one gene at a given level requires the prior expression of another gene at a higher level. The paradigm, or model, organism for flagellar assembly is Salmonella, a bacterium of the family Enterobacteriaceae. My discussion thus pertains principally to Salmonella, unless otherwise indicated.

The flagellar system in Salmonella has three classes of promoters (promoters are akin to a kind of molecular toggle switch which can initiate gene expression when recognised by RNA polymerase and an associated specialised protein called a "sigma factor"). These three classes of promoters are uninspirationally dubbed "Class I," "Class II," and "Class III." This sequential transcription is coupled to the process of flagellar assembly. Class I contains only two genes in one operon (called FlhD and FlhC). Class II consists of 35 genes across eight operons (including genes involved in the assembly of the hook-basal-body and other components of the flagellum, as well as the export apparatus and two regulatory genes called "FliA" and "FlgM"). Those genes which are involved in the synthesis of the filament are controlled by the Class III promoters.

The Class I promoter drives the expression of a master regulator (particular to the Enterobacteriaceae of which Salmonella is a member) called "FldH4C2" (don't worry about remembering it!). This enteric master regulator then turns on the Class II promoters in association with a sigma factor, σ70 (remember, I said that a sigma factor is a type of protein which enables specific binding of RNA polymerase to gene promoters). The Class II promoters are then responsible for the gene expression of the hook-basal-body subunits and its regulators, including another sigma factor called σ28 (which is encoded by a gene called FliA) and its anti-sigma factor, FlgM (anti-sigma factors, as their name suggests, binds to sigma factors to inhibit their transcriptional activity). The sigma factor σ28 is required to activate the Class III promoters. But here we potentially run into a problem. It makes absolutely no sense to start expressing the flagellin monomers before completion of the Hook-Basal-Body construction. Thus, in order to inhibit the σ28, the anti-sigma factor (FlgM) alluded to above inhibits its activity and prohibits it from interacting with the RNA polymerase holoenzyme complex. When construction of the Hook-Basal-Body is completed, the anti-sigma factor FlgM is secreted through the flagellar structures which are produced by the expression of the Class II hook-basal-body genes. The Class III promoters (which are responsible for the expression of flagellin monomers, the chemotaxis system and the motorforce generators) are then finally activated by the σ28 and the flagellum can be completed.

But it gets better. The flagellar export system (that is, the means by which FlgM is removed from the cell) has two substrate-specificity states: rod-/hook-type substrates and filament-type substrates. During the process of flagellar assembly, this substrate-specificity switch has to flick from the former of those states to the latter. Proteins which form part of the hook and rod need to be exported before those which form the filament. But how does this switch in substrate-specificity take place?

A membrane-bound protein called FlhB is the key player in this process. There is also a flagellar hook-length protein which is responsible for making sure that the hook length is of the right size (around 55nm) called FliK. This same protein is also responsible for initiating the switch export substrate specificity. As it turns out, without FliK, both the ability to switch and export filament and the hook length control are completely lost. FliK has two key domains, i.e. the N-terminal and C-terminal domains. During hook assembly, FliKN functions as a molecular sensor and transmitter of information on hook length. When the hook reaches the right length, the information is transmitted to FliKC and FliKCT, resulting in a conformational change, which in turn results in FliKCT binding to FlhBC. This, in turn, results in a conformational change in FlhBC. This causes the substrate specificity switch.

http://www.evolutionnews.org/flagellum%20diagram.jpg

Flagellar assembly begins in the cytoplasmic membrane, progresses through the periplasmic space and finally extends outside the cell. The flagellum basically consists of two main parts: the secretion system and the axial structure. The principle components of the axial structure are FlgG for the rod, FlgE for the hook, and FliC for the filament. All of these assemble with the assistance of a cap protein (FlgJ, FlgD and FliD respectively). Of those, only FliD remains at the tip of the filament in the finished product. Other components of the axial structure (called FlgB, FlgC and FlgF) connect the rod and MS ring complex. The hook and filament are connected by FlgK and FlgL.

When the C ring and C rod attach to the M ring at its cytoplasmic surface, the MS ring complex -- which is the structural foundation of the apparatus -- can begin to secrete flagellar proteins.

