Monday, 13 July 2009

Camera Obscura

A refracting lens is a key component of our image-forming camera eye; however, its evolutionary origin is unknown because precursor structures appear absent in non-vertebrates.

Most living vertebrates possess anterior paired eyes, each with a lens. Although anterior photoreceptors are known to have evolved before the radiation of the major lineages of bilaterally symmetrical animals, the vertebrate lens is a more recent innovation that evolved in the vertebrate lineage. Indeed, the accurate vision facilitated by the lens is one of the key adaptations proposed to underlie the evolution of active predation by ancestral vertebrates and the subsequent evolutionary success of vertebrates themselves. The unique structural properties of the lens are due to its very high content of long-lived proteins, the crystallins. These derive predominantly from two gene families, the α-crystallin family and the βγ-crystallin family. The structure of βγ-crystallins has been elucidated and found to have derived from an ancestral protein domain that comprised two symmetrically organized Greek key motifs.

Vertebrates, together with invertebrate urochordates such as the sea squirt Ciona intestinalis, compose phylum Chordata. C. intestinalis larvae share a basic chordate body plan with vertebrates, including the possession of a notochord and dorsal neural tube in which an anterior photoreceptor resides in a small brain. Urochordates are, however, thought to have split from the vertebrate lineage prior to the evolution of the lens and the associated co-option of crystallin genes into the visual system.

In the larval head is a small brain that includes a neuroectodermal sensory vesicle with two sensory organs, the ocellus and the otolith, together thought responsible for controlling larval locomotion in the search for a suitable site for metamorphosis. Once located, the larva adheres to the substratum with secretion from three anterior epidermal palps and subsequently undergoes a radical metamorphosis during which the majority of the brain and tail are reabsorbed. The remaining tissues are extensively remodeled to produce a sedentary adult. The ocellus is a ciliary-based photoreceptor system that includes a single pigmented cell and is considered homologous to the vertebrate retina. In some urochordate larvae, including those of C.intestinalis, three cells lie above the pigment cell, and because light must pass through them to reach the photoreceptors, these are sometimes referred to as lens cells. However, there is no evidence that these cells are homologous to vertebrate lens cells. Similarly, the otolith is not considered homologous to the vertebrate ear.

The two pigmented cells of the ascidian sensory vesicle share a common developmental origin in that they arise from a bilaterally symmetrical pair of cells in the anterior nervous system. These cells have been shown to be initially equivalent, with the potential to form both types of pigment cell. Which forms ocellus and which forms otolith appears to be regulated by Bmp and chordin signaling. Additionally both ocellus and otolith lineages express opsins. Because anterior photosensory structures are primitive for the bilateria, the parsimonious explanation is that both ocellus and otolith evolved from such photosensory structures.

We therefore conclude that the evolution of the lens did not derive from a new association between a visual system regulatory circuit and co-opted lens structural genes but from the reuse of a pre-existing regulatory interaction linking these components in the central nervous system of a primitive chordate.
http://users.ox.ac.uk/~zool0615/My%20PDFs/Ciona%20crystallin%20CB%202005.pd

The brain of the ascidian larva comprises two pigment cells, termed the ocellus melanocyte and the otolith melanocyte. Cell lineage analysis has shown that the two bilateral pigment lineage cells (a-line blastomeres) in the animal hemisphere give rise to these melanocytes in a complementary manner.

...The two bilaterally positioned cells destined to become the pigment cells in the first step are still equipotent at this stage in that they can give rise to either the ocellus or otolith. Thus, they constitute what is termed an "equivalence group." In the second step, the individual fates of the two cells that compose the equivalence group are determined. Namely, one cell develops into an ocellus and the other cell develops into an otolith.
http://www.ncbi.nlm.nih.gov/pubmed/2494088

Ocellus noun, plural ocelli, adjective ocellate - from Latin, ocellus, a little eye.

1. Simple eyes, small extra eyes, usually situated on the top of the head. The cuticle covering the eye is thickened like a lens. Below the lens there is a layer of transparent cells, continuous with the adjacent epidermal cells. Most insects with complete metamorphosis (holometabolous) have three ocelli on top of the head, arranged in a triangle.
http://bugguide.net/node/view/111296

Dorsal ocelli are light-sensitive organs found on the dorsal (top-most) surface or frontal surface of the head. They tend to be larger and more strongly expressed in flying insects (particularly bees, wasps, dragonflies and locusts), where they are typically found as a triplet.

A dorsal ocellus consists of a lens element (cornea) and a layer of photoreceptors (rod cells). As noted above, ocelli vary widely among insect orders. The ocellar lens may be strongly curved (e.g. bees, locusts, dragonflies) or flat (e.g. cockroaches). The photoreceptor layer may (e.g. locusts) or may not (e.g. blowflies, dragonflies) be separated from the lens by a clear zone (vitreous humour). The number of photoreceptors also varies widely, but may number in the hundreds or thousands for well developed ocelli.
http://www.absoluteastronomy.com/topics/Ocellus

The “otolithic organs,” as they are known, are a pair of sensors—the utricle and the saccule—nestled in the labyrinthine architecture of the inner ear.

Grossly speaking, each consists of a bunch of tiny pebbles (of the white rock known as calcium carbonate) embedded in a gooey wad that sits atop a carpet of delicate hairs. The saccule is roughly vertical in our heads, and the utricle more or less horizontal. Together they orient us in the world, since they work as tiny inertial references: raise your head suddenly (or get in a jerky elevator), and the pebbles of the saccule get momentarily left behind as your skull starts upward; this bends down the hairs against which those pebbles lay, and the sensitive hairs function like switches, sending signals to your brain that you register as a feeling of ascent. The utricle does the same work for motion from side to side, and between them these tiny organs generate the neurological data that give us our normal sense of being in the world. What would it feel like not to have those pebbles? Delete them from a mouse and it spends a lot of time falling over.

Both the utricle and the saccule contain what I have called “pebbles,” but they are little more than mineral crystals really, microscopic sand bound together into a mass by a matrix of protein. Not so the homologous structures in fish, our evolutionary ancestors. They retain, inside their skulls, quite clearly defined, and nearly always large enough to see (and sometimes as large as marbles), healthy little rocks known as otoliths, or “ear stones.” The minute pebbles of our otolithic organs would appear to be the powdered remains of these ancestral lithic pips.

Fish otoliths are among the strangest and most wonderful bits of vertebrate anatomy. They are strikingly sculptural, and their clean surfaces tend to display an alluring opalescent sheen. No one is absolutely sure about all their functions (which would seem to vary from species to species), but it is safe to say that they generally serve in a sensory system very much like the saccule/utricle: they sit atop a mat of sensitive hairs and their sloshing around gives the fish information about its movement in space. Fish that have to deal with complicated spatial environments (reefs, kelp beds) usually have bigger otoliths; those open water predators that stick to swimming fast in straight lines (tuna, billfish) tend to have relatively small ones.



Otoliths also seem to play a role in underwater hearing in many species: because they are stone (and therefore of a different specific gravity than the rest of the fish), their vibrations in response to sound waves are out of phase with those of the animal’s body; these differences can be translated into acoustic information. (Interestingly, although hearing in mammals is now handled by a very different system, it has recently been shown that human beings can “hear” very high frequency sounds by means of their otolithic organs, which appear to retain some acoustic sensitivity, despite having been converted almost entirely into sensors for movement and orientation).

...About thirty years ago a curious geologist, tinkering with an otolith (it was a rock, after all), made the truly shocking discovery that those annual layers can be further resolved, microscopically, down to daily layers, layers that contain, in their chemical composition and size, information about the temperature and the salinity of the water through which the fish moved, the food that it ate, and various environmental contaminants it encountered. The result is a stratigraphy unprecedented in the organic world: the diligent student can peruse the otolith of a long-lived deep sea fish, and reconstruct not merely its age, but (and I am barely exaggerating) what it had for breakfast on 6 March 1964...
http://www.cabinetmagazine.org/issues/31/burnett.php



Apart from the obvious detection of sounds, the inner ear also helps the fish to orient itself in three dimensional space, giving it a feeling of bottom (gravity) and direction.

As sound waves reach a fish, the whole fish moves with the waves, as water is non-compressible. The otoliths, being more dense than the rest of the fish (3X) lag behind the rest of the fish. The otoliths are suspended in liquid and are surrounded by ciliary bundles located on the ends of sensory hair cells. The differential movement of the otoliths bends some of these cilia, which deforms the hair cells, which stimulates neural transmission to the auditory centers of the brain.

With higher frequency sounds, the amplitude of fish displacement is much less and more energy is needed for otolith stimulation. Some fishes have adaptations to increase the sensitivity of their hearing. The gas bubble of the swimbladder of some bony fishes can serve as a sort of amplifier. As gas is more compressible than water, the bladder will pulsate more than the rest of the fish when encountering sound waves. This vibrates the tissues around the bladder, providing the necessary additional movement for auditory nerve stimulation.

As with most vertebrates, the eye is the primary site of photoreception. However, the pineal organ also is photosensitive and is especially important in maintaining circadian (day-night, seasonal) rhythms.

The choroid coat lies under the retina and serves to supply the retinal cells with nutrients and oxygen. Fishes that are heavily vision-dependant have the best developed choroid retina and the highest oxygen concentrations in the vitreous humor of the eye.

Teleosts living below 500m have been found to have a different pigment (chryopsin), this pigment absorbs mainly in the blue region of the spectrum, which is the spectral range of light found in deeper waters.
http://www.montana.edu/ecology/courses/biol415/sens2.doc.

In the frog, light-sensitive pigment cells in the skin and iris, as well as hypothalamic neurones involved in the control of circadian rhythms, express a chromophore—melanopsin. The impact of a photon on melanopsin induces conformational changes in a seven-membrane G-coupled receptor that is subsequently regenerated in neighbouring cells. Invertebrate photoreceptor cells behave similarly, except that the properties of a different G protein allow the chromophore to be regenerated and available within the same cell. This feature reflects the dispersed nature of photoreceptors in invertebrates—the specialized cell-packed structures that allow functional specialization in eyes do not exist.

