Glider

Please stop posting your homework question in forums other than Homework Help.

That's a hell of a question to expect anyone to answer in a forum. Your best bet would be to find a more recent introductory text and compare it with the old book.

That's because, as I said, rod cell activity is supressed by cone cells during photopic vision. So, unless you use your peripheral vision (where there are fewer cones to supress rod activity) you won't detect these scan lines. It's not 'ghosting', it's bleaching. If you look at an extremely bright light, the cells that the image falls on quickly become exhausted and stop functioning until they recover. So, it's not really ghosting because the after image is more like a hole in your visual field rather than a genuine image. Cone cells are slower to respond than rod cells (at least in humans) so we have a flicker fusion threshold (FFT) of about 16Hz in normal photopic vision. Any flicker above this rate will not be detected. Pigeons have a higher FFT so, for example, if you showed a pigeon a cine film (24Hz), the pigeon would see a series of still images, where humans see a continuous moving image. With human retinal cells, if you present a series of images above 16Hz (crt = ~50 - 60Hz) no flicker will be percieved. You have to remember that the eye is not a video camera. There is no 'frame rate' or 'refresh rate' in the eye. Instead there are a series of mechanisms in the eye and the visual cortex that have evolded specifically to detect pattern, motion and detail. Because, whilst retinal cells are specialised to respond to light, mechanical deformation will also trigger action potentials in them. If you press on your eye, the retina gets bent out of shape. This will cause retinal cells to fire. Action potentials are all the same, regardless of what caused them. Action potentials originating in the retina pass down the optic nerve and terminate in the primary visual cortex. Any volley of APs terminating in the visual cortex will always be interpreted as patterns of light because that's what the visual cortex does. It interprets volleys of APs as patterns of light.

The eye produces a continuous image because different cells are being stimulated all the time. The eye is never stationary, it is in constant movement, even in a steady gaze. This is called nystagmus. If you google for the term, you will find that it is more often used to describe a clinical condition of uncontrollable rapid and jerky eye movements. However, at sub-clinical levels, nystagmus is normal and necessary for vision. Experiments have been done where the ocular motor muscles have been temporarily paralysed, eliminating nystagmus. The result is that the cells in the fovea bleach after a few seconds and vision fades. The only way to refresh the image was to move the object. This projected the image onto fresh cells and vision returns Cones don't really retain frequency information. It is simply that in cones, the substance that is sensitive to light (retinoids) in cones is sensitive to different wavelengths and each cone will only respond to its own particular wavelength. I'm not sure what you mean here, but as I said, cones will only respond within their particular band of wavelength sensitivity. The entire retina (at least the dorsal part) contains both rods and cones. However, there are fewer cone cells the further you go from the fovea. During normal daylight vision (photopic) the activity of cone cells in the fovea supresses the activity of rod cells in that area. So photopic vision is primarily mediated by cone cells which are less sensitive to changes in intensity and the flicker of a crt monitor is below their detection threshold. Low light (mesopic) vision is primarily mediated by rod cells which can detect the flicker of a crt monitor, but the light coming from a crt is bright enough for photopic vision (if you can see colour, you are using photopic vision), so rod cell activity in the fovea is suppressed. Thus, the only way to detect the flicker of a crt monitor is to use the rod cells in the periphery of the retina (i.e. out of the 'corner' of your eye) which are not being supressed as there are very few cone cells in the periphery of the retina.

Only in human eyes. Many fish (including goldfish) see well into the infra red spectrum and many birds and insects see in ultraviolet. No they're not. The optic nerves are no different from any other nerve. No, it doesn't reverse itself. The optic chiasm is where all information from the right visual field is routed to the left hemisphere and information from the left visual field is routed to the right hemisphere. There is no reversal. No it isn't. Memory formation happens in the hippocampus in the medial temporal lobes. Presumably you have some evidence for this? Vision at the back, imagination at the front, and this allows the two to superimpose? How, exactly? As with your posts in the Psychology forum, presumably here you are talking about top-down processes, the reality of which which is nothing like you describe here. As in the Psychology forum, you are lecturing and spouting speculation as though it were established fact. You have been told to stop doing it. Changing from Psychology to Physics is not stopping. If you wish to discuss things, feel free to do so. If you wish to lecture ans present speculation and conjecture, do it in the Speculations forum.