The rod structure is built through the peptidoglycan layer. But its growth it isn't able to proceed past the physical barrier presented by the outer membrane without assistance. So, the just-alluded-to outer ring complex cuts a hole in the membrane, so that the hook can grow beneath the FlgD scaffold until it reaches the critical length of 55nm. Then the substrates which are being secreted can switch from the rod-hook mode to flagellin mode, FlgD can be replaced by hook-associated-proteins, and the filament continues to grow. Without the presence of the cap protein FliD, these flagellin monomers become lost. This cap protein is thus essential for the process to take place.

Why the Flagellum Evolution From the T3SS Doesn't Work

One might have thought that the description given above should be more than enough to render the hand-waving gestures of Kenneth Miller et al. trivializations in the extreme. But it gets even worse for the Darwinian story. Why exactly is flagellum biosynthesis so tightly regulated and orchestrated? Not only do the energy demands render the flagellum an extremely expensive system to run, but untimely expression of flagellum proteins may induce a strong immune response in the host system, something no bacterium wants to do.

What is the significance of this from the standpoint of evolutionary rationale? Well, flagellin monomers are somewhat potent cytokine inducers. If you are a Yersinia organism in possession of a Type-III Secretion System the last thing you want to do is display those flagellin peptides to the macrophages. Such would be liable to significantly countermand the Yersinia's anti-inflammatory strategy.

Conclusion

My description, given above, has really only scratched the surface of this spectacular item of nano-technology (for more detail, see here). I have not, for the sake of brevity, even discussed the remarkable processes of chemotaxis, two component signal transduction circuitry, rotational switching, and the proton motive force by which the flagellum is powered (for details on this, see my discussion here or, for more detail, see this review paper). But the bottom line is that modern Darwinian theory -- as classically understood -- has come no where close to explaining the origin of this remarkably complex and sophisticated motor engine. Just as Darwinian "explanations" of the eye may, at first, appear convincing to the uninitiated, largely unacquainted with the sheer engineering marvel of the biochemistry and molecular basis of vision, so too do the evolutionary "explanations" of the flagellum rapidly become void of any persuasiveness when one considers the molecular details of the system. When one couples the above details with demonstrations of the sheer impotence of neo-Darwinism to produce novel protein folds and novel protein-protein binding sites, do you really think that this system can be cobbled together by virtue of slight, successive modification, one small step at a time? Given that neo-Darwinism's key selling point lies in its purported efficacy in explaining away the overwhelming appearance of design, doesn't it stand to reason that its demonstrable impotence throws the design postulate back on the table as a viable and respectable scientific proposition?

Douglas Axe of the Biologic Institute showed in one recent paper in the journal Bio-complexity that the model of gene duplication and recruitment only works if very few changes are required to acquire novel selectable utility or neo-functionalization. If a duplicated gene is neutral (in terms of its cost to the organism), then the maximum number of mutations that a novel innovation in a bacterial population can require is up to six. If the duplicated gene has a slightly negative fitness cost, the maximum number drops to two or fewer (not inclusive of the duplication itself).

It seems that the bacterial flagellum is as much a -- and perhaps a greater -- challenge to Darwinism as it was when Behe first wrote Darwin's Black Box in 1996.

[grigorije22]

[Justin Waters]

Ma kako nije kad naucnici kopiraju ono sto vide u prirodi. Recimo proucavajuci vilinog konjica napravili su helikopter, pa onda mrav koji je milijardu puta slozeniji

od automobila.

У природи има свега, има и фантастичних и нефантастичних примјера што уопште не иде у прилог никаквом дизајну. У природи постоје закони по коме се понаша и тај вилин коњиц, а закон по коме неко сјеме пада правећи хеликоптерске замахе, и то што човјек направи машину сличну том принципу, доказује само да функционишу на истом закону, не и да је нужно коњиц или то хеликоптерско сјеме створено по интелигентном напору творца.

