document_title: Color blindness

question_text: what are the two types of color blindness

question_tokens: what are the two types of color blindness

text: Color blindness

text: Signs and symptoms[edit]

text: In almost all cases, color blind people retain blue–yellow discrimination, and most color-blind individuals are anomalous trichromats rather than complete dichromats. In practice, this means that they often retain a limited discrimination along the red–green axis of color space, although their ability to separate colors in this dimension is reduced. Color blindness very rarely refers to complete monochromatism.[3]

text: Dichromats often confuse red and green items. For example, they may find it difficult to distinguish a Braeburn apple from a Granny Smith or red from green of traffic lights without other clues—for example, shape or position. Dichromats tend to learn to use texture and shape clues and so may be able to penetrate camouflage that has been designed to deceive individuals with normal color vision.[4]

text: Colors of traffic lights are confusing to some dichromats as there is insufficient apparent difference between the red/amber traffic lights and sodium street lamps; also, the green can be confused with a grubby white lamp. This is a risk on high-speed undulating roads where angular cues cannot be used. British Rail color lamp signals use more easily identifiable colors: The red is blood red, the amber is yellow and the green is a bluish color. Most British road traffic lights are mounted vertically on a black rectangle with a white border (forming a "sighting board") and so dichromats can more easily look for the position of the light within the rectangle—top, middle or bottom. In the eastern provinces of Canada horizontally mounted traffic lights are generally differentiated by shape to facilitate identification for those with color blindness.[citation needed] In the United States, this is not done by shape but by position, as the red light is always on the left if the light is horizontal, or on top if the light is vertical. However, a lone flashing light (e.g. red for stop, yellow for caution) is still problematic.

text:
Normal sight

Deuteranopia sight

Tritanopia sight

Monochromacy sight

text: Causes[edit]

text: Color vision deficiencies can be classified as acquired or inherited.

text:
Acquired: Diseases, drugs (e.g., Plaquenil), and chemicals may cause color blindness.[5][6]
Inherited: There are three types of inherited or congenital color vision deficiencies: monochromacy, dichromacy, and anomalous trichromacy.

Monochromacy, also known as "total color blindness", is the lack of ability to distinguish colors (and thus the person views everything as if it were on a black and white television); caused by cone defect or absence. Monochromacy occurs when two or all three of the cone pigments are missing and color and lightness vision is reduced to one dimension.

Rod monochromacy (achromatopsia) is an exceedingly rare, nonprogressive inability to distinguish any colors as a result of absent or nonfunctioning retinal cones. It is associated with light sensitivity (photophobia), involuntary eye oscillations (nystagmus), and poor vision.
Cone monochromacy is a rare total color blindness that is accompanied by relatively normal vision, electroretinogram, and electrooculogram. Cone monochromacy can also be a result of having more than one type of dichromatic color blindness. People who have, for instance, both protanopia and tritanopia are considered to have cone monochromacy. Since cone monochromacy is the lack of/damage of more than one cone in retinal environment, having two types of dichromacy would be an equivalent.

Dichromacy is a moderately severe color vision defect in which one of the three basic color mechanisms is absent or not functioning. It is hereditary and, in the case of protanopia or deuteranopia, sex-linked, affecting predominantly males. Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions. Dichromacy conditions are labeled based on whether the "first" (Greek: prot-, referring to the red photoreceptors), "second" (deuter-, the green), or "third" (trit-, the blue) photoreceptors are affected.

Protanopia is a severe type of color vision deficiency caused by the complete absence of red retinal photoreceptors. Protans have difficulties distinguishing between blue and green colors and also between red and green colors. It is a form of dichromatism in which the subject can only perceive light wavelengths from 400 to 650 nm, instead of the usual 700 nm. Pure reds cannot be seen, instead appearing black; purple colors cannot be distinguished from blues; more orange-tinted reds may appear as very dim yellows, and all orange–yellow–green shades of too long a wavelength to stimulate the blue receptors appear as a similar yellow hue. It is hereditary, sex-linked, and present in 1% of males.
Deuteranopia is a type of color vision deficiency where the green photoreceptors are absent. It affects hue discrimination in the same way as protanopia, but without the dimming effect. Like protanopia, it is hereditary, sex-linked, and found in about 1% of the male population.[7]
Tritanopia is a very rare color vision disturbance in which there are only two cone pigments present and a total absence of blue retinal receptors. Blues appear greenish, yellows and oranges appear pinkish, and purple colors appear deep red. It is related to chromosome 7. Unlike protanopia and deuteranopia, tritanopia and tritanomaly are not sex-linked traits and can be acquired rather than inherited and can be reversed in some cases.

Anomalous trichromacy is a common type of inherited color vision deficiency, occurring when one of the three cone pigments is altered in its spectral sensitivity.

Protanomaly is a mild color vision defect in which an altered spectral sensitivity of red retinal receptors (closer to green receptor response) results in poor red–green hue discrimination. It is hereditary, sex-linked, and present in 1% of males. The difference with protanopia is that in this case the L-cone is present but malfunctioning, whereas in the former case the L-cone is completely missing.[8]
Deuteranomaly, caused by a similar shift in the green retinal receptors, is by far the most common type of color vision deficiency, mildly affecting red–green hue discrimination in 5% of European males. It is hereditary and sex-linked. The difference with deuteranopia is that in this case the green sensitive cones are not missing but malfunctioning.[9]
Tritanomaly is a rare, hereditary color vision deficiency affecting blue–green and yellow–red/pink hue discrimination. It is related to chromosome "7".[10] The difference is that the S-cone is malfunctioning but not missing.[11]

text: Genetics[edit]

text: Color blindness is typically an inherited genetic disorder. It is most commonly inherited from mutations on the X chromosome but the mapping of the human genome has shown there are many causative mutations—mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man (OMIM)). Two of the most common inherited forms of color blindness are protanomaly (and, more rarely, protanopia – the two together often known as "protans") and deuteranomaly (or, more rarely, deuteranopia – the two together often referred to as "deutans").[12] Both "protans" and "deutans" (of which the deutans are by far the most common) are known as "red–green color-blind" which is present in about 8 percent of human males and 0.6 percent of females of Northern European ancestry.[13]

text: Some of the inherited diseases known to cause color blindness are:

text:
cone dystrophy
cone-rod dystrophy
achromatopsia (a.k.a. rod monochromatism, stationary cone dystrophy or cone dysfunction syndrome)
blue cone monochromatism (a.k.a. blue cone monochromacy or X-linked achromatopsia)
Leber's congenital amaurosis
retinitis pigmentosa (initially affects rods but can later progress to cones and therefore color blindness).

