Here, Cornelius Hunter discusses merely the most recent finding of *real* science (as distinct from the 'Science!' so beloved of DarwinDefenders) that shows Dawkins and the other DarwinDefenders to be *wrong* in claiming that our eyes are "wired backward" -- It’s Just Getting Worse: Our Retina Structure is “optimized for our vision purposes”
Here is a little something I first read about a good decade ago -- The Retinal Pigment Epithelium in Visual Function
AbstractTo put this into plain English: the supposed "backwards" design of the retina is actually critical to "maintain the photoreceptor excitability" of the cone and rod cells -- that is, to allow us to see as efficiently as we.
Located between vessels of the choriocapillaris and light-sensitive outer segments of the photoreceptors, the retinal pigment epithelium (RPE) closely interacts with photoreceptors in the maintenance of visual function. Increasing knowledge of the multiple functions performed by the RPE improved the understanding of many diseases leading to blindness. This review summarizes the current knowledge of RPE functions and describes how failure of these functions causes loss of visual function. Mutations in genes that are expressed in the RPE can lead to photoreceptor degeneration. On the other hand, mutations in genes expressed in photoreceptors can lead to degenerations of the RPE. Thus both tissues can be regarded as a functional unit where both interacting partners depend on each other.
I. INTRODUCTION
The retinal pigment epithelium (RPE) is a monolayer of pigmented cells forming a part of the blood/retina barrier (72, 372, 492, 558). The apical membrane of the RPE faces the photoreceptor outer segments (Fig. 1). Long apical microvilli surround the light-sensitive outer segments establishing a complex of close structural interaction. With its basolateral membrane the RPE faces Bruch’s membrane, which separates the RPE from fenestrated endothelium of the choriocapillaris (Fig. 1).
[figure 1]
Summary of retinal pigment epithelium (RPE) functions. PEDF, pigment epithelium-derived growth factor; VEGF, vascular epithelium growth factor; Epithel, epithelium.
As a layer of pigmented cells the RPE absorbs the light energy focused by the lens on the retina (72, 86). The RPE transports ions, water, and metabolic end products from the subretinal space to the blood (144, 236, 369, 402, 558). The RPE takes up nutrients such as glucose, retinol, and fatty acids from the blood and delivers these nutrients to photoreceptors. Importantly, retinal is constantly exchanged between photoreceptors and the RPE (30, 58, 596). Photoreceptors are unable to reisomerize all-trans-retinal, formed after photon absorption, back into 11-cis-retinal. To maintain the photoreceptor excitability, retinal is transported to the RPE reisomerized to 11-cis-retinal and transported back to photoreceptors. This process is known as the visual cycle of retinal. Furthermore, the voltage-dependent ion conductance of the apical membrane enables the RPE to stabilize ion composition in the subretinal space, which is essential for the maintenance of photoreceptor excitability (144, 558, 559). Another function in the maintenance of photoreceptor excitability is the phagocytosis of shed photoreceptor outer segments (72, 170, 187, 575). The photoreceptor outer segments are digested, and essential substances such as retinal are recycled and returned to photoreceptors to rebuild light-sensitive outer segments from the base of the photoreceptors. In addition, the RPE is able to secrete a variety of growth factors helping to maintain the structural integrity of choriocapillaris endothelium and photoreceptors. Furthermore, the secretory activity of the RPE plays an important role in establishing the immune privilege of the eye by secreting immunosuppressive factors (280, 581). With these complex different functions, the RPE is essential for visual function. A failure of any one of these functions can lead to degeneration of the retina, loss of visual function, and blindness. In the following sections these functions will be described in more detail. ...
To put it another way, if Dawkins, being a "tidy minded engineer", had designed our eyes, our vision wouldn't be nearly as good as it is, and it wouldn't be nearly as fitted to how we actually live as it is. Since the photoreceptor cells couldn't react as quickly as they do to the *next* photon to strike them, we'd need to have much bigger eyes, with far more photoreceptor cells,to send the same amount of visual information to the brain. Or, perhaps our visual experience of the world would have to be as a series of stills, instead of smoothly flowing.
So, if it really were the case that our eyes were "wired backward" ... and that this were then proof that Darwinism, and atheism, are the truth about the nature of reality ... does the *real* scientific finding that they're not "wired backward" count as proof that Darwinism, and atheism, are falsehoods about the nature of reality? Of course not! For the "our eyes are wired backward" argument (ahem!) was never offered ion good-faith in the first place.
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