Иначе у природи не би смјело да постоји несавршених стварi ако је све последица беспрекорног дизајна, а управо примјер једног несавршеног - неинтелигентног дизајна је и људско ждријело:

гдје на једном кратком потезу од пар центиметара постоји заједнички канал за струјање ваздуха и пролазак хране. На том потезу постоји срећмо поклопац - епиглотис који при сваком гутљају рефлексно се затвара и спречава да храна уђе у душник, али то и даље не чини гутање потпуно сигурним, јер храна и течност ипак може доспјети до душника без обзира на сигурносне мјере које даје епиглотис и сасвим је могуће угушити се од хране ако се гута пуних уста или једе у лежећем положају, а до непријатности се може доћи и ако задихани и жедни хоћемо да угушимо жећ па потрегнемо за течношћу у стању напетих мишића и загрцнемо се ко од шале....Ждријело према томе није интелигентно дизајнирано, јер представља потенцијалну опасност за угрожавање живота. Да је душник одвојен од једњака на други начин, и да нема мјешања са једњаком, то би онда било интелигентно. Овако стање ждријела је слично као шахту у коме се сустичу канализација и водовод, а кад би тако нешто у пракси било изведено свакако би тај потез био окарактерисан као не баш интелигентан.

Исти је случај са цријевима гдје може доћи до запетљаја без икакве болести. Интелигентно би било да цријева функционишу, а да не може доћи до тако једне баналне ситуације да се запетљају и угрозе живот.

[Avocado]

Michael Behe Hasn't Been Refuted on the Flagellum

http://www.evolution...e-flagellum.jpg

Ovo zaista prolazi samo kod neukih...

IC argument se zasniva na ideji da se pojedini delovi IC sistema ne mogu ukloniti a da sistem i dalje funkcioniše. To je suština. Otud reč "irreducible" u "irreducible complexity"...

Autor članka navodi naučnike koji su pokazali nesporno da se pojedini delovi flagelluma mogu ukloniti a da sistem i dalje funkcioniše... i pita se da li je time ovaj argument odbačen... zatim zaključuje da nije jer taj odgovor "trivijalizuje kompleksnost i sofisticiranost celog sistema" budući da je stvaranje flageluma u svakoj bakteriji mnogo sofisticiran proces?!?!

On bukvalno tvrdi da iako je "nesvodljivost" pobijena, argument "nesvodljive kompleksnosti" i dalje stoji jer je sistem kompleksan. Nadam se da ne moram da ti objašnjavam koliko je ta tvrdnja retardirana.

[Avocado]

I došlo je i to doba godine...

glasanje traje do 14. oktobra.... glasa se ovde: http://www.crocoduck.org.uk/

nominovane klipove možete videti na ovoj listi:

http://www.youtube.c...5D5D2570BE5EA14

(Golden Crocoduck is awarded every year for the biggest breach of the 9th Commandment in pursuit of the creationist cause.)

[grigorije22]

Koliko ja znam Behe je tvrdio kako nema mehanizama koji bi mogao da evoluira deo po deo a da flagelum prezivljava eonima dok se

ceo sistem ne dovrsi. Kasnije je ovo pokusao da demantuje Kent Miler koristeci misolovku, gde je on isao od unapred ka nazad odnosno on

je na misolovci od nekoliko delova pokazivao kako kako rastavljanjem na jednostavnije forme, misolovka moze da se prilagodi da bude drzac za kravatu. Ali onda mu je Behe jasno objasnio da njegova refutacija nema nikakvu logicku podlogu na prvom mestu jer trebao bi da pokaze kako su od jednostavnijih formi misolovke uspvale da ujedno prezivljavaju, te idu ka kompleksnijim delovima sve dok se nije razvio citav danasnji sistem misolovke koja se ,,hrani misevima,, (a plus sve to treba objasniti koristeci cisto naturalne procese, odnosno prirodne zakone)

[grigorije22]

У природи има свега, има и фантастичних и нефантастичних примјера што уопште не иде у прилог никаквом дизајну. У природи постоје закони по коме се понаша и тај вилин коњиц, а закон по коме неко сјеме пада правећи хеликоптерске замахе, и то што човјек направи машину сличну том принципу, доказује само да функционишу на истом закону, не и да је нужно коњиц или то хеликоптерско сјеме створено по интелигентном напору творца.