text: Inherited color blindness can be congenital (from birth), or it can commence in childhood or adulthood. Depending on the mutation, it can be stationary, that is, remain the same throughout a person's lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, certain forms of color blindness can progress to legal blindness, i.e., an acuity of 6/60 (20/200) or worse, and often leave a person with complete blindness.

text: Color blindness always pertains to the cone photoreceptors in retinas, as the cones are capable of detecting the color frequencies of light.

text: About 8 percent of males, and 0.6 percent of females, are red-green color blind in some way or another, whether it is one color, a color combination, or another mutation.[14] The reason males are at a greater risk of inheriting an X linked mutation is that males only have one X chromosome (XY, with the Y chromosome carrying altogether different genes than the X chromosome), and females have two (XX); if a woman inherits a normal X chromosome in addition to the one that carries the mutation, she will not display the mutation. Men do not have a second X chromosome to override the chromosome that carries the mutation. If 8% of variants of a given gene are defective, the probability of a single copy being defective is 8%, but the probability that two copies are both defective is 0.08 × 0.08 = 0.0064, or just 0.64%.

text: Other causes[edit]

text: Other causes of color blindness include brain or retinal damage caused by shaken baby syndrome, accidents and other trauma which produce swelling of the brain in the occipital lobe, and damage to the retina caused by exposure to ultraviolet light (10–300 nm). Damage often presents itself later on in life.

text: Color blindness may also present itself in the spectrum of degenerative diseases of the eye, such as age-related macular degeneration, and as part of the retinal damage caused by diabetes. Another factor that may affect color blindness includes a deficiency in Vitamin A.[15]

text: Some subtle forms of colorblindness may be associated with chronic solvent-induced encephalopathy (CSE), caused by longtime exposure to solvent vapors.[16]

text: Red–green color blindness can be caused by ethambutol,[17] a drug used in the treatment of tuberculosis.

text: Types[edit]

text: Based on clinical appearance, color blindness may be described as total or partial. Total color blindness is much less common than partial color blindness.[18] There are two major types of color blindness: those who have difficulty distinguishing between red and green, and who have difficulty distinguishing between blue and yellow.[19][20]

text: Immunofluorescent imaging is a way to determine red–green color coding. Conventional color coding is difficult for individuals with red–green color blindness (protanopia or deuteranopia) to discriminate. Replacing red with magenta or green with turquoise improves visibility for such individuals.[21]

text: The different kinds of inherited color blindness result from partial or complete loss of function of one or more of the different cone systems. When one cone system is compromised, dichromacy results. The most frequent forms of human color blindness result from problems with either the middle or long wavelength sensitive cone systems, and involve difficulties in discriminating reds, yellows, and greens from one another. They are collectively referred to as "red–green color blindness", though the term is an over-simplification and is somewhat misleading. Other forms of color blindness are much more rare. They include problems in discriminating blues from greens and yellows from reds/pinks, and the rarest forms of all, complete color blindness or monochromacy, where one cannot distinguish any color from grey, as in a black-and-white movie or photograph.

text: Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two primary colors (whereas normally humans are trichromats and require three primary colors). These individuals normally know they have a color vision problem and it can affect their lives on a daily basis. Two percent of the male population exhibit severe difficulties distinguishing between red, orange, yellow, and green. A certain pair of colors, that seem very different to a normal viewer, appear to be the same color (or different shades of same color) for such a dichromat. The terms protanopia, deuteranopia, and tritanopia come from Greek and literally mean "inability to see (anopia) with the first (prot-), second (deuter-), or third (trit-) [cone]", respectively.

text: Anomalous trichromacy is the least serious type of color deficiency.[22] People with protanomaly, deuteranomaly, or tritanomaly are trichromats, but the color matches they make differ from the normal. They are called anomalous trichromats. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. From a practical standpoint though, many protanomalous and deuteranomalous people have very little difficulty carrying out tasks that require normal color vision. Some may not even be aware that their color perception is in any way different from normal.

text: Protanomaly and deuteranomaly can be diagnosed using an instrument called an anomaloscope, which mixes spectral red and green lights in variable proportions, for comparison with a fixed spectral yellow. If this is done in front of a large audience of males, as the proportion of red is increased from a low value, first a small proportion of the audience will declare a match, while most will see the mixed light as greenish; these are the deuteranomalous observers. Next, as more red is added the majority will say that a match has been achieved. Finally, as yet more red is added, the remaining, protanomalous, observers will declare a match at a point where normal observers will see the mixed light as definitely reddish.[citation needed]

text: Red–green color blindness[edit]

text: Protanopia, deuteranopia, protanomaly, and deuteranomaly are commonly inherited forms of red–green color blindness which affect a substantial portion of the human population. Those affected have difficulty with discriminating red and green hues due to the absence or mutation of the red or green retinal photoreceptors.[12][23] It is sex-linked: genetic red–green color blindness affects males much more often than females, because the genes for the red and green color receptors are located on the X chromosome, of which males have only one and females have two. Females (46, XX) are red–green color blind only if both their X chromosomes are defective with a similar deficiency, whereas males (46, XY) are color blind if their single X chromosome is defective.[24]

text: The gene for red–green color blindness is transmitted from a color blind male to all his daughters who are heterozygote carriers and are usually unaffected. In turn, a carrier woman has a fifty percent chance of passing on a mutated X chromosome region to each of her male offspring. The sons of an affected male will not inherit the trait from him, since they receive his Y chromosome and not his (defective) X chromosome. Should an affected male have children with a carrier or colorblind woman, their daughters may be colorblind by inheriting an affected X chromosome from each parent.[24]