The reason for this is that rods are more numerous than cones in the periphery of the retina. Cones are concentrated around the fovea. Rods are more sensitive to light and changes in intensity. In low light where you want to see something (e.g. a dim star or a person in the shadows), you will see better if you look slightly to one side of the object. As to your CRT monitor, the same principle applies. The flicker that exists in all CRTs is better detected by the high concentration of rod cells in the periphery of the retina. Retinal cells don't have a 'frame rate' per se, so there is no 'ghosting' of frames. In good light, the cones are as active as the rods, it's just that they're responding to different qualities of light (wavelength rather than intensity).

Well, essentially, after your mid 30s, osteoblast activity slows down. Osteoclasts on the other hand, tends to remain quite active, so in most of us, more bone is being removed than laid down. This is a normal part of getting old, except in cases of osteoporosis where the bone loss process accelerates. It's further confounded if normal bone density wasn't achieved in adolescence. Yeah. The media harps on about calcium but it's really not as simple as that. Firstly, it's not really the amount of dietary calcium that's important. It's the absorbtion and metabolism of calcium that's important. There needs to be a balance of other nutrients and minerals to allow calcium to be metabolised usefully. Secondly, think of a building site where you have brickies building walls, and some 'reverse' brickies taking the bricks away again. If these 'reverse; brickies are working harder than the normal brickies, it really doesn't matter how many bricks are available. The result will be that the walls get smaller. The trick is to slow the reverse brickies activity (cut their overtime or something). In any particular case of osteoporosis, the aetiology is multifactorial and so each case has to be taken on its own merits. Probably the two main factors are inadequate bone mineral formation by the end of childhood and accelerated bone depletion in later life. This suggests that prevention (i.e. ensuring good bone density in childhood and preventing accelerated loss in later life) is simpler than cure in this case.

It is said because it is true However, that is not to say that calcium uptake stops after 17 years. It is just that calcium uptake is greatest during the period of most rapid bone growth. Calcium uptake drops off after 17, but still happens at a level sufficient for the slow turnover required. When it drops off further than that, you get osteoporosis as there is insufficient calcium to replace that being removed.

Bone marrow isn't bone. Bone marrow is the soft fatty tissue that can be found inside certain hollow bones (e.g. femur, illiac crest, sternum etc.). It is highly vascular and contains stem cells which differentiate to procuce erythrocytes, white cells and platelets.

Teeth are made of dentine and enamel, which is different from bone. They don't regenerate, but they do survive fires that bone doesn't. Bone itself is not a living tissue. It doesn't regenerate in the same way that e.g. skin does (i.e. cell division). Bone is a matrix of calcium and collagen that is inert. The periosteum is a nighly vascular layer of tissue surrounding bone. When a bone is broken, blood is released around the break (in fact bone healing is an inflammatory process) and within this pool of blood, two types of cell concentrate at the site and are responsible for healing; oteoclasts and osteoblasts. Osteoclasts are responsible for 'eating' away fragments and cleaning up the rough edges. Basically, they disolve the bone chemically. Osteoblasts lay down the new bone within the matrix formed by the blood clot in the form of a callus which, if you X-ray a newly healing bone, looks like a swollen mass around the break. Once the callus has been laid down, osteoclasts trim it down and smooth it off to more or less the right size and shape. As for the original post, I have no idea what the teacher could be taliking about. As Silkworm says, bone is constantly being replaced through balanced oteoclast/osteoblast action. Out entire skeleton is replaced something like 7 times throughout our lives.