Иначе у природи не би смјело да постоји несавршених стварi ако је све последица беспрекорног дизајна, а управо примјер једног несавршеног - неинтелигентног дизајна је и људско ждријело:

гдје на једном кратком потезу од пар центиметара постоји заједнички канал за струјање ваздуха и пролазак хране. На том потезу постоји срећмо поклопац - епиглотис који при сваком гутљају рефлексно се затвара и спречава да храна уђе у душник, али то и даље не чини гутање потпуно сигурним, јер храна и течност ипак може доспјети до душника без обзира на сигурносне мјере које даје епиглотис и сасвим је могуће угушити се од хране ако се гута пуних уста или једе у лежећем положају, а до непријатности се може доћи и ако задихани и жедни хоћемо да угушимо жећ па потрегнемо за течношћу у стању напетих мишића и загрцнемо се ко од шале....Ждријело према томе није интелигентно дизајнирано, јер представља потенцијалну опасност за угрожавање живота. Да је душник одвојен од једњака на други начин, и да нема мјешања са једњаком, то би онда било интелигентно. Овако стање ждријела је слично као шахту у коме се сустичу канализација и водовод, а кад би тако нешто у пракси било изведено свакако би тај потез био окарактерисан као не баш интелигентан.

Исти је случај са цријевима гдје може доћи до запетљаја без икакве болести. Интелигентно би било да цријева функционишу, а да не може доћи до тако једне баналне ситуације да се запетљају и угрозе живот.

Recurrent Laryngeal Nerve Is Not Evidence of Poor Design

by Jerry Bergman, Ph.D. *

Introduction

A common claim by evolutionists is that the human body is poorly designed, which to them is evidence that it was not intelligently designed, but rather cobbled together by the unintelligent process of evolution. One of the most frequent examples of poor design cited by evolutionists today is the recurrent laryngeal nerve (RLN), which controls the mammalian larynx (voice box) muscles. Paleontologist Donald Prothero wrote that examples of "poor or at least very puzzling design can be accumulated endlessly," thus proving evolution, with one of the best examples being "the recurrent laryngeal nerve, which connects the brain to the larynx and allows us to speak."

In mammals, this nerve avoids the direct route between brain and throat and instead descends into the chest, loops around the aorta near the heart, then returns to the larynx. That makes it seven times longer than it needs to be.

¹

Although the laryngeal nerve does not take the shortest route to the larynx, this is also true for many other nerves. The optic nerves do not take the shortest route to the occipital lobe of the brain (the lobe near the back of the head), but rather cross over at the optic chiasm (where the two tracts cross over in the form of an "X") for reasons now known to be based on good design. The nerves from the right side of the brain go to the left side of the body (except for the right and left frontal branches of a facial nerve, which are supplied by both sides of the brain) also for good reasons.

Likewise, the left RLN has a different anatomical trajectory than one would first expect, and for very good reasons. In contrast to Prothero's claim, the vagus nerve (the longest of the cranial nerves) travels from the neck down toward the heart, and then the recurrent laryngeal nerve branches off from the vagus just below the aorta (the largest artery in the body, originating from the left ventricle of the heart and extending down the abdomen). The RLN travels upward to serve several organs, some near where it branches off of the vagus nerve, and then travels back up to the larynx.²

This is the reason it is called the left recurrent laryngeal nerve. In contrast, the right laryngeal nerve loops around the subclavian artery just below the collarbone, and then travels up to the larynx. Of note is the fact that the longer left RLN works in perfect harmony with the right laryngeal nerve, disproving the faulty design claim.

Reasons for This Design

The most logical reason is that the RLN design is due to developmental constraints. Eminent embryologist Professor Erich Blechschmidt wrote that the recurrent laryngeal nerve's seemingly poor design in adults is due to the "necessary consequences of developmental dynamics," not historical carryovers from evolution.³

Human-designed devices, such as radios and computers, do not need to function until their assembly is complete. By contrast, living organisms must function to a high degree in order to thrive during every developmental stage from a single-cell zygote to adult. The embryo as a whole must be a fully functioning system in its specific environment during every second of its entire development. For this reason, adult anatomy can be understood only in the light of development. An analogy Blechschmidt uses to help elucidate this fact is the course of a river, which "cannot be explained on the basis of a knowledge of its sources, its tributaries, or the specific locations of the harbors at its mouth. It is only the total topographical circumstances that determine the river's course."⁴

Due to variations in the topographical landscape of the mammalian body, the "course of the inferior [meaning lower] laryngeal nerve is highly variant" and minor anatomic differences are common.⁵ Dissections of human cadavers found that the paths of the right and left recurrent laryngeal nerves were often somewhat different from that shown in the standard literature, illustrating Blechschmidt's analogy.⁶