Invertebrate-type opsins may have survived in vertebrate skin to provide light sensitivity in tissues remote from the eye, but light-dependent intracellular pigment redistribution may also have evolved for thermoregulation and photoprotection. Arnheiter thinks that pigment cells may have been the evolutionary precursors of photoreceptor cells, since the role of pigment cells in eyes is to act as a screen blocking access of light to one side of a receptor cell to endow it with directional sensitivity. Although photoreception has developed along a number of evolutionary pathways, it seems probable that the starting point was always a rhodopsin-expressing pigment cell in the skin.
http://qjmed.oxfordjournals.org/cgi/content/full/95/1/61

For equilibrium control in man, the inner ear contains some tiny 'stones' called otoliths (from the Greek: otos=ear andlithos=stone). In fact these stones are crystals of minerals like calcium carbonate. The stones are inside three semi-circular canals, each one working in one of the three dimensions. As these stones are mineral, they are heavier than surrounding biological tissues: when they move they push on ciliated cells which produce a nervous stimulation, which is used by the brain to compute our body position. Another ear part called the vestibule, is used to detect rotation and acceleration movements by using a similar principle.

It's surprising to find such a sophisticated process in other creatures, but particularly in marine zooplankton, including the larval stages of primitive animals. Some examples are described below.

Equilibrium organs are called statocysts. They contain statoliths (stones) made with dense material such as calcium or magnesium salts crystals which are in contact with specialized cells. Many research studies are in progress on this topic and a hypothesis would be that actin fibers connect the statoliths to the cells.

Many experiments of seed growing in micro-gravity have been made during space flights of the American Shuttle and in this case roots are observed to grow in any direction. (Sorry, I have been unable to rent the Shuttle to try this experiment myself!)
http://www.microscopy-uk.org.uk/mag/indexmag.html?http://www.microscopy-uk.org.uk/mag/artdec02/jmcstatolit.html


I guess by now you are getting a good idea of how my brain works. I tend to try and find a relationship between various bits of information, and then keep on leap-frogging from source to source from there on in.

Some things will catch my eye. Sometimes things will really stand-out for me. I'm not sure why, but some things will just feel right. I had previously published a small extract from a paper on statoliths in Phycomyces, which right now, feels like it belongs here too:

Statoliths in Phycomyces: Characterization of octahedral protein crystals.

The crystals, which are present throughout the central vacuoles of the sporangiophore, function as statoliths.

Absorption spectra of isolated crystals and in situabsorption spectra of growing zones indicate the presence of chromophores, probably oxidized and reduced flavins. The flavin nature of the chromophores is also indicated by their fluorescence properties. It appears likely that the chromophores represent an essential part of the statoliths and thus the gravitropic transduction chain.
http://linkinghub.elsevier.com/retrieve/pii/S108718450091199X


The common origin (monophyly) of all animal eyes is now widely accepted as fact based on shared anatomical and genetic features of all eyes; that is, all modern eyes, varied as they are, have their origins in a proto-eye believed to have evolved some 540 million years ago.

As the eye ages certain changes occur that can be attributed solely to the aging process. Most of these anatomic and physiologic processes follow a gradual decline.

With aging a prominent white ring develops in the periphery of the cornea- called arcus senilis. Aging causes laxity and downward shift of eyelid tissues and atrophy of the orbital fat. These changes contribute to the etiology of several eyelid disorders such as ectropion, entropion, dermatochalasis , and ptosis. The vitreous gel undergoes liquefaction (posterios vitreous detachment or PVD) and its opacities — visible as floaters — gradually increase in number.
http://www.omnipelagos.com/entry?n=eye

Vertebrates have evolved two types of eyes; the lateral eyes (paired eyes) and the median eyes (pineal or parietal eyes). The urochordate ascidian larva has an eye-spot (ocellus) in its brain. Putative photoreceptor organs have also been reported in adult ascidians. Understanding evolutionary relationships between the ascidian photoreceptors and the vertebrate eyes is a key to uncover the origin and evolution of the vertebrate eyes. In C. intestinalis, we have characterized and examined expression patterns of homologues of genes involved in function or development of the vertebrate eyes.

The results suggest that ascidians have photoreceptor systems more similar to those of vertebrates than to those of other invertebrates. The larval ocellus expresses a vertebrate-type opsin gene and the surrounding brain cells express visual cycle genes similar to those found in the retinal pigment epithelium of vertebrates. A number of genes related to eye function and development are also expressed in part of the primordial pharynx and atrial primordia, suggesting that adult photoreceptors develop in these regions, possibly oral and atrial siphons.

Based on comparisons of the developmental origins, gene expression patterns, and functions of eyes between vertebrates and ascidians, we propose a hypothesis that the larval ocellus and the adult anterior photoreceptors (of the oral siphon) are homologous to the vertebrate median eye and lateral eyes, respectively. The last common ancestor of urochordates and vertebrates may have possessed distinct precursors of the lateral eyes and the median eye of vertebrates.

Another interesting modification in the larval nervous system in ascidians is found in the diversity of the brain sensory organs. The larval brain of Ciona and Halocynthia contains two sensory organs, the otolith (gravity-sense organ) and the ocellus (photoreceptor organ). In some ascidian species, such as those in the genus Molgula, however, the brain contains only the otolith. On the other hand, other species, including Botryllus schlosseri, have a single sensory organ, the photolith, responding to both gravity and light. We intend to compare development of the brain sensory organ in these species with that of Ciona. This study will contribute to our understanding how developmental pathways can be modified during evolution.
http://www.sci.himeji-tech.ac.jp/life/bioinfo/kusakabe/research.html




The tuatara is a reptile endemic to New Zealand which, though it resembles most lizards, is actually part of a distinct lineage, order Sphenodontia. The two species of tuatara are the only surviving members of its order, which flourished around 200 million years ago. Their most recent common ancestor with any other extant group is with the squamates (lizards and snakes). For this reason, tuatara are of great interest in the study of the evolution of lizards and snakes, and for the reconstruction of the appearance and habits of the earliest diapsids (the group that also includes birds and crocodiles).



The tuatara has a third eye on the top of its head called the parietal eye. It has its own lens, cornea, retina with rod-like structures, and degenerated nerve connection to the brain, suggesting it evolved from a real eye. The parietal eye is only visible in hatchlings, which have a translucent patch at the top centre of the skull. After four to six months it becomes covered with opaque scales and pigment. Its purpose is unknown, but it may be useful in absorbing ultraviolet rays to manufacture vitamin D, as well as to determine light/dark cycles, and help with thermoregulation. Of all extant tetrapods, the parietal eye is most pronounced in the tuatara. The parietal eye is part of the pineal complex, another part of which is the pineal gland, which in tuatara secretes melatonin at night. It has been shown that some salamanders use their pineal body to perceive polarised light, and thus determine the position of the sun, even under cloud cover, aiding navigation.

Together with turtles, the tuatara has the most primitive hearing organs among the amniotes. There is no eardrum and no earhole, and the middle ear cavity is filled with loose tissue, mostly adipose tissue. The stapes comes into contact with the quadrate (which is immovable) as well as the hyoid and squamosal. The hair cells are unspecialized, innervated by both afferent and efferent nerve fibres, and respond only to low frequencies. Even though the hearing organs are poorly developed and primitive with no visible external ears, they can still show a frequency response from 100-800 Hz, with peak sensitivity of 40 dB at 200 Hz.

Tuatara probably have the slowest growth rates of any reptile, continuing to grow larger for the first 35 years of their lives. The average lifespan is about 60 years, but they can live to be well over 100 years old. Some experts believe that captive tuatara could live as long as 200 years
http://en.wikipedia.org/wiki/Tuatara

The pineal gland or epiphysis synthesizes and secretes melatonin, a structurally simple hormone that communicates information about environmental lighting to various parts of the body. Ultimately, melatonin has the ability to entrain biological rhythms and has important effects on reproductive function of many animals. The light-transducing ability of the pineal gland has led some to call the pineal the "third eye".

The pineal gland is a small organ shaped like a pine cone (hence its name). It is located on the midline, attached to the posterior end of the roof of the third ventricle in the brain. The pineal varies in size among species; in humans it is roughly 1 cm in length, whereas in dogs it is only about 1 mm long. To observe the pineal, reflect the cerebral hemispheres laterally and look for a small grayish bump in front of the cerebellum. The images below shows the pineal gland of a horse in relation to the brain.



Histologically, the pineal is composed of "pinealocytes" and glial cells. In older animals, the pineal often is contains calcium deposits ("brain sand").
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/otherendo/pineal.html



The gland will sometimes shrink and then fill up with specific types of mineral salts that are referred to as "brain sand." The condition has been traced directly to poor nutrition. When this condition exists in the pineal gland, thinking and sexual processes are affected. The pineal gland will respond quickly to proper nutrition even after being "starved" and degeneration has begun. The pineal contains more lecithin than any other body part.

The pineal isn't an actual gland; it's a neuroendocrine transducer: meaning it converts incoming nerve impulses into outgoing hormones. Most glands are triggered by changes in the body or hormones secreted by other glands. The pineal gland releases hormones in response to bioelectrical messages from the outside environment received through the eyes. The optic nerve sends information to the visual portion of the brain through nerve fibers. The impulses from the brain are carried to the superior cervical ganglia (a cluster of nerve cells) in the upper part of the neck by smaller nerve fibers. From there the autonomic nervous system relays the information to the pineal.
http://hubpages.com/hub/Human_Growth_Hormone__Melatonin_And_The_Pineal_Gland

In some lower vertebrates, the Epiphysis Cerebri - Pineal Gland, has a well developed eye - like structure; in others, though not organized as an eye, it functions as a light receptor. In lower vertebrates, the pineal gland has an eye like structure and it functions as a light receptor and also is considered by some, to be the evolutionary forerunner of the modern eye.
http://www.strayreality.com/Lanis_Strayreality/thirdtyepinealgland.htm

The human pineal gland, in the centre of the brain, has been found to contain large numbers of calcite micro-crystals that “bear a striking resemblance” to calcite crystals found in the inner ear. The ones found in the inner ear have been shown to exhibit the quality of piezoelectricity. If those found in the pineal gland also have this quality then this would provide a means whereby an external electromagnetic field might directly influence the brain.