text: Because one X chromosome is inactivated at random in each cell during a woman's development, deuteranomalous heterozygotes (i.e. female carriers of deuteranomaly) are potentially tetrachromats, because they will have the normal long wave (red) receptors, the normal medium wave (green) receptors, the abnormal medium wave (deuteranomalous) receptors and the normal autosomal short wave (blue) receptors in their retinas.[25][26][27] The same applies to the carriers of protanomaly (who have two types of short wave receptors, normal medium wave receptors, and normal autosomal short wave receptors in their retinas). If, by chance, a woman is heterozygous for both protanomaly and deuteranomaly she could be pentachromatic. This situation could arise if, for instance, she inherited the X chromosome with the abnormal long wave gene (but normal medium wave gene) from her mother who is a carrier of protanomaly, and her other X chromosome from a deuteranomalous father. Such a woman would have a normal and an abnormal long wave receptor, a normal and abnormal medium wave receptor, and a normal autosomal short wave receptor – 5 different types of color receptors in all. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. In many cases it is almost unnoticeable, but in a minority the tetrachromacy is very pronounced.[25][26][27] However, Jameson et al.[28] have shown that with appropriate and sufficiently sensitive equipment all female carriers of red-green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) are tetrachromats to a greater or lesser extent.

text: Since deuteranomaly is by far the most common form of red-green blindness among men of northwestern European descent (with an incidence of 8%), then the carrier frequency (and of potential deuteranomalous tetrachromacy) among the females of that genetic stock is 14.7% (= [92% × 8%] × 2).[24]

text: Protanopia (1% of males): Lacking the red cones for long-wavelength sensitive retinal cones, those with this condition are unable to distinguish between colors in the green–yellow–red section of the spectrum. They have a neutral point at a cyan-like wavelength around 492 nm (see spectral color for comparison) – that is, they cannot discriminate light of this wavelength from white. For a protanope, the brightness of red, orange, and yellow are much reduced compared to normal. This dimming can be so pronounced that reds may be confused with black or dark gray, and red traffic lights may appear to be extinguished. They may learn to distinguish reds from yellows primarily on the basis of their apparent brightness or lightness, not on any perceptible hue difference. Violet, lavender, and purple are indistinguishable from various shades of blue because their reddish components are so dimmed as to be invisible. For example, pink flowers, reflecting both red light and blue light, may appear just blue to the protanope. A very few people have been found who have one normal eye and one protanopic eye. These unilateral dichromats report that with only their protanopic eye open, they see wavelengths shorter than neutral point as blue and those longer than it as yellow. This is a rare form of color blindness.

text: Deuteranopia (1% of males): Lacking the green cones for medium-wavelength cones, those affected are again unable to distinguish between colors in the green–yellow–red section of the spectrum. Their neutral point is at a slightly longer wavelength, 498 nm, a more greenish hue of cyan. A deuteranope suffers the same hue discrimination problems as protanopes, but without the abnormal dimming. Purple colors are not perceived as something opposite to spectral colors; all these appear similarly. This form of colorblindness is also known as Daltonism after John Dalton (his diagnosis was confirmed as deuteranopia in 1995, some 150 years after his death, by DNA analysis of his preserved eyeball). Equivalent terms for Daltonism in Romanic languages such as daltonismo (Spanish, Portuguese and Italian), daltonisme (French), daltonism (Romanian) are still used to describe color blindess in a broad sense or deuteranopia in a more restricted sense. Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths shorter than neutral point as blue and longer than it as yellow.[29]

text: Protanomaly (1% of males, 0.01% of females):[30] Having a mutated form of the long-wavelength (red) pigment, whose peak sensitivity is at a shorter wavelength than in the normal retina, protanomalous individuals are less sensitive to red light than normal. This means that they are less able to discriminate colors, and they do not see mixed lights as having the same colors as normal observers. They also suffer from a darkening of the red end of the spectrum. This causes reds to reduce in intensity to the point where they can be mistaken for black. Protanomaly is a fairly rare form of color blindness, making up about 1% of the male population. Both protanomaly and deuteranomaly are carried on the X chromosome.

text: Deuteranomaly (most common—6% of males, 0.4% of females):[30] These individuals have a mutated form of the medium-wavelength (green) pigment. The medium-wavelength pigment is shifted towards the red end of the spectrum resulting in a reduction in sensitivity to the green area of the spectrum. Unlike protanomaly the intensity of colors is unchanged. The deuteranomalous person is considered "green weak". For example, in the evening, dark green cars appear to be black to deuteranomalous people. Similar to the protanomates, deuteranomates are poor at discriminating small differences in hues in the red, orange, yellow, green region of the spectrum. They make errors in the naming of hues in this region because the hues appear somewhat shifted towards green. One very important difference between deuteranomalous individuals and protanomalous individuals is deuteranomalous individuals do not have the loss of "brightness" problem.

text: Blue–yellow color blindness[edit]

text: Those with tritanopia and tritanomaly have difficulty discriminating between bluish and greenish hues, as well as yellowish and reddish hues.

text: Color blindness involving the inactivation of the short-wavelength sensitive cone system (whose absorption spectrum peaks in the bluish-violet) is called tritanopia or, loosely, blue–yellow color blindness. The tritanope's neutral point occurs near a yellowish 570 nm; green is perceived at shorter wavelengths and red at longer wavelengths.[31] Mutation of the short-wavelength sensitive cones is called tritanomaly. Tritanopia is equally distributed among males and females. Jeremy H. Nathans (with the Howard Hughes Medical Institute) demonstrated that the gene coding for the blue receptor lies on chromosome 7, which is shared equally by males and females. Therefore, it is not sex-linked. This gene does not have any neighbor whose DNA sequence is similar. Blue color blindness is caused by a simple mutation in this gene.

text: Tritanopia (less than 1% of males and females): Lacking the short-wavelength cones, those affected see short-wavelength colors (blue, indigo and a spectral violet) greenish and drastically dimmed, some of these colors even as black. Yellow is indistinguishable from pink, and purple colors are perceived as various shades of red. This form of color blindness is not sex-linked.