Developmental Variations

The human body begins as a sphere called a blastocyst and gradually becomes more elongated as it develops. Some structures, such as the carotid duct, are simply obliterated during development, and some are eliminated and replaced. Other structures, including the recurrent laryngeal nerve, move downward as development proceeds. The movement occurs because the neck's formation and the body's elongation during fetal development force the heart to descend from the cervical (neck) location down into the thoracic (chest) cavity.⁷

As a result, various arteries and other structures must be elongated as organs are moved in a way that allows them to remain functional throughout this entire developmental phase. The right RLN is carried downward because it is looped under the arch that develops into the right subclavian artery, and thus moves down with it as development proceeds.⁸

The left laryngeal nerve recurs around the ligamentum arteriosum (a small ligament attached to the top surface of the pulmonary trunk and the bottom surface of the aortic arch) on the left side of the aortic arch. It likewise moves down as the thoracic cavity lengthens. The body must operate as a living, functional unit during this time, requiring ligaments and internal connections to secure various related structures together while also allowing for body and organ movement. For the laryngeal nerve, the ligamentum arteriosum functions like a pulley that lifts a heavy load to allow movement.

As a result of the downward movement of the heart, "the course of the recurrent laryngeal nerves becomes different on the right and left sides."⁹ These nerves cannot either be obliterated or replaced because many of them must function during every fetal development stage. Blechschmidt notes that "no organ could exist that is functionless during its development," an axiom that also applies to the nervous system.¹⁰ This movement appears designed to position the left RLN downward as the body elongates.

In addition, "the laryngeal branch splits up into other branches before entering the larynx at different levels."¹¹ These many RLN branches serve several other organs with both motor and sensory branches, including the upper esophagus, the trachea, the inferior pharynx, and the cricopharyngeus muscle, the lowest horizontal bandlike muscle of the throat just above the esophagus.¹² Neuroanatomists describe larynx innervation as "complicated" and they are still trying to work out the specific targets of its nerve branches. The fact that the left RLN also gives off some fibers to the cardiac plexus is highly indicative of developmental constraints because the nerve must serve both the larynx (in the neck) and the heart (in the chest).

As noted, after looping around the aorta, the RLN travels back up to innervate the larynx. The superior (meaning upper) and recurrent laryngeal nerves then innervate an area known as Galen's anastamosis. Other cases exist of one nerve splitting off early and providing direct innervations, and another taking what seems like a circuitous route. One example is the phrenic nerve that arises in the neck and descends to connect to the diaphragm. This is a necessary path, since the pericardium and diaphragm arise in the septum transversum (a thick mass of tissue that gives rise to parts of the thoracic diaphragm and the ventral mesentery of the foregut) in the neck area of the early embryo.

It then migrates caudally (toward the tailbone) as the embryo enlarges by differential growth of the head and thorax areas, taking the nerve with it. The diaphragm cannot have evolved step-wise, since a partial diaphragm results in an imperfect chest-abdomen separation. Even a small defect results in herniation of the gut contents into the chest--which either compresses the lungs or results in strangulation of the gut.

A complicated issue still being researched is how the incredibly complex nerve-muscle system, the component nerve fibers, and the laryngeal muscles arise from the neural crest (cells between the epidermis and the neural tube that develop into the brain and spinal cord) and dorsal somites (cells that develop into muscles and vertebrae) respectively in the early embryo, and then migrate anteriorly (towards the front of the body) into their final positions. Without explaining the nerve structure's design system, function, and ultimate connections, alleging that the RLN is a poor design is a meaningless assertion.

Thus, the claim that it has to loop up the distance from the ligamentum arteriosum for no reason is invalid. For all these reasons, Prothero's conclusions are incorrect and poorly considered:

Not only is this design wasteful, but…the bizarre pathway of this nerve makes perfect sense in evolutionary terms. In fish and early mammal embryos, the precursor of the recurrent laryngeal nerve [is] attached to the sixth gill arch, deep in the neck and body region.