It’s interesting to note, though, that paragraph 18 does refer to a suggestion by Frohlich that a biological system might behave in some way like a radio receiver, amplifying a very small signal through a process of resonance; this idea is dismissed due to the unlikelihood of biological material resonating in this way – but of course one of the earliest types of radio was the ‘crystal set’, in which a mineral crystal was made to resonate (by tuning with a ‘cats whisker’) with an incoming radio wave, which is simply an electromagnetic wave of rather lower frequency than microwaves. The conclusion of this section was that “…there is little evidence to support resonant behaviour…”. The existence in the pineal gland of crystals which may prove to exhibit piezoelectric properties puts the whole issue in a totally different light – particularly in a scenario where the absolute requirement is to ‘play it safe’ (Stewart’s ‘Precautionary Principle’).
http://www.starweave.com/pinealsummary/

The organ where calcification is so widely accepted that it is almost considered a natural consequence of aging, is the pineal gland. In Japan, a study of 2877 people of all ages, after pathological cases were excluded, showed a 81% pineal calcification rate in people between 70 and 79 year old. The youngest person they found to have calcification of the pineal gland was 8 years old. They found that calcification increased with age. Another Japanese study of 450 subjects, found a 70% pineal calcification rate in people over 30 years, and also found the rate of calcification was proportional to increase in age. A German study focused on pineal calcification in 1044 children found calcification in 3% of children under 1 year, rising gradually to 7% at 10 years of age, and 33% by 18 years of age.

The composition of the calcification in the pineal gland has been shown to have calcium and phosphorus as the major elements and accumulations of calcium associated with phosphorus have been localized in vesicles,vacuales, lipid droplets, lipopigments, and mitochondria of dark pinealocytes.

There is also one bacteria that deserves special attention, due to its role in calcification. In 1998, Drs. O Kajander and N Ciftcioglu came across a very slow growing bacteria, which they called nanobacteria sanguineum, while they were researching something else. This bacteria, so small that it needs highly specialized instruments for it to be detected, protects itself by building a calcium shell around itself. It has been implicated in the plaque that forms on artery walls, and has been found in kidney stones and implicated in polycystic kidney disease.
http://www.customhps.com/Pres_Foc_Pineal.htm

“We can’t publish this. It’s too small to be alive. It must be a contaminant”

The turbidity in Kajander and Ciftcioglu’s culture flask turned out to be biofilm, elaborated by a previously undescribed bacterial species, which they named Nanobacterium sanguineum.

Nanobacteria readily bind to mammalian cells, trick the cells into internalizing them, and then trigger target cell apoptosis - including killing those cells responsible for our natural defenses like T-Lymphocytes (fig1-Nanobacteria killing a T6 Lymphocyte). N. sanguineum demonstrates unique radioresistance, related to its unique nucleic acid makeup and low division rate.
http://www.amri-ohio.com/Nanobacterium/NB%20-%20Literature%20Review/What%20is%20it%20-%20Small%20size.htm


At the moment I'm a sucker for the word "turbid". We have not only turbid waters and turbid skies, but also turbid amber, and turbid urine. Cloudy, murky, or turbid (muddy) urine is characteristic of a urinary tract infection, which may also have an offensive smell. Turbidity is also sometimes applied to describe cataracts in the eye.

The word cataract comes from the Greek meaning "waterfall". Until the mid 1700s, it was thought that a cataract was formed by opaque material flowing, like a waterfall, into the eye.

Cataracts are a common occurrence, often in the elderly, where the lens of the eye loses its transparency and becomes turbid. Cataracts usually occur in one eye first, followed by the other later. Cataracts are protein crystals which grow in the lens of the eye. They begin very small and grow until they obstruct vision; if untreated they can cause blindness.

Think of your eyeball as a balloon full of water, but instead of being rubber, it is a protein membrane. Optical tissue normally allows fluids to flow through the membrane wall which acts like a filter, cleaning out harmful particles, keeping your eyes clear and your vision good as it allows nutrients to permeate. But should the membranes become tough like leather, the fluids are trapped and particles begin to accumulate. If this buildup continues, your vision will seem as if you're looking through frosted glass, a condition known as cataracts.



It all started when NASA senior scientist Rafat Ansari developed a low-powered laser light device to help astronauts with experiments growing crystals in space.

Ansari, with NASA's John Glenn Research Center in Cleveland, knew physics, not medicine. Then his father developed cataracts, where the eye's normally clear lens becomes permanently clouded. Surgery to replace the lens is the only fix.

Surprised at the lack of options, Ansari read up on cataracts and learned the lens is largely made up of proteins and water. One type of protein, called alpha-crystallin, is key to keeping it transparent. When other proteins get damaged — by the sun's UV radiation or cigarette smoke or aging — alpha-crystallins literally scoop them up before they can stick together and clog the lens. But we're born with a certain amount of alpha-crystallin. Once the supply's gone, cataracts can form.
http://www.chinadaily.com.cn/life/2009-01/21/content_7417903.htm

Nanobacterium Sanguineum is a Nanobacteria that is approximately 10,000 times smaller than regular bacteria. It replicates from 1000 to 10,000 times slower than regular bacteria as well. It grows in the human system in blood, and has been found by various medical researchers and scientists to cause many human problems.

Some of the various diseases that it has either been implicated to be involved with or to cause are: calcification in atherosclerotic plaque, kidney stones, calcification in the lenses of eyes that ultimately causes "cataracts", soft tissue calcification in scleroderma, calcification in tumors, calcification in arthritis or osteoarthritis and other pathological disease states in humans. These nanobacteria colonize and secrete a "biofilm" over themselves that causes them to be covered by a calcium "shell". These nanobacteria are implicated to be the cause of all calcification in the human system that you were not born with, that you subsequently develop as you age. These nanobacteria are also implicated in causing some forms of cancer and "apoptosis" or cell death.
http://www.amazon.com/review/R2LR8ATD124FNW


We're all a little weary of a new darnfangled disease, aren't we? Does this new research carry any weight? I think that there could be some very exciting ground to be covered in the future regarding nanobacteria. I'm fascinated by the role nanobacteria might play in cataracts.

And here's a thing. I thought I had tonsilitis a few days back. I had found tiny greenish lumps on my tonsils. I had had a funny taste in my mouth, especially when swallowing food, for a good month or so. It was not a pleasant taste - almost rancid. Well, I looked it up on the web and found they were called tonsil stones, and that they are not so much an infection, but are more related to dental plaque. Nanobacteria has been implied in the formation of dental plaque. Am I growing a culture of nanobacteria at the back of my throat? Further still, after describing all these ailments to my wife, I remain unsure to whether she will ever kiss me again.

A role for Melatonin in the regulation of energy production and tissue calcification has been proposed: When Melatonin is plentiful, it is easy to incorporate phosphorus into ATP, and cellular energy is plentiful. When Melatonin is in short supply, ATP production is blunted. The phosphorus will then be incorporated into calcium pyrophosphate, and the mitochondria will begin to calcify. This process occurs first in energy intensive organs, such as the heart, the kidney, and the pineal gland itself. As the pineal begins to calcify, its output of Melatonin falls off further, so pineal and extra-pineal calcification will progress. The Pineal gland appears to be the first organ to calcify in man – the beginning of the end.

Could it be that N. sanguineum puts a brake on human longevity, or that impaired immune function or recurrent Nanobacteremia leads to organ system dysfunction and premature senescence, via the mechanism of Pineal Gland calcification? Could they be everywhere? Rather, why wouldn’t we assume that they are everywhere in our tissues?
http://www.heartfixer.com/Nanobacterium/NB%20-%20Literature%20Review/Brain_sand.htm







Many thanks:


http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2636888
http://www.a4t.org/Health/nanobacteria.html
http://life.bio.sunysb.edu/ee/seatrout/Cynoscion_sagittae_pictures.html
http://www.heartfixer.com/Nanobacterium/NB%20-%20Literature%20Review/Kidney%20stones.htm
http://www.crystalinks.com/thirdeyepineal.html
http://www.nsbri.org/HumanPhysSpace/focus7/ep_structure.html
http://www.medicine.mcgill.ca/physio/cullenlab/Notes209.htm
http://%20flrec.ifas.ufl.edu/entomo/ants/ant_anatomy.htm
http://www.tchain.com/otoneurology/disorders/bppv/bppv.html
http://www.newmediaexplorer.org/chris/2003/09/03/cataract_msm_eye_drop_solution.htm
http://www.otmagazine.co.uk/articles/docs/232fd150ab01c6cd7514ac1d1e306ac7_brown20010406.pdf

Sunday, 12 July 2009

History of Ultraviolet Photobiology

The following are extracts from a paper called "History of Ultraviolet Photobiology", and it really lives up to the title. The paper is a very thorough background to the study of ultraviolet light, and its effects. It was written by Philip E. Hockberger. I thought it was sheer brilliant, and very, very well researched. It was the kind of stuff that can make one feel a bit like a diver swimming around the coral reef. Loads of interesting things going on, lots to take on-board. Below are a few juicy bits which caught my eye....

Starting in the late 17th century, a new mythology arose in Europe that was based upon scientific principles and provided the basis for a more reliable understanding of the relationship between humans and sunlight. By the start of the 19th century, the application of these principles led to the realization that sunlight is not a single stimulus but, rather, a collection of stimuli of different wavelengths (e.g., infrared, visible, ultraviolet). This realization inspired additional studies aimed at determining whether different wavelengths might be responsible for the different effects of sunlight

In 1801, Ritter made the hallmark observation. He noticed that invisible rays just beyond the violet end of the spectrum were even more effective at darkening silver chloride-soaked paper. He called them "deoxidizing rays" to emphasize their chemical reactivity and to distinguish them from the "heat rays" at the other end of the visible spectrum.

In 1832, Picton (44) was the first to document the detrimental effects of sunlight on patients with smallpox. He reported that soldiers confined to dungeons during a smallpox epidemic contracted the disease but recovered without suppuration or scarring.

In 1866, Schutze (cited in 31) demonstrated that vertebrate eyes possess two kinds of photoreceptors: rods for dim vision and cones for color vision. In 1877, Boll (131, 132) and Kühne (133, 134) independently published their classical studies on visual purple (rhodopsin), the photoreceptor pigment of rods, and established that it was involved in the detection of light. Sixty years later, Hosoya (135) showed that rhodopsin absorbs UV as well as visible rays.

In 1875, Von Platen (112) found that illumination of the frog retina stimulated oxygen uptake, CO2 production, and increased metabolism. The same year, Pott (113) showed that an individual mouse produced more CO2 under green or yellow light than under violet, red or sunlight. It also produced less CO2 at night.

In 1883, Graber (141) showed that blinded salamaders and naturally blind ringworms avoided UV and violet-blue light, and he suggested that the response was mediated through the skin.

In 1885, Moleschott (117) reported that light-induced CO2 production in frogs was mediated locally through the skin as well as through the visual system. By 1887, Fubini & Spallitta (118) showed that all colors were effective at increasing CO2 production, though not to the same degree.