text: Tritanomaly (equally rare for males and females [0.01% for both]):[30] Having a mutated form of the short-wavelength (blue) pigment. The short-wavelength pigment is shifted towards the green area of the spectrum. This is the rarest form of anomalous trichromacy color blindness. Unlike the other anomalous trichromacy color deficiencies, the mutation for this color blindness is carried on chromosome 7. Therefore, it is equally prevalent in both male and female populations. The OMIM gene code for this mutation is 304000 "Colorblindness, Partial Tritanomaly".[32]

text: Total color blindness[edit]

text: Total color blindness is defined as the inability to see color. Although the term may refer to acquired disorders such as cerebral achromatopsia also known as color agnosia, it typically refers to congenital color vision disorders (i.e. more frequently rod monochromacy and less frequently cone monochromacy).[33][34]

text: In cerebral achromatopsia, a person cannot perceive colors even though the eyes are capable of distinguishing them. Some sources do not consider these to be true color blindness, because the failure is of perception, not of vision. They are forms of visual agnosia.[34]

text: Monochromacy is the condition of possessing only a single channel for conveying information about color. Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness. It occurs in two primary forms:

text:
Rod monochromacy, frequently called achromatopsia, where the retina contains no cone cells, so that in addition to the absence of color discrimination, vision in lights of normal intensity is difficult. While normally rare, achromatopsia is very common on the island of Pingelap, a part of the Pohnpei state, Federated States of Micronesia, where it is called maskun: about 10% of the population there has it, and 30% are unaffected carriers. The island was devastated by a storm in the 18th century (an example of a genetic bottleneck) and one of the few male survivors carried a gene for achromatopsia. The population grew to several thousand before foreign troops introduced diseases to the island in the 1940s.
Cone monochromacy is the condition of having both rods and cones, but only a single kind of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues. Blue cone monochromacy (X chromosome) is caused by lack of functionality of L and M cones (red and green). It is encoded at the same place as red–green color blindness on the X chromosome. Peak spectral sensitivities are in the blue region of the visible spectrum (near 440 nm). People with this condition generally show nystagmus ("jiggling eyes"), photophobia (light sensitivity), reduced visual acuity, and myopia (nearsightedness).[35] Visual acuity usually falls to the 20/50 to 20/400 range.

tag: ol

text: Mechanism[edit]

text: The typical human retina contains two kinds of light cells: the rod cells (active in low light) and the cone cells (active in normal daylight). Normally, there are three kinds of cone cells, each containing a different pigment, which are activated when the pigments absorb light. The spectral sensitivities of the cones differ; one is most sensitive to short wavelengths, one to medium wavelengths, and the third to medium-to-long wavelengths within the visible spectrum, with their peak sensitivities in the blue, green, and yellow-green regions of the spectrum, respectively. The absorption spectra of the three systems overlap, and combine to cover the visible spectrum. These receptors are known as short (S), medium (M), and long (L) wavelength cones, but are also often referred to as blue, green, and red cones, although this terminology is inaccurate.[36]

text: The receptors are each responsive to a wide range of wavelengths. For example, the long wavelength "red" receptor has its peak sensitivity in the yellow-green, some way from the red end (longest wavelength) of the visible spectrum. The sensitivity of normal color vision actually depends on the overlap between the absorption ranges of the three systems: different colors are recognized when the different types of cone are stimulated to different degrees. Red light, for example, stimulates the long wavelength cones much more than either of the others, and reducing the wavelength causes the other two cone systems to be increasingly stimulated, causing a gradual change in hue.

text: Many of the genes involved in color vision are on the X chromosome, making color blindness much more common in males than in females because males only have one X chromosome, while females have two. Because this is an X-linked trait, an estimated 2–3% of women have a 4th color cone[25] and can be considered tetrachromats. One such woman has been reported to be a true or functional tetrachromat, as she can discriminate colors most other people can't.[26][27]

text: Diagnosis[edit]

text: The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose red–green color deficiencies.[37] A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

text: Position yourself about 75cm from your monitor so that the colour test image you are looking at is at eye level, read the description of the image and see what you can see!! It is not necessary in all cases to use the entire set of images. In a large scale examination the test can be simplified to six tests; test, one of tests 2 or 3, one of tests 4, 5, 6, or 7, one of tests 8 or 9, one of tests 10, 11, 12, or 13 and one of tests 14 or 15.[this quote needs a citation]

text: Because the Ishihara color test contains only numerals, it may not be useful in diagnosing young children, who have not yet learned to use numbers. In the interest of identifying these problems early on in life, alternative color vision tests were developed using only symbols (square, circle, car).

text: Besides the Ishihara color test, the US Navy and US Army also allow testing with the Farnsworth Lantern Test. This test allows 30% of color deficient individuals, whose deficiency is not too severe, to pass.

text: Another test used by clinicians to measure chromatic discrimination is the Farnsworth-Munsell 100 hue test. The patient is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps.[38]

text: The HRR color test (developed by Hardy, Rand, and Rittler) is a red–green color test that, unlike the Ishihara, also has plates for the detection of the tritan defects.[39]

text: Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect thorough datasets, identify copunctal points, and measure just noticeable differences.[40]

text: Management[edit]

text: There is generally no treatment to cure color deficiencies. ″The American Optometric Association reports a contact lens on one eye can increase the ability to differentiate between colors, though nothing can make you truly see the deficient color.″[41]

text: Lenses[edit]

text: Optometrists can supply colored spectacle lenses or a single red-tint contact lens to wear on the non-dominant eye, but although this may improve discrimination of some colors, it can make other colors more difficult to distinguish. A 1981 review of various studies to evaluate the effect of the X-chrom contact lens concluded that, while the lens may allow the wearer to achieve a better score on certain color vision tests, it did not correct color vision in the natural environment.[42] A case history using the X-Chrom lens for a rod monochromat is reported[43] and an X-Chrom manual is online.[44]

text: Lenses that filter certain wavelengths of light can allow people with a cone anomaly, but not dichromacy, to see better separation of colors, especially those with classic "red/green" color blindness. They work by notching out wavelengths that strongly stimulate both red and green cones in a deuter- or protanomalous person, improving the distinction between the two cones' signals. As of 2013, sunglasses that notch out color wavelengths are available commercially.[45]

text: Apps[edit]

text: Many applications for iPhone and iPad have been developed to help colorblind people to view the colors in a better way. Many applications launch a sort of simulation of colorblind vision to make normal-view people understand how the color-blinds see the world. Others allow a correction of the image grabbed from the camera with a special "daltonizer" algorithm.