¹³

The Redundant Pathway Design

Some innervations to the larynx go directly to the larynx, including the sensory internal laryngeal nerve and the motor external laryngeal nerve. Other nerves, the left and right superior laryngeal nerves, branch off close to the larynx to provide this structure with direct innervation. The superior laryngeal nerve branches off of the vagus at a location called the ganglion nodosum and receives a nerve branch from the superior cervical ganglion (group of nerve cells near the neck) of the sympathetic nervous system (a branch of the autonomic nervous system).¹⁴

Aside from the developmental reasons for the circuitous route, certain benefits of overlapping sensory and motor innervations result when one of the nerves is slightly longer. One reason why laryngeal nerve branches are located both above and below the larynx (both branch off the vagus) is because this design allows some preservation of function if either one is interrupted. The redundant pathway also provides some backup in case of damage to one of the nerves.

Knowledge of the laryngeal innervation will help us to understand the necessity for the slightly longer route for a nerve, and a hint is provided from the fact that the two nerves regulate different vocal responses. Paralysis of the superior laryngeal nerve (the non-circuitous nerve) causes difficulty in increasing voice loudness, producing a high pitch, vocal fatigue, and an inability to sing because the vocal cords lack their normal tone and cannot sufficiently lengthen. In contrast, paralysis of the recurrent nerve results in a weak voice that sounds like Mickey Mouse.

In one patient, a traumatic rupture of the aortic arch in a car accident required an aortic graft that left him with a severed left RLN. Although his voice was slightly feeble, his articulation was unaffected. He speaks perfectly well, but cannot project his voice because the laryngeal muscles have multiple innervations and the set as a unit controls its function.

Finally, several studies found that the existing path occupies a relatively safe position in a groove that renders it less prone to damage or injury than a more direct route.¹⁵

Conclusions

Arguing that the left RLN is poorly designed implies that God should have used different embryo developmental trajectories for all the structures involved to avoid looping the left RLN around the aorta. One who asserts that the RLN is a poor design assumes that a better design exists, a claim that cannot be asserted unless an alternative embryonic design from fertilized ovum to fetus--including all the incalculable molecular gradients, triggers, cascades, and anatomical twists and tucks--can be proposed that documents an improved design. Lacking this information, the "poor design" claim uses evolution to fill in gaps in our knowledge. Furthermore, any alternative embryonic design pathway would likely result in its own unique set of constraints, also giving the false impression of poor design.

The left recurrent laryngeal nerve is not poorly designed, but rather is clear evidence of intelligent design:

• Much evidence exists that the present design results from developmental constraints.
  
• There are indications that this design serves to fine-tune laryngeal functions.
  
• The nerve serves to innervate other organs after it branches from the vagus on its way to the larynx.
  
• The design provides backup innervation to the larynx in case another nerve is damaged.
  
• No evidence exists that the design causes any disadvantage.
  

The arguments presented by evolutionists are both incorrect and have discouraged research into the specific reasons for the existing design.

References

1. Prothero, D. 2008. Evolution: What the Fossils Say and Why It Matters. New York: Columbia University Press, 37-38.
   
2. Sadler, T. W. 2010. Langman's Medical Embryology, 11th ed. Philadelphia, PA: Williams & Wilkins.
   
3. Blechschmidt, E. 2004. The Ontogenetic Basis of Human Anatomy: A Biodynamic Approach to Development from Conception to Birth. B. Freeman, transl. New York: North Atlantic Books, 188.
   
4. Ibid, 108.
   
5. Sturniolo, G. et al. 1999. The Recurrent Laryngeal Nerve Related to Thyroid Surgery. The American Journal of Surgery. 177: 487-488.
   
6. Steinberg, J. L., G. J. Khane, C. M. C. Fernanades and J. P. Nel. 1986. Anatomy of the recurrent laryngeal nerve: A redescription. The Journal of Laryngology and Otology. 100: 919.
   
7. Sadler, T. W. 1990. Langman's Medical Embryology, 6th ed. Philadelphia, PA: Williams & Wilkins, 211.
   
8. Schoenwolf, G. C., S. B. Bleyl, P. R. Brauer and P. H. Francis-West. 2009. Larsen's Human Embryology. Philadelphia, PA: Churchill Livingstone, 407.
   