Several studies showed that light stimulated the motility of contractile tissues. Between 1844-59, Arnold (146), Reinhardt (147) and Brown-Sequard (148) observed that artificial light induced contraction of the iris muscle in the extracted eyes of eels and frogs. Brown-Sequard further demonstrated that it was due to a direct effect of light on the pupillary sphincter muscle. In 1892, Steinach (149) extended these results to fish and amphibians by showing contraction of the papillary muscle in response to light in isolated eyes even after carefully removing the optic and oculomotor nerves.

In 1888, Gaillard (260) found that sunlight was damaging to many kinds of bacteria and spores but not to molds or yeast. He agreed that the rate of destruction was dependent upon the intensity of sunlight, the composition of the medium, and the presence of oxygen.

Between 1893-95, Ward (260) performed a remarkable series of experiments demonstrating superb technical skill and ingenuity. Using improved versions of Buchner's assay and Geisler's apparatus, he showed that violet-blue and near UV (UVA) rays were the most damaging part of sunlight on bacteria. He also noted that pigmented fungi were resistant, consistent with the notion that pigments serve as protective filters. Finsen (50) showed that sunlight concentrated by a lens and passed through the ear of a white rabbit was capable of bactericidal action. In 1896, Westbrook (265, 266) showed that the bactericidal effect of sunlight was greatest at the surface of cultures, whereas bacterial growth was facilitated deeper in the medium due to elevated temperature and decreased oxygen availability.

In 1893, Richardson (267) showed that sunlight had a sterilizing effect on human urine, and that irradiation of urine in the presence of oxygen resulted in the generation of hydrogen peroxide. D'Arcy & Hardy (268) showed that UVA and violet-blue rays from a high intensity electric arc lamp stimulated production of an oxidizing substance in water, possibly ozone. This, they suggested, might explain the bactericidal action reported by Ward. In 1927, Bedford (269) showed that UV light stimulated hydrogen peroxide production in culture medium. This led him to suggest that the destructive action of UV light on bacteria is caused by the interaction of light with photosensitizers in the medium resulting in hydrogen peroxide production leading to irreparable damage to the bacteria.

In 1898, Anderson (70) reported that two patients exhibiting seasonal sunburn (hydroa aestivale) possessed an unusual porphyrin-like pigment in their urine. Ehrman (71) suggested that this pigment was hematoporphyrin, although Günther (72) noted that not all patients with porphyrinuria were light-sensitive. In 1913, Meyer-Betz (73) confirmed the photosensitizing properties of hematoporphyrin by administering it to himself.

In 1916, Jüngling (94) showed that melanin production was enhanced by light rays longer than 330 nm, whereas sunburn was induced by rays below 330 nm.

In 1921, Fabry & Buisson measured the spectral composition of sunlight and the absorption characteristics of ozone. They surmised that ozone in the upper atmosphere is responsible for filtering most of the solar UV radiation. In 1919, Dorno demonstrated that the intensity of UV radiation penetrating the atmosphere varies throughout the day (greatest when directly overhead) and with the seasons of the year (greatest in summer).

They [biologists] used the term "UVC" to refer to the solar region that was absorbed by the ozone layer in the Earth's upper atmosphere, i.e., below 290 nm, and therefore had no biological impact. The term "UVA" was used for the region 320-400 nm that penetrated window glass and had physiological effects on organisms. The term "UVB" was applied to the region between the UVC and UVA, i.e., 290-320 nm, and this region was believed to be responsible for the deleterious effects of sunlight on living organisms.

In 1919, Adler (154) showed that UV, but not visible, rays stimulated smooth muscle contraction in the frog, rabbit, and guinea pig. In 1954, Giese & Furshpan (155) showed that low intensity UV rays increased the frequency of discharge of the stretch receptor of a crayfish muscle, whereas high intensity UV rays decreased it. In 1957, Pierce & Giese (156) found that high intensity UV rays reduced the amplitude of action potentials in the axons of frogs and crabs, but irradiation with blue light immediately afterwards reversed the effect (photoreactivation)

Very recently, Berson, Yau and colleagues (185, 186) have demonstrated that rat retinal ganglion cells are photosensitive, due to the photosensitive pigment melanopsin that absorbs throughout the UV and visible spectrum, and that these cells are responsible for setting the circadian clock.

Wykoff (289, 290) reported that the energy required to kill bacteria with X-rays was 100 times less than that required with even the most potent UV rays (i.e., 265 nm). He calculated that only one in four million absorbed UV photons is capable of causing cell death.

Raab (245) found that Paramecia stained with the fluorescent dye acridine red were killed when exposed to visible light. He also showed that animals treated with eosin and exposed to visible light suffered from edema and necrosis in the irradiated area. While investigating the cause of the toxicity, he found that neither the light nor the dye was toxic when given alone. Furthermore, the dye was non-toxic if exposed to light separately and then applied. He concluded that it was the combination of dye and light that was responsible for the effect.

Between 1900-1910, von Tappeiner (Raub's mentor), Jodlbauer, and their colleagues went on to show that this toxic effect (which they called "photodynamic sensitization") could be produced using any fluorescent dye and any wavelength (UV or visible) that excited the dye. This led von Tappeiner (246) to propose that it was the emitted light that was responsible for the toxicity.

In 1932, Blum (3) reviewed the results of 121 papers related to this topic, and he concluded that it was not the light but rather some chemical toxin produced by the interaction of light with the dyes. This effect, he pointed out, was clearly distinct from the direct effect of UV rays on cells. Photodynamic actions required a dye or some other chemical to interact with the light, and the response was dependent upon the presence of oxygen. The latter was demonstrated by Straub (247) who hypothesized that the photodynamic effect was due to direct oxidation of cellular constituents. Blum (3) surmised that cellular damage was an indirect effect caused by photooxidation of the dye resulting in the generation of a toxic by-product, probably a peroxide. He also ventured that the photosensitivity of range animals feeding on either buckwheat or St. John's wort was due to the same kind of photochemical reaction.

In 1964, Setlow & Carrier (304) and Pettijohn & Hanawalt (305) independently found that DNA is spontaneously repaired in bacteria following UV exposure.

Webb (15) reviewed the literature showing that UVA rays cause lethal and mutagenic effects in microorganisms even in the absence of exogenous photosensitizers. Unlike UVB effects, UVA effects are oxygen-dependent. In 1980, D'Aoust and colleagues (298) showed that flavins are endogenous photosensitizers which underly the damaging effect of visible light in bacteria. Hartman (299) reported that irradiation of E. coli with UV rays (300-400 nm) induced hydrogen peroxide production, a process that probably involves flavins (300).

Most studies of UVA and violet-blue light responses have implicated carotenoids and flavins as molecular photoreceptors. In 1935-37, Castle (332) and Bünning (333) proposed that carotenes were involved in phototropism in the fruiting bodies of Phycomyces and Pilobolus (fungi) and in the coleoptiles of the plant Avena. In 1950, Galston (334) proposed the alternative "flavin hypothesis" in which riboflavin acts as a photosensitizing agent in the photooxidation and stimulation of the growth hormone (auxin) indole acetic acid. Forty years later, Galland (335) reported that flavins are still regarded as the most common photoreceptors in blue light responses, although carotenoids and pterins have been implicated in some cases.


Many thanks:


Philip E. Hockberger

Northwestern University, Feinberg School of Medicine
Department of Physiology, M211
303 E. Chicago Ave., Chicago, IL 60611-3008, USA
p-hockberger@northwestern.edu
http://www.photobiology.info/Hockberger.html

Statoliths in Phycomyces

Statoliths in Phycomyces: Characterization of octahedral protein crystals.

The crystals, which are present throughout the central vacuoles of the sporangiophore, function as statoliths.

Absorption spectra of isolated crystals and in situabsorption spectra of growing zones indicate the presence of chromophores, probably oxidized and reduced flavins. The flavin nature of the chromophores is also indicated by their fluorescence properties. It appears likely that the chromophores represent an essential part of the statoliths and thus the gravitropic transduction chain.
http://linkinghub.elsevier.com/retrieve/pii/S108718450091199X

Monday, 6 July 2009

Little Sun


If you swallow a vitamin B2 supplement, and the amount is more than your body needs, the vitamin is excreted in the urine. The urine will be a very bright yellow - almost fluorescent. Unfortunately though, for those who like to have fun and want to experiment at home, it doesn't mean your piss will glow in the dark. Vitamin B2 is an easily absorbed micronutrient also known as riboflavin. Like the other B vitamins, it plays a key role in energy metabolism, and is required for the metabolism of fats, ketone bodies, carbohydrates, and proteins. Riboflavin is fluorescent under ultraviolet light.

In animals, riboflavin deficiency results in lack of growth, failure to thrive, and eventual death. Experimental riboflavin deficiency in dogs results in growth failure, weakness, ataxia, and inability to stand. The animals collapse, become comatose, and die. During the deficiency state, dermatitis develops together with hair-loss. Other signs include corneal opacity, lenticular cataracts, hemorrhagic adrenals, fatty degeneration of the kidney and liver, and inflammation of the mucus membrane of the gastrointestinal tract.

Aqueous solutions of riboflavin are yellow with a yellowish-green fluorescence. Under the influence of light and alkaline pH riboflavin is transformed into lumiflavin, an inactive compound with a yellowish-green fluorescence. Under acid conditions riboflavin is transformed into another inactive derivative, lumichrome and ribitol. This compound has a blue fluorescence.

Probably the oldest known example of a blue-light response is the growth toward light(phototropism) of various fungal and plant structures; examples include the aerial fruiting bodies (sporangiophores) of the fungi Phycomyces.

Sporangiophores of the fungus Phycomyces are exquisitely sensitive to light, the action of which is to induce a transient increase in the velocity of growth of the sporangiophore. When illumination is asymmetric, the lens properties of the sporangiophore focus the light such that a net growth increase occurs on the side away from the light source; this results in growth toward the light, i.e., photo-tropism. A similar mechanism is probably operative in sporangiophores of the related fungus Pilobolus. Phototropism enables the fruiting bodies of these fungi to grow out from the depths of crevices in order to disperse their spores somewhere other than the present home of the organism. It is thus a tremendously valuable ability for these organisms to have.

Thus both riboflavin and g-carotene are molecules which enjoy wide biological prevalence. Carotenoids, in particular ß-carotene, have long been candidates for the role of photoreceptor for the various blue light-controlled pro-cesses. The main points supporting this candidacy were the presence of carotenoids in the blue light-sensitive organisms, the general similarity of the g-carotene absorption spectrum and the various physiological action spectra, and the fact that carotenoids are closely related to retinal, the molecule already well known as the photoreceptor for vision in animals.