text: The GNOME desktop environment provides colorblind accessibility using the gnome-mag and the libcolorblind software. Using a gnome applet, the user may switch a color filter on and off, choosing from a set of possible color transformations that will displace the colors in order to disambiguate them. The software enables, for instance, a colorblind person to see the numbers in the Ishihara test.

text: Epidemiology[edit]

text:
Rates of color blindness[clarification needed][46]

Males
Females

Dichromacy
2.4%
0.03%

Protanopia (red deficient: L cone absent)
1.3%
0.02%

Deuteranopia (green deficient: M cone absent)
1.2%
0.01%

Tritanopia (blue deficient: S cone absent)
0.001%
0.03%

Anomalous trichromacy
6.3%
0.37%

Protanomaly (red deficient: L cone defect)
1.3%
0.02%

Deuteranomaly (green deficient: M cone defect)
5.0%
0.35%

Tritanomaly (blue deficient: S cone defect)
0.0001%
0.0001%

text: Color blindness affects a large number of individuals, with protanopia and deuteranopia being the most common types.[12] In individuals with Northern European ancestry, as many as 8 percent of men and 0.4 percent of women experience congenital color deficiency.[47]

text: The number affected varies among groups. Isolated communities with a restricted gene pool sometimes produce high proportions of color blindness, including the less usual types. Examples include rural Finland, Hungary, and some of the Scottish islands.[citation needed] In the United States, about 7 percent of the male population—or about 10.5 million men—and 0.4 percent of the female population either cannot distinguish red from green, or see red and green differently from how others do (Howard Hughes Medical Institute, 2006[clarification needed]). More than 95 percent of all variations in human color vision involve the red and green receptors in male eyes. It is very rare for males or females to be "blind" to the blue end of the spectrum.[48]

text:
Prevalence of red–green color blindness among males[49]

Population
Number
studied
%

Arabs (Druzes)
337
10.0

Aboriginal Australians
4,455
1.9

Belgians
9,540
7.4

Bosnians
4,836
6.2

Britons
16,180
6.6

Chinese
1,164
6.9

DR Congolese
929
1.7

Dutch
3,168
8.0

Eskimo
297
2.5

Fijians
608
0.8

French
1,243
8.6

Germans
7,861
7.7

Hutu
1,000
2.9

Indians (Andhra Pradesh)
292
7.5

Iranians
16,180
6.6

Japanese
259,000
4.0

Mexicans
571
2.3

Navajo
571
2.3

Norwegians
9,047
9.0

Russians
1,343
9.2

Scots
463
7.8

Swiss
2,000
8.0

Tibetans
241
5.0

Tswana
407
2.0

Tutsi
1,000
2.5

Serbs
4,750
7.4

text: History[edit]

text: The first scientific paper on the subject of color blindness, Extraordinary facts relating to the vision of colours, was published by the English chemist John Dalton in 1798[50] after the realization of his own color blindness. Because of Dalton's work, the general condition has been called daltonism, although in English this term is now used only for deuteranopia.

text: Society and culture[edit]

text: Design implications[edit]

text: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (August 2012) (Learn how and when to remove this template message)

text: Color codes present particular problems for those with color deficiencies as they are often difficult or impossible for them to perceive.

text: Good graphic design avoids using color coding or using color contrasts alone to express information;[51] this not only helps color blind people, but also aids understanding by normally sighted people by providing them with multiple reinforcing cues.[citation needed]

text: Designers need to take into account that color-blindness is highly sensitive to differences in material. For example, a red–green colorblind person who is incapable of distinguishing colors on a map printed on paper may have no such difficulty when viewing the map on a computer screen or television. In addition, some color blind people find it easier to distinguish problem colors on artificial materials, such as plastic or in acrylic paints, than on natural materials, such as paper or wood. Third, for some color blind people, color can only be distinguished if there is a sufficient "mass" of color: thin lines might appear black, while a thicker line of the same color can be perceived as having color.[citation needed]

text: Designers should also note that red–blue and yellow–blue color combinations are generally safe. So instead of the ever-popular "red means bad and green means good" system, using these combinations can lead to a much higher ability to use color coding effectively. This will still cause problems for those with monochromatic color blindness, but it is still something worth considering.[52]

text: When the need to process visual information as rapidly as possible arises, for example in an emergency situation, the visual system may operate only in shades of gray, with the extra information load in adding color being dropped.[citation needed] This is an important possibility to consider when designing, for example, emergency brake handles or emergency phones.

text: Occupations[edit]

text: Color blindness may make it difficult or impossible for a person to engage in certain occupations. Persons with color blindness may be legally or practically barred from occupations in which color perception is an essential part of the job (e.g., mixing paint colors), or in which color perception is important for safety (e.g., operating vehicles in response to color-coded signals). This occupational safety principle originates from the Lagerlunda train crash of 1875 in Sweden. Following the crash, Professor Alarik Frithiof Holmgren, a physiologist, investigated and concluded that the color blindness of the engineer (who had died) had caused the crash. Professor Holmgren then created the first test using different-colored skeins to exclude people from jobs in the transportation industry on the basis of color blindness.[53] However, there is a claim that there is no firm evidence that color deficiency did cause the collision, or that it might have not been the sole cause.[54]

text: Color vision is important for occupations using telephone or computer networking cabling, as the individual wires inside the cables are color-coded using green, orange, brown, blue and white colors.[55] Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, yellow, green, blue, violet, gray, white, silver, gold.[56]

text: Driving[edit]

text: Some countries have refused to grant driving licenses to individuals with color blindness. In Romania, there is an ongoing campaign to remove the legal restrictions that prohibit colorblind citizens from getting drivers' licenses.[57]

text: The usual justification for such restrictions is that drivers of motor vehicles must be able to recognize color-coded signals, such as traffic lights or warning lights.[52]