No need. I understand what you're saying and I know it to be true. This is a problem of misdiagnosis as in these overly PC times, GPs can't get away with saying "You have no real problems. Deal with it". I just wanted to avoid the common lay interpretation that 'stress' isn't really a problem. Real stress is a killer. That there are so many who without real cause go whining to their GP tends to dilute that fact and often leads people to dismiss stress as the product of a weak mind. This in itself is a problem because it begins to generate a certain stigma which deters genuine cases from presenting as they don't want to appear 'weak'. It is more often those who feel they should be strong enough to cope that suffer stress conditions anyway as they tend to take so much on themselves. All those who present to a GP at the drop of a hat because they're feeling a little pi**ed off one day are a) less likely to actually be suffering stress, and b) actually doing harm by changing the general perception of the condition from a serious problem to something made up to cater for whiney neurotics who can't cope with normal life. PS Sorry about the 'off topic'.

Stress isn't really an illness. It's more an aetiological factor in certain illnesses (e.g. coronary heart disease, chronic hypertension, depression etc.). Even then, it's only a certain kind of stress, not yer everyday just being pi**ed off with somebody. It needs to be chronic for a start.

MDMA has an effect similar to amphetamine. It elevates levels of dopamine (DA) in the reward centres of the brain. All drugs of abuse share this common effect, although their specific effects differ. Increased DA in the reward centres results in feeling of euphoria (reward). Whilst this chemically induced euphoria could be said to be an alteration in your reality, insofar as you are happy with no real reason, it doesn't alter your reality in the same way that LSD does. No. There is a condition related to amphetamine based drugs though. If you take too much, then too much DA is released and you develop Amphetamine Psychosis. This is clinically indistiguishable from an acute schitzophrenic episode (schitzophrenia is also associated with elevated levels of DA). I wouldn't call amphetamine psychosis a euphoric state, but it is temporary and passes as the drug is metabolised.

So, you're part cetacean? Cool! My father's brother is in to geneology. He has found that his (and obviously, my father's) side of the family are from North Wales from as far back as anyone can find. My mother's side are English, but no in depth search has been done on them.

Yeah. If you think about it that way, life is a sexually transmitted terminal condition. It's the only one contracted by someone not involved in the act too.

I don't know that it does not. I said I didn't think so, but I can't be sure. I haven't looked at it for a while; it's still in a box somewhere from my move. Most people would open the book to ensure it contained what they wanted before they bought it. Even better, libraries allow you to open books all the time and they don't even make you buy it. You should try it, it's really neat.

You're doing it again sunspot, making stuff up and giving it an impressive sounding term. What exactly is unconscious sensory projection? The process you describe makes no sense at all. You are confusing the optic and ocular motor systems. These are different systems and use different nerves. The optic nerve is afferent (sensory) and conducts information from the retina to the primary visual cortex. The ocular motor is efferent (motor) and controls eye movement (including REM). You are (partly) talking about top down processes; the process that things like the Rorschach test rely on. This happens in the brain, not the eye. The rest of what you are saying is just pants. You didn't make a lot of sense in that thread either, as you were making stuff up there too.

So, in short, if a person is dying, ignore them; their wishes don't count?

Hehehe

But what does brain activity have to do with pain? As I said, there are no 'pain' centres in the brain, and activity in 'nociceptive' pathways is not pain. You can activate nociceptive pathways without experiencing pain. There is no objective physiological measure of pain. No scanning method (EEG, fMRI, PET, SPET etc.) can show pain because pain is a psychological state.

I know, I'm sorry we can't be more helpful, but I think collecting a bunch of ill-informed guesses would do more harm than good in terms of your peace of mind.

True, they are an amazing example of specialised adaptation. If it weren't for the fact that in terms of mortality, they are the most lethal animal on the planet, they'd be very cool. They have specialised chemoreceptors on their antennae.

I guess it would depend on which stage you chose to call 'human'. Australopichicus (bipedal tool user) lived around 5 million years ago, but there have been intermediate stages since then. As for remaining unchanged, well, average height and weight for adult humans has changed significantly within the last 500 years, so I guess you'd have to define 'change' also. Change is still happening too. For example, the female pelvis is becoming more android (male-like) leading to more difficult births. This change has been noted comparitively recently. Speaking more generally though, humans haven't changed that much in the last 50-100,000 years.