The notion that riboflavin, rather than a carotenoid, might be playing the role of blue-light receptor has had its ups and downs since Galston first raised the point three decades ago. However, over the past ten years the consensus has come to be that riboflavin is probably functioning as the receptor for blue light-mediated physiological responses in most of the organisms that have been studied. One strong argument providing support for a flavin rather than a caro-tenoid photoreceptor is the presence of a band in the long.

Among the many organisms that exhibit physiological responses to blue light there may in fact exist several different blue-light receptors with differing mechanisms of action. Retinal was apparently discovered and put to use by life as a photoreceptor at several independent points in evolution, the results being retinal-based vision in animals and retinal-based energy and sensory phototrans-duction in the Halobacteria. Given the ubiquity of riboflavin among living organisms,it would be far less surprising here than it was for retinal that life would put to use the photochemical properties of this molecule at several independent points in evolution.
http://etd.caltech.edu/etd/available/etd-08042006-134847/unrestricted/Presti_de_1979.pdf.


Some inks glow faintly (fluoresce) when under an ultraviolet lamp. This is a property of many substances, particularly organic substances and body fluids. When the British Secret Intelligence Service (SSB) discovered that semen made a good invisible ink, Sir George Mansfield Smith-Cumming noted of his agents that "Every man carries his own stylo".

There's a popular urban myth that energy drinks contain the ingredient taurine which comes from bull's semen. Taurine is a lesser known amino acid. Adults can produce sulphur-containing taurine from cysteine with the help of pyridoxine, B6. Taurine functions in electrically active tissues such as the brain and heart to help stabilize cell membranes. While taurine is present in both bull semen and urine, the taurine used in energy drinks such as Red Bull is not taken from these sources. If the story were true - could you imagine the ramifications in trying to gather it?

Most specimens of bull semen are almost white, but during the course of unrelated studies on spermatozoa it was observed that the semen from one particular bull was quite yellow. The colour was confined to the plasma fraction and ultra-violet light produced a green fluorescence similar to that emitted by riboflavin. Other reports have since been noted which suggest that the yellow pigmentation of bull semen may be attributed to riboflavin, and recently eight bulls producing yellow semen have been located, thus permitting a more critical and extensive investigation.

The pigmentation apparently does not affect the fertility of the semen since the bulls were in use at artificial insemination centres and the spermatozoal concentration and morphology were normal.
http://www.nature.com/nature/journal/v182/n4636/abs/182667a0.html


Riboflavin also helps our bodies make glutathione, a free radical scavenger that’s produced by cells. Some people simply can’t produce glutathione because of an inherited abnormality, and they have a marked increase in cell damage. Red blood cells break down more easily, while white blood cells and nerves are also affected. With more riboflavin to support the production of glutathione, it seems reasonable to assume that people would experience less cellular damage.

Animal research has led some scientists to believe that people who are deficient in riboflavin are more likely to develop cataracts, because glutathione helps to protect the eyes from damage by sunlight.

In one study on animal tissue, researchers found that riboflavin can help protect tissues from damage from oxygen that occurs when blood flow stops, then starts again. That stop-start pattern is exactly what develops when someone has a heart attack or stroke.
http://www.mothernature.com/library/bookshelf/books/23/56.cfm

"Glutathione is a very interesting, very small molecule that's [produced by the body and] found in every cell," says Gustavo Bounous, MD, director of research and development at Immunotec and a retired professor of surgery at McGill University in Montreal, Canada. "It's the [body's] most important antioxidant because it's within the cell."

Evidence for the important role that glutathione plays in health comes from studies in people who are severely ill.

"If you look in a hospital situation at people who have cancer, AIDS, or other very serious disease, almost invariably they are depleted in glutathione," says Appleton. "The reasons for this are not completely understood, but we do know that glutathione is extremely important for maintaining intracellular health."
http://www.medicinenet.com/script/main/art.asp?articlekey=50746


Glutathione is a tripeptide. It contains an unusual peptide linkage between the amine group of cysteine and the carboxyl group of the glutamate side chain. Tissue and sperm glutathione concentrations can be raised by increased intake of the precursor cysteine, a necessary building block of glutathione. Worthy of note at this stage perhaps, is that glutathione inhibits and blocks tryrosinase, the enzyme responsible for dark melanin pigments.

Glutathione has recently been used as an inhibitor of melanin in the cosmetics industry. In countries like the Philippines, this product is sold as a whitening soap. Glutathione dose dependently inhibit melanin synthesis in the reaction of tyrosinase and L-DOPA. These results indicate that glutathione inhibits the synthesis and agglutination of melanin by interrupting the function of L-DOPA.
http://en.wikipedia.org/wiki/Glutathione


With a thiol side chain, cysteine is classified as a hydrophobic amino acid. Because of the high reactivity of this thiol, cysteine is an important structural and functional component of many proteins and enzyme. Due to the ability of thiols to undergo redox reactions, cysteine has anti-oxidant properties.

Cysteine is a sulfur-containing amino acid. Cysteine is present in keratin, the main protein that makes up nails, skin and hair. It aids in the production of collagen and provides elasticity in the skin. Cysteine is important in energy production because it can be converted to the sugar glucose which the body can burn. Cysteine also assists in the supply of insulin to the pancreas, which is needed for the assimilation of sugars and starches.

Cysteine is more easily absorbed by the body than cystine, so most supplements contain cysteine rather than cystine. In nature, E.coli bacteria produce cysteine from sugar, salts and trace elements for their own metabolism. At the present time, the cheapest source of material from which food-grade L-cysteine may be purified in high yield is by hydrolysis of human hair.

The basic building block of hair, responsible for 91 percent of its dry weight, is keratin. A strand of hair consists of 3 primary structures: the cuticle (which is the outermost, shingle-like layer); the cortex (the inside of the hair consisting of bundles of protein filaments; and the medula (a soft spongy-like core in the center of the cortex.) The cortex contains densely packed keratin. The inner part of the hair is sometimes referred to as the "pith"



Keratin, a simple protein of albuminoid nature, is the chief constituent of hair, indeed of all epidermal tissue—nails, feathers, horns and hoofs. Keratin is peculiar, in that it has a high sulphur content, the sulphur being present almost entirely in the form of the amino-acid cystine. No other protein is so high in cystine as the keratin of human hair. It would appear,therefore, that the metabolism of sulphur probably plays an important role in the development and growth of these tissues.
http://archderm.ama-assn.org/cgi/content/summary/27/4/584


As with all other amino acids, the vital role of cysteine is to contribute to the structure of protein, which it does in the form of cystine. Cysteine is in the same class as methionine. When it is exposed to air, cysteine oxidizes to form cystine, which is a dimer of two cysteine molecules joined by a weak disulfide bond. Cystine holds proteins in shape and determines the form and properties of animal and plant proteins.

A decrease in the cystine content of human head hair following moderate bleaching has been found. During hair bleaching the primary consequence of the treatment is oxidation of the melanin. Photochemical degradation of hair proteins occurs primarily near 254 to 350 nm, the primary absorbance region of unpigmented hair. Although several amino acids are degraded by light, the primary degradation occurs at cystine.

Hair pigments function to provide some photochemical protection to hair proteins, especially at lower wavelengths, where both the pigments and the proteins absorb light (254 to 350 nm). Hair pigments accomplish this protection by absorbing and filtering the impinging radiation and subsequently dissipating this energy as heat. However, in the process of protecting the hair proteins from light, the pigments are degraded or bleached.

THE sun can make your hair turn grey, new research shows. The same ultraviolet light in the sun's rays which damages skin can also inflict "genotoxic stress" on the adult stem cells which give hair its colour. Japanese researchers have shown that some types of biological body stress, such as ultraviolet light, some chemicals and ionising radiation, damage our DNA. The "irreparable" DNA damage causes the melanocyte stem cells to change the way thay act.
http://www.news.com.au/adelaidenow/story/0,22606,25623374-5006301,00.html


The color of hair is due to the presence in the cortex of granules of a pigment called melanin, which is formed in special pigment-producing cells (melanocytes) in the hair bulb during the growing phase (anagen) of each hair. The melanin granules lie along the amino acid chains of the proteins, looking under the microscope rather like a string of pearls.

Two types of melanin are produced by melanocytes. Eumelanins are black/brown melanins with high photoprotective properties and pheomelanins are red/yellow sulfur containing pigments that provide no protection against the noxious effects of solar irradiation.

Genes determine hair color by directing the type and amount of pigment that epidermal melanocytes produce. If these cells produce an abundance of melanin, the hair is dark. If an intermediate quantity of pigment is produced, the hair is blond. If no pigment is produced, the hair appears white. A mixture of pigmented and unpigmented hair is usually gray. Another pigment, trichosiderin, is found only in red hair.

The following extract is taken from Harriet Hubbard Ayer’s Beauty Book. Though it contains sound advise "on the sin of dowdiness", I am unsure about the exact science behind Harriet's musings on hair pigments. Hair does contain trace elements of metals but these amount to less than 1%. I've included Harriet's wisdom here because I am absorbed by her name, and her cheeky Victorian bed-side manner. And who knows? Maybe one day we'll find out she was right.

The coloring matter of the hair has been scientifically shown to consist of the mineral ingredients in the pigment of the cells. These minerals change with age and health, and vary in individuals. Very blond hair contains a large proportion of magnesia; iron predominates in black hair; chestnut and browns contain a large amount of sulphur.

When the iron or sulphur pigment fails, the hair becomes gray, and as iron appears to fail earlier than sulphur, black hair is oftener found turning gray in youth than any other color. Sulphur comes next, and the magnesia resists longer than any of the others, for which reason blond hair often retains its youthful beauty and luster far beyond middle age.

The reason the golden hair of little children darkens as they grow older is because the hair pigment changes, the sulphur or iron increasing and becoming more powerful than the magnesia. http://www.2020site.org/beauty/hair.html


Current thinking is that hair pigment plays some role in the incorporation of trace elements and not the other way around. Hair is hydroscopic and the absorption of water is very rapid, enabling liquids (sweat, shampoo, dyes, etc) including ions of trace element pollutants to enter the hair. Some experiments have shown hair to behave, to some extent, as an ion exchanger (Bate 1966).

Trace amounts of metals are needed in the structure of pigments though. Bright red hair contains an iron pigment (trichosiderin) that does not occur in hair of any other colour. There's also copper, which is incorporated into the melanin molecule through the amino acid tyrosine. Tyrosinase, a copper-containing enzyme, converts tyrosine to melanin, which is the pigment that gives hair and skin its color.