text: Piloting aircraft[edit]

text: While many aspects of aviation depend on color coding, only a few of them are critical enough to be interfered with by some milder types of color blindness. Some examples include color-gun signaling of aircraft that have lost radio communication, color-coded glide-path indications on runways, and the like. Some jurisdictions restrict the issuance of pilot credentials to persons who suffer from color blindness for this reason. Restrictions may be partial, allowing color-blind persons to obtain certification but with restrictions, or total, in which case color-blind persons are not permitted to obtain piloting credentials at all.[citation needed]

text: In the United States, the Federal Aviation Administration requires that pilots be tested for normal color vision as part of their medical clearance in order to obtain the required medical certificate, a prerequisite to obtaining a pilot's certification. If testing reveals color blindness, the applicant may be issued a license with restrictions, such as no night flying and no flying by color signals—such a restriction effectively prevents a pilot from holding certain flying occupations, such as that of an airline pilot, although commercial pilot certification is still possible, and there are a few flying occupations that do not require night flight and thus are still available to those with restrictions due to color blindness (e.g., agricultural aviation). The government allows several types of tests, including medical standard tests (e.g., the Ishihara, Dvorine, and others) and specialized tests oriented specifically to the needs of aviation. If an applicant fails the standard tests, they will receive a restriction on their medical certificate that states: "Not valid for night flying or by color signal control". They may apply to the FAA to take a specialized test, administered by the FAA. Typically, this test is the "color vision light gun test". For this test an FAA inspector will meet the pilot at an airport with an operating control tower. The color signal light gun will be shone at the pilot from the tower, and they must identify the color. If they pass they may be issued a waiver, which states that the color vision test is no longer required during medical examinations. They will then receive a new medical certificate with the restriction removed. This was once a Statement of Demonstrated Ability (SODA), but the SODA was dropped, and converted to a simple waiver (letter) early in the 2000s.[58]

text: Research published in 2009 carried out by the City University of London's Applied Vision Research Centre, sponsored by the UK's Civil Aviation Authority and the US Federal Aviation Administration, has established a more accurate assessment of color deficiencies in pilot applicants' red–green and yellow–blue color range which could lead to a 35% reduction in the number of prospective pilots who fail to meet the minimum medical threshold.[59]

text: Art[edit]

text: Inability to distinguish color does not necessarily preclude the ability to become a celebrated artist. The 20th century expressionist painter Clifton Pugh, three-time winner of Australia's Archibald Prize, on biographical, gene inheritance and other grounds has been identified as a protanope.[60] 19th century French artist Charles Méryon became successful by concentrating on etching rather than painting after he was diagnosed as having a red–green deficiency.[61]

text: Rights of the color blind[edit]

text: Brazil[edit]

text: A Brazilian court ruled that people with color blindness are protected by the Inter-American Convention on the Elimination of All Forms of Discrimination against Person with Disabilities.[62][63][64]

text: At trial, it was decided that the carriers of color blindness have a right of access to wider knowledge, or the full enjoyment of their human condition.

text: United States[edit]

text: In the United States, under federal anti-discrimination laws such as the Americans with Disabilities Act, color vision deficiencies have not been found to constitute a disability that triggers protection from workplace discrimination.[65]

text: A famous traffic light on Tipperary Hill in Syracuse, New York, is upside-down due to the sentiments of its Irish American community,[66] but has been criticized due to the potential hazard it poses for color-blind persons.[67]

text: Research[edit]

text: Some tentative evidence finds that color blind people are better at penetrating certain color camouflages. Such findings may give an evolutionary reason for the high rate of red–green color blindness.[4] There is also a study suggesting that people with some types of color blindness can distinguish colors that people with normal color vision are not able to distinguish.[68] In World War II, color blind observers were used to penetrate camouflage.[69]

text: In September 2009, the journal Nature reported that researchers at the University of Washington and University of Florida were able to give trichromatic vision to squirrel monkeys, which normally have only dichromatic vision, using gene therapy.[70]

text: In 2003, a cybernetic device called eyeborg was developed to allow the wearer to hear sounds representing different colors.[71] Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004; the eyeborg allowed him to start painting in color by memorizing the sound corresponding to each color. In 2012, at a TED Conference, Harbisson explained how he could now perceive colors outside the ability of human vision.[72]


document_title: Mamluk dynasty (Delhi)

question_text: name the ruler who shifted capital from lahore to delhi

root

text: Mamluk dynasty (Delhi)

text: History

text: The Mamluk, literally meaning owned, was a soldier  of slave origin who had converted to Islam. The phenomenon started in the 9th century and gradually the Mamluks became a powerful military caste in various Muslim societies. Mamluks held political and military power most notably in Egypt, but also in the Levant, Iraq, and India.

tag: p

text: In 1206, Muhammad of Ghor, Sultan of the Ghurid Empire was assassinated.[8] Since he had no children, his empire split into minor sultanates led by his former mamluk generals. Taj-ud-Din Yildoz became the ruler of Ghazni. Muhammad bin Bakhtiyar Khilji got Bengal. Nasir-ud-Din Qabacha became the sultan of Multan. Qutb ud-Din Aibak became the sultan of Delhi, and that was the beginning of the Slave dynasty.

text: Aibak rose to power when a Ghorid superior was assassinated.[9] However, his reign as the Sultan of Delhi was short lived as he died in 1210 and his son Aram Shah rose to the throne, only to be assassinated by Iltutmish in 1211.