9. Sadler, 1990, Langman's Medical Embryology, 211.
   
10. Blechschmidt, The Ontogenetic Basis of Human Anatomy, 91.
    
11. Sturniolo et al, The Recurrent Laryngeal Nerve Related to Thyroid Surgery, 487.
    
12. Ibid.
    
13. Prothero, Evolution: What the Fossils Say and Why It Matters, 37-38.
    
14. Sanders, I. and L. Mu. 1998. Anatomy of the Human Internal Superior Laryngeal Nerve. The Anatomical Record. 252: 646-656.
    
15. Armstrong, W. G. and J. W. Hinton. 1951. Multiple Divisions of the Recurrent Laryngeal Nerve. AMA Archives of Surgery. 62 (4): 539.
    

* Dr. Bergman is an Adjunct Associate Professor at the University of Toledo Medical School in Ohio.

Cite this article: Bergman, J. 2010. Recurrent Laryngeal Nerve Is Not Evidence of Poor Design. Acts & Facts. 39 (8): 12-14.

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Koliko ja znam Behe je tvrdio kako nema mehanizama koji bi mogao da evoluira deo po deo a da flagelum prezivljava eonima dok se

ceo sistem ne dovrsi. Kasnije je ovo pokusao da demantuje Kent Miler koristeci misolovku, gde je on isao od unapred ka nazad odnosno on

je na misolovci od nekoliko delova pokazivao kako kako rastavljanjem na jednostavnije forme, misolovka moze da se prilagodi da bude drzac za kravatu. Ali onda mu je Behe jasno objasnio da njegova refutacija nema nikakvu logicku podlogu na prvom mestu jer trebao bi da pokaze kako su od jednostavnijih formi misolovke uspvale da ujedno prezivljavaju, te idu ka kompleksnijim delovima sve dok se nije razvio citav danasnji sistem misolovke koja se ,,hrani misevima,, (a plus sve to treba objasniti koristeci cisto naturalne procese, odnosno prirodne zakone)

Pa slabo znaš.... i pusti mišolovku...

Sam koncept koji iznosiš (da evoluira deo po deo a da flagelum prezivljava) je fundamentalno pogrešan... ne može da postoji flagellum a da mu delovi evoluiraju... već, nema flageluma, postoji samo jedan deo koji nešto radi, pa se pojavi još jedan deo koji nešto radi i tako dalje... i u jednom trenutku svi ti delovi zajedno čine flagelum.

Nađene su bakterije koje imaju samo pojedine delove, dakle, ranije stadijume u evoluiciji flageluma, čime je Beheov argument opovrgnut.

Takođe, veoma bitna stvar koju kreacionisti previđaju kada govore o ovoj temi je i da mogu postojati delovi koji su postojali pa prestali da postoje.

Vidi ovaj most...

On nema malter, i stoji usled svog oblika... on je "nesvodljivo kompleksan" jer bilo koji deo da mu skloniš, ceo most će da se sruši. Koristeći IC argument, mogao bi da tvrdiš da je ovaj most jedino mogao da nastane ako je svaki kamen u istom trenutku postavljen... što se naravno nije desilo, već je postojala drvena ili kamena platforma koja je nakon pravljenja mosta sklonjena.

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Recurrent Laryngeal Nerve Is Not Evidence of Poor Design

by Jerry Bergman, Ph.D. *

Jel neko iz ovog članka razumeo zašto RLN mora da ide dužim putem? Pošto ja zaista ne kontam šta je pisac hteo da kaže...

[Justin Waters]

• No evidence exists that the design causes any disadvantage.
  

Не нема, осим што можеш да се удавиш приликом обављања једне фундаменталне радње, узимања хране.

Јесу ли креационисти објаснили како је то птица киви тако интелигентно дизајнирана да јаје када је бременита заузима знатан волумен њеног тијела, што је јединствен примјер у птичијем свијету, чиме сама птица доживљава болове и тешкоће док се јаје не излеже.

Нема никаквог интелигентнот разлога зашто је јаје птице толико велико, а не нормалне величине у односу на тијело као што је кокошије или препеличино. Она би могла да преживљва и са мањим јајетом, као што преживљва са овим великим. Са овим великом, кад јаје нарасте довољно, вуче се доњи дио тијела по земљи, некад мора да уђе у хладну воду само да би олакшала напор, а прије изласка јајета, не може ништа јести 2 - 3 дана јер нема мјеста да желудац прошири.

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