Melanin or an associated product in the retinal pigment epithelium (RPE) regulates retinal maturation, because in albino mammals the central retina is underdeveloped and there is a cell specific deficit in the rod population.
http://linkinghub.elsevier.com/retrieve/pii/0165380696000752%20-


Melanin means 'black amino' and is a color pigment composed of a hydrocarbon chain which has various amino (nitrogen-based) compounds attached to it. It is carbon that gives melanin its blackness. Carbon is the organizing molecule that gives melanin its structure. It is carbon that gives melanin the ability to absorb energy and bind with other molecules while retaining stability and coherence. Another element important to the structure of melanin is sulphur.

Sulphur is incorporated into the melanin molecule through the amino compound cysteine. Cysteine is an amino compound that is organized around sulphur, nitrogen, and carbon. This amino acid facilitates melanin’s heat and energy transference. In other words, it allows melanin to create or release heat as is needed for the body. Cysteine also cleanses and purifies melanin by ‘burning off’ toxic elements that have been absorbed within melanin.

Cystine is created when two cystines oxidize and bond together. Cystine is a chemical substance which naturally occurs as a deposit in the urine, and can form a calculus (hard mineral formation) when deposited in the bladder or kidney. Cystine crystals are transparent and hexagonal and their solubility is increased in an alkaline medium. The crystals have a brilliant silvery birefringence when viewed under polarized light.



Cystinosis is a rare genetic disorder that causes an accumulation of cystine within cells, forming crystals that can build up and damage the cells. These crystals negatively affect many systems in the body, especially the kidneys and eyes. The accumulation is caused by abnormal transport of cystine from lysosomes, resulting in a massive intra-lysosomal cystine accumulation in tissues. Via an as yet unknown mechanism, lysosomal cystine appears to amplify and alter apoptosis in such a way that cells die inappropriately, leading to loss of renal (kidney) epithelial cells.

A symptom of cystinosis is the accumulation of cystine crystals in the eyes, leading to damage to the retina and loss of sight. With the continued build-up of cystine crystals, the cornea becomes opacified, resulting in decreased vision and the need for corneal transplantation in some patients. The deposition of cystine crystals in the cornea causes photophobia (sensitivity to bright light). Patients endure disabled vision, blurring, redness, pain, irritation, and itching in their eyes. The following paragraph is taken from a story about four-year-old Tina, who has been diagnosed with cystinosis:

Cystine crystals are clearly building up in Tina’s eyes, as is evident by her growing sensitivity to sunlight. Bright light causes the eye crystals to act as a prism, causing severe eye pain and discomfort. Eventually, Tina will start on cysteamine eye drops, which will keep her from developing retinopathy, or blindness. The eye drops must be taken every waking hour and sting considerably. They must remain refrigerated at all times. They are not FDA approved, making them difficult to purchase.
http://www.natalieswish.org/Community-Info/3


I was blown away by Tina's courage. I am starting to appreciate that cystinosis is not simply a problem with the eyes and kidneys. It is something which effects Tina "from head-to-toe". Sadly, cystinosis disrupts Tina's quality of life. Cystinosis, and the treatment of her cystinosis, is something that consumes practically every moment of Tina's life. I have nothing but admiration for Tina, and her parents.

Light sensitivity is usually due to too much light entering the eye, which causes over stimulation of the photoreceptors in the retina and subsequent excessive electric impulses to the optic nerve. This leads to a reflex aversion to light, and discomfort or pain. Some cystinosis patients have been known to display an unusual accompanying reflex - sneezing when exposed to a sudden bright light (photic sneezing). The stimulus might not only be sunlight, but also artificial light, and UV.

The role of intra-orbital trigeminal nerve stimulation was proposed by Katz et al, who found a high incidence of photic sneezing in patients with corneal crystals secondary to nephropathic
cystinosis. They suggested that cystine crystal deposition results in dysfunction of the peripheral branches of the trigeminal nerve, leading to supersensitivity and hence photophobia and photic sneezing.

The theory of parasympathetic generalisation invokes co-activation by one stimulus of neighbouring parasympathetic branches. Light falling on the retina stimulates pupillary constriction (via the third cranial nerve) and lacrimation (via the seventh). A stimulus of
sufficient intensity could generate enough parasympathetic activity to cause nasal congestion and secretions, and stimulate sneezing by an effect on the maxillary branch of the trigeminal nerve.
http://www.madsci.org/posts/archives/2004-04/1081644543.Im.r.html

Patients with infantile cystinosis have hypopigmentation with, for Caucasian subjects, blond hair, blue eyes and a clear skin. However it seems that some patients, in particular African American patients, but also few Caucasian patients have no hypopigmentation. Unfortunately no correlation between cutaneous phenotype, severity of renal disease and genotype has been carried out. The causes of hypopigmentation have not been so far elucidated. In humans, pigmentation results from the synthesis and distribution of melanin in skin, hair bulbs, and eyes.
http://natalieswish.org/files/ProgressReportDrBalloti6-08.pdf.


Hypopigmentation is the loss of skin colour. It is caused by melanocyte or melanin depletion, or a decrease in the amino acid tyrosine, which is used by melanocytes to make melanin. Hypopigmentation of the skin and hair can result from copper deficiency in humans; the depigmentation associated with chronic excessive molybdenum intake is related to a decreased storage of copper in the liver.

Under the trade name Cystagon, cysteamine is used in the treatment of disorders of cystine excretion. Cysteamine is a cystine-depleting agent. It works by reducing the amount of cystine in the body. Cysteamine was first used in the cold war for radiation treatment. Cysteamine is currently under investigation as a protective agent in radiation therapy. A lot of experiments have been done on mice which reveal that cysteamine has a tendency to protect normal healthy tissue from radiation damage, without protecting the tumour tissue.

It is well known that when cells become hypoxic they become radioresistant. Hypoxia is where the body as a whole, or a region of the body, is deprived of oxygen. Increasing the oxygen concentration above atmospheric levels leads to increased radiation sensitivity in most mammals, and is known as the "oxygen effect".

It has been reported that the intracellular level of cAMP in moderately hypoxic cells markedly increases, therefore the radioresistance of hypoxic cells may, in-part, be related to a rise in cellular cAMP. Cysteamine is known to elevate intracellular levels of cAMP.

Cyclic adenosine monophosphate (cAMP) is a second messenger that is important in many biological processes. Many water soluble hormones do not cross the cell membrane, but instead cause effects within the cell via a second messenger. cAMP is used for intracellular signal transduction, such as transferring the effects of hormones like glucagon and adrenaline, which cannot get through the cell membrane. It is involved in the activation of protein kinases and regulates the effects of adrenaline and glucagon. It also regulates the passage of Ca2+ through ion channels.

A possible mode of action of cysteamine is that it might react with extracellular cystine to form cysteine which then is readily taken up into the cell and transformed into glutathione (gamma-glutamyl-cysteinyl-glycine; GSH)

Glutathione itself is does not enter easily into cells, even when given in large amounts. However, glutathione precursors do enter into cells and have been shown to be effective in the treatment of conditions such as acetaminophen toxicity by preventing significant GSH depletion (Prescott & Critchley, 1983). Examples of GSH precursors include cysteine, N-acetylcysteine, methionine and other sulphur-containing compounds such as cysteamine (Prescott, Park & Proudfoot, 1976).
http://www.clinicalconnection.com/exp/ExpandedPatientViewStudy211427.aspx


Glutathione, as you may remember, is an antioxidant which inhibits and blocks tyrosinase, the enzyme responsible for dark melanin pigments. Melanin reduces the penetration of UV radiation through the epidermal layers, and scavenges reactive oxygen species that are generated in the skin on sun exposure. It's a reminder that in the early 19th century, when ultraviolet wavelengths were first being discovered, some knew them as "deoxidizing rays".

A hallmark of sun exposure is increased melanin synthesis by cutaneous melanocytes which protects against photodamage and photocarcinogenesis. Irradiation of human keratinocytes or melanocytes with ultraviolet (UV) rays stimulates the synthesis and releaseof a-melanotropin (a-MSH) and adrenocorticotropic hormone (ACTh), which induce cyclicAMP (cAMP) formation and increase the proliferation and melanogenesis of human melanocytes. We report that stimulation of cAMP formation is obligatory for the melanogenic response of cultured normal human melanocytes to UVB radiation. In the absence of cAMP inducers, UVB radiation inhibited, rather than stimulated, melanogenesis....

...Our results underscore the importance of the CAMP pathway and its physiological inducers in mediating the response of human melanocytes to UV radiation.
http://cancerres.aacrjournals.org/cgi/reprint/58/1/47.pdf


Although the entire process of pigment formation involves many complex interactions - the crucial element of the melanogenic pathway is the action of the principal oxidizing enzyme, tyrosinase.

Protection against UV rays is guaranteed by the tanning response in which UV radiation triggers the production of melanin in the melanocytes. These are specialized cells localized in the basal layer of the epidermis that synthesize melanin in organelles called melanosomes. The melanosomes are transferred via dendrites to the neighboring keratinocytes where they generate a protective screen around the cell nucleus.

Two key upstream components of the melanin cascade process are the α-melanocyte-stimulating hormone (α-MSH) and its receptor, the G-protein coupled melanocortin-1 receptor
(MC1R). The expression of their genesis UV-inducible. Binding of α-MSH to MC1R increases the intracellular level of cAMP, which finally leads to an increased expression of the tyrosinase gene that encodes the rate-limiting enzyme in the synthesis of melanin.
http://www.mibellebiochemistry.com/pdfs/Self-tanning_Based_on_Stimulation_of_Melanin_Biosynthesis_CandT_07_2007.pdf.

[Researchers] showed Mc1r-deficient mice (i.e., mice analogous to red-haired humans) to be incapable of tanning in response to ultraviolet radiation (UVR). When these mice were exposed to topical forskolin, a compound that permeates cells and increases intracellular cAMP levels, their skin darkened dramatically (which correlates with profound eumelanin production). Thus, when nature cannot generate cAMP in response to UVR because of defects in MSH signaling, compounds that directly increase cAMP offer a pharmacologic approach to eumelanization.
http://dermatology.jwatch.org/cgi/content/full/2006/1103/1


In vivo, Phycomyces shows a positive growth response to blue light. It is demonstrated that blue light can increase the chitin synthetase activity in vitro. The following extract also shows a marked effect upon cAMP levels by blue light:

At the University of Florida, I initiated several lines of biochemical and biochemical genetic investigations of Phycomyces. We studied the chemistry of the cell wall and the enzymology of chitinase and chitin synthetase to try to obtain a clue about the regulation of cell growth...