text: The Sultanate under Iltutmish established cordial diplomatic contact with the Abbasid Caliphate between 1228–29 and had managed to keep India unaffected by the invasions of Genghis Khan and his successors.[6] Following the death of Iltutmish in 1236 a series of weak rulers remained in power and a number of the noblemen gained autonomy over the provinces of the Sultanate. Power shifted hands from Rukn ud din Firuz to Razia Sultana until Ghiyas ud din Balban rose to the throne and successfully repelled both external threats to the Sultanate from the Chagatai Khanate invasions and internal threats from the rebellious sultanate nobles.[6][9] The Khalji dynasty came into being when Jalal ud din Firuz Khalji overthrew the last of the Slave dynasty rulers, Muiz ud din Qaiqabad, the grandson of Balban, and assumed the throne at Delhi.[10]

text: Sultans

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tag: table

text: The first Sultan of the Mamluk dynasty was Qutb ud-Din Aibak (قطب الدین ایبک), who had the titular name of Sultan (سلطان) and reigned from 1206 to 1210. He temporarily quelled the rebellions of Nasir-ud-Din Qabacha of Multan and Tajuddin Yildoz of Ghazni. Making Lahore his capital, he consolidated his control over North India through an administrative hold over Delhi. He also initiated the construction of Delhi's earliest Muslim monuments, the Quwwat-ul-Islam mosque and the Qutb Minar. In 1210, he died due to injuries received from an accident while playing a game of polo in Lahore; his horse fell and he was impaled on the pommel of his saddle. He was buried near the Anarkali Bazaar in Lahore.

text: The second Sultan was Aram Shah (آرام شاہ), who had the titular name of Sultan and reigned from 1210 to 1211. An elite group of forty nobles named Chihalgani ("the Forty") conspired against Aram Shah and invited Shams-ud-din Iltutmish, then Governor of Badaun, to replace Aram. Iltutmish defeated Aram in the plain of Jud near Delhi in 1211. It is not quite certain what became of Aram.

text: The third Sultan was Shams-ud-din Iltutmish (شمس الدین التتمش), who had the titular name of Nasir Amir-ul-Mu'minin (ناصرامیر المؤمنین ) and reigned from 1211 to 1236. He shifted the capital from Lahore to Delhi and trebled the exchequer. He defeated Nasir-ud-Din Qabacha of Multan and Tajuddin Yildoz of Ghazni, who had declared themselves contenders of Delhi. Mongols invaded India in pursuit of Jalal-ud-din Mangabarni who was defeated at the Battle of Indus by Genghis Khan in 1221. After Genghis Khan's death, Iltutmish consolidated his hold on northern India by retaking many of the lost territories. In 1230, he built the Hauz-i-Shamsi reservoir in Mehrauli, and in 1231 he built Sultan Ghari, which was the first Islamic mausoleum in Delhi.

text: The fourth Sultan was Rukn-ud-din Feroze (رکن الدین فیروز), who had the titular name of Sultan and reigned from April 1236 to November 1236. He ruled for only seven months and his mother, Shah Turkan, for all practical purposes was running the government. He abandoned himself to the pursuit of personal pleasure and debauchery, to the considerable outrage of the citizenry. On 9 November 1236, both Rukn-ud-din Feroze and his mother Shah Turkan were assassinated by the Chihalgani.

text: The fifth Sultana was Razia al-Din (رضیہ الدین ), who had the titular name of Jalâlat-ud-dîn Raziyâ Sultana (جلالۃ الدین رضیہ سلطانہ ) and reigned from 1236 to 1240. As the first female Muslim ruler in Inda, she initial managed to impress the nobles and administratively handled the Sultanate well. However, she began associating with the African Jamal-ud-Din Yaqut, provoking racial antagonism amongst the nobles and clergy, who were primarily Central Asian Turkic and already resented the rule of a female monarch. She was defeated by the powerful nobleman Malik Altunia whom she agreed to marry. Her half-brother Muiz-ud-din Bahram, however, usurped the throne with the help of the Chihalgani and defeated the combined forces of the Sultana and her husband. The couple fled and reached Kaithal, where their remaining forces abandoned them. They both fell into the hands of Jats and were robbed and killed on 14 October 1240.

text: The sixth Sultan was Muiz-ud-din Bahram (معز الدین بہرام), who had the titular name of Sultan and reigned from 1240 to 15 May 1242. During his reign, the Chihalgani became disorderly and constantly bickered among each other. It was during this period of unrest that the Mongols invaded the Punjab and sacked Lahore. Muiz-ud-din Bahram was too weak to take any action against them, and the Chihalgani besiged him in the White Fort of Delhi and put him to death in 1242.

text: The seventh Sultan was Ala-ud-din Masud (علاءالدین مسعود), who had the titular name of Sultan and reigned from 1242 to 1246. He was effectively a puppet for the Chihalgani and did not actually have much power or influence in the government. Instead, he became infamous for his fondness of entertainment and wine. By 1246, the chiefs had become upset with Ala-ud-din Masud's increasing hunger for more power and replaced him with his cousin Nasir-ud-din Mahmud, who was another grandson of Iltutmish.

text: The eighth Sultan was Nasir-ud-din Mahmud (نصیر الدین محمود ), who had the titular name of Nasir-ud-din Feroze Shah (نصیر الدین فیروز شاہ) and reigned from 1246 to 1266. As a ruler, Mahmud was known to be very religious, spending most of his time in prayer and was renowned for aiding the poor and the distressed. It was his Deputy Sultan, Ghiyath-ud-din Balban, who primarily dealt with state affairs.

text: The ninth Sultan was Ghiyath-ud-din Balban (غیاث الدین بلبن), who had the titular name of Sultan and reigned from 1266 to 1287. Balban ruled with an iron fist and broke up the Chihalgani group of noblemen. He tried to establish peace and order in India and built many outposts with garrisons of soldiers in areas where there had been disorder. Balban wanted to make sure everyone was loyal to the crown, so he established an efficient espionage system.

text: The tenth and final Sultan was Muiz-ud-din Muhammad Qaiqabad (معز الدین قیق آباد), who had the titular name of Sultan and reigned from 1287 to 1290. Being still young at the time, he ignored all state affairs. After four years, he suffered a paralytic stroke and was later murdered in 1290 by a Khalji chief. His three-year-old son Kayumars nominally succeeded him, but the Slave dynasty had ended with the rise of the Khaljis.

text: Architecture

text: The architectural legacy of the dynasty includes the Qutb Minar by Qutb ud-Din Aibak in Mehrauli, the Mausoleum of Prince Nasiru'd-Din Mahmud, eldest son of Iltumish, known as Sultan Ghari near Vasant Kunj, the first Islamic Mausoleum (tomb) built in 1231, and Balban's tomb, in the Mehrauli Archaeological Park.