...We also showed that cAMP and cGMP levels were quickly changed by blue light.
http://www.med.ufl.edu/biochem/rcohen/oldres.html


The following extract is taken from a paper entitled the "History of Ultraviolet Photobiology". It was written by Philip E. Hockberger. I thought the paper to be a fantastic read. Below, a few paragraphs taken from the paper seem to tie together the elements that I've drawn out in this post. I feel like it's gone full circle. The post was certainly longer than I thought it would be. I am, as yet, unable to draw any real conclusions. I feel like this post needs to be condensed, squashed up like an accordion, and injected into my brain, before I can begin to formalise ideas.

Webb (15) reviewed the literature showing that UVA rays cause lethal and mutagenic effects in microorganisms even in the absence of exogenous photosensitizers. Unlike UVB effects, UVA effects are oxygen-dependent. In 1980, D'Aoust and colleagues (298) showed that flavins are endogenous photosensitizers which underly the damaging effect of visible light in bacteria. Hartman (299) reported that irradiation of E. coli with UV rays (300-400 nm) induced hydrogen peroxide production, a process that probably involves flavins (300).

Curry & Gruen (326) demonstrated positive phototropism to violet-blue light using Phycomyces (fungus). In 1960, Delbrück & Shropshire (327) showed that the action spectrum for phototropism in Phycomyces corresponded to the absorption spectrum of flavinoids.

Most studies of UVA and violet-blue light responses have implicated carotenoids and flavins as molecular photoreceptors. In 1935-37, Castle (332) and Bünning (333) proposed that carotenes were involved in phototropism in the fruiting bodies of Phycomyces and Pilobolus (fungi) and in the coleoptiles of the plant Avena. In 1950, Galston (334) proposed the alternative "flavin hypothesis" in which riboflavin acts as a photosensitizing agent in the photooxidation and stimulation of the growth hormone (auxin) indole acetic acid. Forty years later, Galland (335) reported that flavins are still regarded as the most common photoreceptors in blue light responses, although carotenoids and pterins have been implicated in some cases.
http://www.photobiology.info/Hockberger.html


But if I was asked to leave a final thought here today, it would be something about pressure. If I was trying to simplify the above post I might be tempted to say that it all has something to do with pressure.... pressure inside cells .... blood pressure ... aether field pressures.... ????







Many, many thanks:

Chemical and physical behavior of human hair By Clarence R. Robbins
The invertebrates By Richard Stephen Kent Barnes, Peter Calow, Peter Olive
http://www.pg.com/science/haircare/hair_twh_59.htm
http://%20http//www.pjbs.org/pjnonline/fin295.pdf..
http://brewery.org/library/Maillard_CS0497.html
http://www.jbc.org/cgi/reprint/75/2/443.pdf
http://en.wikipedia.org/wiki/Pith
http://en.wikipedia.org/wiki/Samson
http://blog.taragana.com/n/detecting-sulphur-in-just-one-hair-could-help-nab-a-terrorist-66430/
http://www.insidecosmeceuticals.com/articles/delivery-systems/83h251461319032.html
http://www.eurekalert.org/pub_releases/2006-09/uok-sst092606.php
http://comparative%20action%20spectrum%20for%20ultraviolet%20light%20killing%20of%20mouse%20.../
Nutrient requirements of dogs and cats By National Research Council (U.S.). Ad Hoc Committee on Dog and Cat Nutrition, National Research Council
http://dujs.dartmouth.edu/2000S/06-Biolumen.pdf.
http://en.wikipedia.org/wiki/Riboflavin
http://www.newton.dep.anl.gov/newton/askasci/1993/biology/bio021.htm
http://www.answers.com/topic/glutathione
http://www.absoluteastronomy.com/topics/Invisible_ink
http://www.revoptom.com/HANDBOOK/SECT42a.HTM
http://en.wikipedia.org/wiki/Cystinosis
Harley's pediatric ophthalmology By Robison D. Harley, Leonard B. Nelson, Scott E. Olitsky
http://www.cystinosis.org.uk/techArticle.php?id=13
http://www.fxmed.co.nz/Pat/HairBro.html..
http://www.mgwater.com/taurine.shtml
http://www.assatashakur.org/forum/afrikan-wholistic-health/11586-melanin-wellness-part-i-melanin-sacred-metals-stones.html
http://www.vitsaf.org/Vitamins.doc.
http://etd.caltech.edu/etd/available/etd-05182006-082819/unrestricted/Jan_yn_1975.pdf.
http://www.springerlink.com/content/x12w531x5418m476/
International review of cytology By Geoffrey Howard Bourne, International Society for Cell Biology
Handbook of radiobiology By Kedar N. Prasad
http://www.koreamed.org/SearchBasic.php?RID=176031&DT=1
http://www.absoluteastronomy.com/topics/Photophobia






Sunday, 5 July 2009

Wet-type earwax fluoresces weakly under ultraviolet (UV or "black") light. One of the ways of testing the authenticity of amber is to pass it under a fluorescent light - amber should fluoresce. The crystalline structure of dried urine causes it to fluoresce a dull yellow color under UV light.

The hardness of amber varies from 1-3, and it is transparent to opaque, with the cloudy turbidity due to air bubbles and inclusions. It has no cleavage, conchoidal fracture, and is tough to brittle (Baltic amber tends to be tough, while Dominican amber, brittle). The luster is resinous and amber fluoresces bluish-white, yellow-green, or blue (more fluorescence with higher sulfur content). The color of amber varies, with white, yellow, and orange common, as well as red, brown, green, "black" (deep shades of other colors), and bluish colors possible.
http://www.emporia.edu/earthsci/amber/go340/ambers.htm

Blue amber can be found, predominately in the Dominican Republic. It is also found in the Baltic. An amber researcher Sawkiewicz determined that Baltic blue amber was formed through the optical effect of closely concentrated bubbles of the same size, 0.00007 mm.The author has in his possession a tiny piece which shows some blue colouring and is pictured here. Green fossil resin can be found, again from the Dominican Republic and also in copal from Colombia. Burmite from Burma has a deep red colour.
http://www.gplatt.demon.co.uk/properti.htm


Chlorophyll will fluoresce in the red part of the spectrum and also give off heat. Chlorophyll is a green pigment found in most plants, algae, and cyanobacteria. Chlorophyll is the molecule that absorbs sunlight and uses its energy to synthesise carbohydrates from CO2 and water. This process is known as photosynthesis and is the basis for sustaining the life processes of all plants.

Chlorophyll molecules are specifically arranged in and around pigment protein complexes called photosystems which are embedded in the thylakoid membranes of chloroplasts. Light energy absorbed by chlorophyll molecules in a leaf can undergo one of three fates: it can be used to drive photosynthesis, excess energy can be dissipated as heat, or it can be re-emitted as light - chlorophyll fluorescence. The spectrum of fluorescence is different to that of absorbed light, with the peak of fluorescence emission being of longer wavelength than the absorption.

Light energy absorbed initially by the antenna and transferred to the reaction centers is channeled by a number of different processes including photochemistry, photo-protective heat dissipation, other heat dissipation and about 3%-9% of the light energy absorbed by chlorophyll pigments is re-emitted as fluorescence. The emission peak is of a longer wavelength than the excitation energy. This effect was first observed more than 100 years ago, when N.J.C. Müller (1874) by visually using colored glass filters. He also noted that fluorescence changes that occur in green leaves are correlated with photosynthetic assimilation. Lack of appropriate technical equipment prevented a more detailed investigation of this phenomenon. The light energy drives photosynthetic electron transport through PSII and PSI leading to the oxidation of water, oxygen evolution, the reduction of NADP+ to NADPH, membrane proton transport and ATP synthesis.
http://www.optisci.com/cf.htm

Lutein and zeaxanthin belong to the class of carotenoids known as xanthophylls and both contain hydroxyl groups. In photosynthetic plants lutein and zeaxanthin are located in chloroplasts where they are integrated with light-harvesting chlorophyll proteins. Lutein and zeaxanthin are phytochemicals found most often in leafy green vegetables, but also in other fruits and vegetables. Chicken egg yolks are a rich food source of lutein and zeaxanthin. Lutein is only obtained through the diet, while zeaxanthin can be produced by conversion from lutein in the eye.

Xanthophylls serve as accessory light-gathering pigments and to protect these organisms against the toxic effects of ultra-violet radiation and oxygen. Both lutein and zeaxanthin absorb blue light (peak absorption is 446 nm) The absorption of blue light protects plants from damage but does not prevent photosynthesis. Absorption of blue light is responsible for the colour of lutein and zeaxanthin, causing yellow pigmentation at low concentrations and orange-red at high concentrations. The name lutein is derived from Latin for "yellow".

Lutein and zeaxanthin are two dietary carotenoids which accumulate in the ‘yellow spot’ or macula lutea of the retina. The macula is located roughly in the center of the retina, temporal to the optic nerve. It is a small and highly sensitive part of the retina responsible for detailed central vision. The fovea is the very center of the macula. The macula allows us to appreciate detail and perform tasks that require central vision such reading. It is interesting to note that lutein and zeaxanthin are the only carotenoids known to concentrate specifically in the eye tissues.


Macular pigment has been implicated as a risk factor in age-related macular degeneration (AMD), the most prevalent cause of vision loss in the elderly. Vision loss in AMD is due to the irreversible death of photoreceptors and/or the invasion of leaky, unwanted blood vessels into the retina. At advanced stages of this progressive disease, everyday activities such as reading, driving, or even seeing the face of a loved one become impossible.

In the short-term study, reported in the November 2002 issue of Investigative Ophthalmology and Visual Science (IOVS), the team divided the carotenoid-deficient quail into two groups, and for one week preceding light damage, they fed one group zeaxanthin-supplemented diet. The study established that photoprotection was strongly correlated with the concentration of zeaxanthin in the retinas of the quail. Retinas with low concentrations of zeaxanthin had suffered severe light damage, as evidenced by a very high number of apoptotic photoreceptor cells, while the group with high zeaxanthin concentrations had minimal damage. Apoptosis is programmed cell death, the final common pathway for photoreceptor death in retinal degeneration.

The macular pigment acts like "sunglasses" by protecting the critically important central sight from damaging light waves. The distribution of lutein and zeaxanthin in the eye may indicate they have different functions. Zeaxanthin is the dominant component in the center of the macula, while lutein dominates at the outer edges. The eye is selective and preferentially places dietary zeaxanthin in the very center of the macula, the most critical area for central vision with the greatest need for protection. This selective uptake of zeaxanthin occurs even though lutein is more available in the diet by a 20:1 ratio.

Previous investigations may have obscured evidence of zeaxanthin's greater protective role by looking at the two carotenoids together, rather than separately. Although both of these carotenoids protect the retina, zeaxanthin has been shown to be a better photoprotector and a recent animal study supports the photoprotective activity of zeaxanthin. Additionally, zeaxanthin's chemical structure makes it a much more effective antioxidant than lutein.

The human study concluded that decreased blood plasma zeaxanthin, but not blood plasma lutein, is significantly associated with the risk of age-related macular degeneration. This correlation strongly indicates that a high level of dietary zeaxanthin intake may directly affect the risk of developing macular degeneration. Increasing intake through diet or supplementation may help to slow down or stop vision loss with those who have been diagnosed with AMD.

http://www.mdsupport.org/library/zeaxanthin.html


Many thanks:

Safety of Dietary Supplements for Horses, Dogs, and Cats By National Research Council (U.S.)
http://www.chm.bris.ac.uk/motm/carotenoids/carotenoids.htm
http://www.nature.com/nature/journal/v209/n5028/abs/2091135a0.html
http://jxb.oxfordjournals.org/cgi/reprint/51/345/659.pdf
http://www.naturalnews.com/024847_magnesium_insulin_medicine.html
http://www.ch.ic.ac.uk/local/projects/steer/chloro.htm
http://www.ab.ipw.agrl.ethz.ch/~yfracheb/flex.htm
http://www.geocities.com/CapeCanaveral/Hall/1410/lab-B-26.html
http://en.wikipedia.org/wiki/Macula
http://www.ghuth.com/2005/10/03/a-thought-experiment-on-retinal-design/#more-16
http://www.mdsupport.org/library/zeaxanthin.html
http://www.healthyeyes.org.uk/index.php?id=23
http://omlc.ogi.edu/spectra/PhotochemCAD/html/riboflavin.html
http://anrvitamins.com/glossary/zeaxan.html

Saturday, 4 July 2009

Thursday, 2 July 2009

More Than Meets The Eye


At the moment, daylight pours into the room where I am writing this. The light is pretty much invisible to me. I see very well all the objects, and the walls, and everything else in the room - but not the light itself. If I hold my hand up to the light coming into the room, I can see it strike my hand making it suddenly brighter, and if I leave my hand in the light long enough, I can feel warmth. If I were to shake a dusty cushion, the daylight might strike the dust and therefore I would see the light, but otherwise no, I don't physically see the light until it reaches an object. This light is known as "white light", and it is supposed that it is made up of all the colours of the visible spectrum.

Books tell me that the white light in this room is moving very fast, approaching speeds of 300,000 km/s. It is supposed that white light is refracted by an object. The material absorbs certain frequencies of the visible spectrum, and it reflects others. It is the frequencies which are reflected that we see as the colour of the object. I now struggle with this theory.

I struggle with the theory mainly because we are told that white light has no frequency. Surely white light should have a frequency? Everything in the Universe has a frequency. All electromagnetic radiation, ranging from X-rays to radiowaves has a frequency - except, we are told, white light. White light apparently, is the sum of all the frequencies in the visible spectrum. By combining these frequencies into white light then the light has no frequency. I am not convinced.

Light leaves the Sun and travels to our planet. On its journey it does not fill space with light. The space between the Earth and the Sun remains black. The light that left the Sun is not visible until it hits the Earth. It's as if the atmosphere of the Earth transforms the energy from the Sun into visible light. Right now, in this room, the light from the Sun enters through the window as white light.

All matter emits EMR. Only when something is at absolute zero will it no longer emit EMR. A small fraction of the EMR spectrum is taken up by the visible spectrum, but if you look at the world around us, everything - absolutely everything - is made up of colour (the possible exception being black which is considered to be the absence of colour). Colours are not a property of an object though, they actually belong to the eye.

The pigment in a material will behave in such a way that it somehow activates receptor cells in the eye which the brain then interprets as colour. I don't believe the material absorbs some frequencies of white light and reflects others. I think matter generates EMR due to the electric fluid of the aether.

The aether field has a constant applied pressure, somewhat similar to a hydraulic system. We write this pressure as the speed of light in a vacuum: 300,000 km/s; except it's not really a speed, but rather a volumetric flow rate. This volume is normally measured in cubic metres per second. Should the volumetric flow rate of the aether therefore be written as 300, 000 cubic kilometres per second?

The fluid of the aether is induced to flow through matter. Molecules act as motors which suck in and blow out the fluid of the aether. The aether is manoeuvred through the atomic vortices of matter, generating a difference in pressure between the applied pressure constant of the aether field, and the pressure of the aether inside matter.

In water, the speed of light is said to be about 3/4 the speed of light in a vacuum, around 225,000 km/s. These kids pulled a simple, but also brilliant, experiment to show how the different values for the speed of light can be measured.
http://www.ms.uky.edu/~skim/SpeedOfLight/

As said before, the pressure of the aether field is an applied constant of 300,000 km/s. The aether has been way-laid by being forced to pass through an atomic obstacle course. The fluid of the aether has become choppier. The peaks and troughs of the EM waves move closer together. The speed of light in water has a value of 225, 000 km/s - is this illustrating a pressure drop in the aether field in water?

The speed of light in glass, which has a higher refractive index than water, is supposed to be something in the region of 200, 000 km/s. Once again, do we have a pressure drop?

Refracted light inside a glass prism produces the colours of the rainbow - the visible spectrum - in a process known as dispersion. A ray of white light enters the glass and is bent towards the normal. The colours of the visible spectrum leaving glass are bent away from the normal. It's as if the light enters the prism at an angle, then makes a bee-line for the other side like it's a speedboat on flat water, before being reflected out through the otherside at an angle.

I remember once swimming in the beautiful crystal waters off Corsica, and being struck by just how blue it was. It wasn't grey like the waters I'm used to back home in Brighton - this stuff was really blue. The other thing I noticed was my reflection on the surface of the water - no surprises there - but at the time I was immersed in the water looking up, just below the surface of the water. The surface of the water was acting as a mirror, and this is something known as total internal reflection. Is something inside the prism acting like the surface of water?

We see the colours of the rainbow inside the prism, and then we see them leave the prism. EMR is a wave which propagates in the medium of the aether. Inside the glass prism the fluid of the aether gets choppier. The peaks and troughs come closer together. The frequencies of light get higher. These higher frequencies are what we recognise as the visible spectrum. The visible spectrum thus emerges from the prism and out into the big bad world. The fluid of the aether is maintaining the higher frequencies outside the prism in order to support the visible spectrum. The glass medium of the prism is effectively making waves in the aether field which it then transmits into the air. And one cannot help but make the analogy of a pebble being thrown and making ripples on a pond.

It is often handy to think of light as a wave – like the wave you make by dropping a stone in a pond – because light has many wave-like properties. When you drop a stone in a pond, you create ripples, and you could actually measure the distance between the ripples. This distance is called the wavelength. Each color of light has a unique wavelength.

Christian Huygens, a Dutch physicist fond of optics, was one of the first to suggest visible light is a wave disturbance, like the ripples on a pond or the vibrations of a violin string. Huygens kept at his research and showed that light waves interfere with each other in the same way as waves of water, and in the same way as waves from musical instruments.

Thomas Young devised a light-slit experiment which showed light as a wave disturbance. The crests and troughs from two diffracted rays alternately added together and cancelled each other out. The interference effect is not restricted to light. Waves produced on the surface of a pool or pond will spread in all directions and undergo an identical behavior. Where two waves meet in step, they will add together to make a larger wave by constructive interference. Colliding waves that are out of step will cancel each other via destructive interference and produce a level surface on the water.

In one of Newton's experiments, he cast the spectra of three prisms onto one another so that they overlapped without coinciding. In the centre, where all the colours fell, the combined spectrum was white. Is this an example of destructive interference, where the vibrant frequencies of the visible spectrum cancel each other out?

What of the fluid of the aether as it moves from the vibrant frequencies of the spectra into the lower frequencies of white light? We are told that white light has no frequency, so we should therefore expect to find the fluid of the aether perfectly still. But is that quite the case as I look around my room? The molecules of the air are surely inducing the aether to wobble. Indeed, the speed of light in air is slightly lower than the speed of light in a vacuum. There's a pressure drop in the aether field inside this room compared to the constant applied pressure of the Universe. I suspect white light is really low frequency EMR.

Sunlight is directional. It starts at the Sun, and then it arrives at our planet. My back garden at this moment is half in sunlight, while the other half is shaded by the house. The half that is exposed to the Sun is much brighter. The colours on that side are much more vivid than those of the garden dulled by the shade.

I look at the bright green grass. The grass contains a pigment which my eye detects as green. The grass is somehow creating a pressure drop in the aether field, which generates a frequency of EMR that I see as the colour green. Why is it that the grass always looks greener on the otherside? Why does the grass look so much brighter in the sunlight?

When a photo is taken, the shutter in the camera opens for a fraction of a second to allow light from the scene to enter. The light is focused by the camera lens onto a piece of light sensitive film. The film contains chemicals which break down when exposed to light and thus the image is recorded on the film by the pattern of chemicals, broken down or otherwise. The more the chemicals are broken down, the brighter the resulting photo will be.
http://freespace.virgin.net/hugo.elias/graphics/x_posure.htm


Can this process not only be applied to cameras, but also to how we visualize the world around us? Is an object brighter because receptor cells in the eye have a longer exposure to brighter colours? This longer exposure is only possible if light from brighter objects is reaching my eye before the light of dull objects. Is the light from the grass in the sunlight travelling with a greater velocity to reach my eye - or is it that these changes in velocity take place inside the eye - or is it both?

As I write this I feel like I've ended up somewhere very strange. Somewhere unexpected. I've long suspected that white light has no frequency because I imagined it had been mistaken for heat, but maybe there's more to it than that. Is there, quite literally, more than meets the eye?


Many thanks:

Physics demystified By Stan Gibilisco
http://www.hartnell.edu/faculty/pmoth/Files/AST1LAB/Spectroscope.doc.
http://home.vicnet.net.au/~colmusic/clario2.htm
http://arstechnica.com/old/content/2007/08/faster-than-the-speed-of-light-no-i-dont-think-so.ars
http://www.glenbrook.k12.il.us/GBSSCI/PHYS/Class/light/u12l2c.html