document_title: The Sandlot 2

question_text: what is the dogs name in sandlot 2

question_tokens: what is the dogs name in sandlot 2

text: The Sandlot 2

text: Plot[edit]

text: This article's plot summary may be too long or excessively detailed. Please help improve it by removing unnecessary details and making it more concise. (December 2016) (Learn how and when to remove this template message)

text: The start of the movie flashes back to 1962 when Benny becomes Benny "the Jet" Rodriguez. The main part of the movie is set in 1972, ten years after the events of The Sandlot. New kids have moved into the neighborhood of San Fernando Valley in Los Angeles. They have started playing baseball in the sandlot. The previous kids have all grown up and moved away. A young boy named Johnnie Smalls, the little brother of Scott Smalls (the protagonist of the first film), has heard the legend of "The Great Fear" (a beastly mutated dog, as he puts it when he later on tells the group about The Beast) owned by Mr. Mertle, who lives behind the Sandlot. David Durango (Max-Lloyd Jones) is the leader of the boys. Behind the Sandlot, next to Mr. Mertle's home, lives the Goodfairer family. Hayley Goodfairer (Samantha Burton), the daughter and her two friends initially befriend the other boys in a census to share the Sandlot, but their relationship burgeons potently into a friendship when they find themselves in a big problem with The Beast next door, despite Hayley calling David a little baby, and David calling Hayley a spoiled brat.

text: The next day, David and his friends Mac, Tarqell, Saul and Saul's deaf little brother Sammy (referred to as "Fingers"), repeatedly demand Johnnie to tell the girls to leave the sandlot, but they keep refusing. Johnnie then suggests that they share the sandlot. The others agree but David doesn't feel good with the idea. Although since the girls are amazing at playing ball, he plans to make a deal with them; that they have to be on their team, they agree. Friday afternoon, the kids play a game with a little league team. But when the team captain, Singleton (Reece Thompson), ends up hitting Hayley in the stomach for playing with them, David responds by punching Singleton in the face and forces him to leave, but not before telling him that the sandlot is theirs forever.

text: One day, when Mac gets an aluminum baseball bat, he hits the ball over the junk wall, and afterward they attempt to retrieve it. But just as they are about to cross over through a passage in the fence, Johnnie stops them and tells them the story of "The Great Fear": how it was born to bite and was different from its sibling puppies. There was a boy who loved the comic book hero named Rapid Rocket, and believed he ran as fast as him. On his first day of school, he went past the house belonging to Mr. Mertle (who forgot to lock the back gate where the Great Fear was), and The Great Fear got out and chased the boy. It was unknown what happened to him after he was cornered by "The Great Fear." Soon afterward, a wall made of assorted junk was built. Ever since, if anything went over the fence, nothing would ever come out.

text: The main conflict comes when Johnnie accidentally launches a model Space Shuttle. The model was built by Hayley's father, a NASA engineer.  It was said to be the future of NASA. Unfortunately, Mr. Goodfarier's rocket lands in Mr. Mertle's back yard (which is now the home of the "Great Fear").  Hayley, along with everyone else, frantically attempts many ideas of getting it back, including hiring the boy called "The Retriever" (Griffin Reilly Evans), but every time he fails, and decides to retire and go home. Then, just like Benny Rodriguez from the first movie, David decided to go over the wall himself to retrieve the rocket. (Here it is revealed that the little boy who was bitten by "The Great Fear" in the story was David himself.) He retrieves it and escapes the Great Fear's yard. The Sandlot kids soon discover (just like The Beast) that The Great Fear got loose. David then hops on his bike and rides out of the sandlot. The Great Fear then chases after David. David then goes through a construction site, and then David gets off his bike and runs back to the sandlot. David hops over the junk wall back to Mr. Mertle's yard and falls through the tunnel that Mac used to try to get the rocket back. The dog knocks over the wall and saves David from suffocating. When David defeats the dog, it's revealed that the dog's real name is Goliath; after that, the kids can be seen running to the sandlot because Goliath got away, and realize that he only wanted to get out to see his girlfriend dog, Tiny (who was also behind a fence). As all the kids are leaving, Hayley and David share a kiss, and Mr. Mertle, tired of kids thinking he's grouchy, decides not to build a new fence.

text: In the final moments of the movie, the narrator tells what happened to all the sandlot kids. Mac joined the army when he graduated from high school, and received a Purple Heart when he was injured in the Gulf War, and then joined the Peace Corps. Saul and Fingers started a record label for a "new" kind of music called hip hop, and they named their company Def Jam Records; with the money Fingers made in the music industry, he started a successful gum company known as Kissing Booth Bubblegum. Jenny and Penny both raised three kids and had a happy life with their families. Tarquell was believed to be abducted by aliens and was never seen again. Hayley became a supermodel and a pitcher for the United States Olympic Softball team, winning two gold medals in the process. David earned the nickname "Rocket" after he defeated Goliath, and he eventually went on to marry Hayley, while Johnnie went to work for the Jet Propulsion Laboratories, as rockets were still his life.

text: Cast[edit]

text: This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (December 2016) (Learn how and when to remove this template message)

text:
Max Lloyd-Jones as David "Rocket" Durango
Samantha Burton as Hayley Goodfairer
James Willson as Johnnie Smalls
Brett Kelly as Mac McKing
Cole Evan Weiss as Saul Samuelson
Neilen Benvegnu as Tarquell
Sean Berdy as Sammy "Fingers" Samuelson
Jessica King as Penny
McKenzie Freemantle as Jenny
Griffin Reilly Evans as The Retriever
Reece Thompson as Singleton
Teryl Rothery as Mrs. Goodfairer
Greg Germann as Mr. Goodfairer
James Earl Jones as Mr. Mertle
Steve Garvey as Little League Coach
Austin Dunn as Kid David
Barbara Kottmeier as Hot Young Lady
Michael Antonakos as Boyfriend
Celia Bond as Man at Movie
David Mickey Evans as Narrator

tag: ul

text: Reception[edit]

text: The Sandlot 2 has received negative reviews from critics. It currently holds a 40% "rotten" rating on the review aggregator website, Rotten Tomatoes.[1]