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The International Society for Clinical Electrophysiology of Vision (ISCEV) standard for full-field electroretinography (ERG) describes a minimum procedure for testing generalized retinal function but encourages more extensive testing. This extended protocol describes a method of assessing the function of the short-wavelength-sensitive cone (S-cone) retinal pathway, using a short-wavelength flash superimposed on a background that saturates the rods and adapts the L/M-cones to elicit a response, known as the S-cone ERG. Stimulus parameters such as the strength and luminance of the flash and background, respectively, and their spectral and temporal characteristics are specified. As a complement to the ISCEV standard, testing the S-cone ERG enables further characterization of light-adapted retinal function and may refine diagnosis of some retinal disorders. Typical applications are described including use in the diagnosis of rod monochromacy and S-cone monochromacy, identification and investigation of cone On-bipolar cell dysfunction and use of the technique to confirm the diagnosis of enhanced S-cone syndrome.

Color blindness is when someone is unable to see color in a normal way or make out the differences in certain colors. The color-sensitive cells in our eyes react differently to various wavelengths of light giving our brain the information needed to create the ‘perceived’ color in our vision. There is no way to rectify the cells. In other words, color blind people cannot be treated. This paper uses image processing techniques to make Ishihara Test (test for color deficiency) images visible to partially and totally color blind people. Authors have targeted the following types of dichromatic color blindness—deuteranopia, protanopia, tritanopia and also monochromatic color blindness. All of this is achieved by applying various state-of-the-art image processing and mathematical operations in the image pixels to allow the user to ‘perceive’ the color as it was intended. To give a kind of proof of concept of the image processing for complete color blindness, a machine learning model has been implemented and trained on the widely known MNIST dataset.

Bats are a diverse radiation of mammals of enduring interest for understanding the evolution of sensory specialization. Colour vision variation among species has previously been linked to roosting preferences and echolocation form in the suborder Yinpterochiroptera, yet questions remain about the roles of diet and habitat in shaping bat visual ecology. We sequenced OPN1SW and OPN1LW opsin genes for 20 species of leaf-nosed bats (family Phyllostomidae; suborder Yangochiroptera) with diverse roosting and dietary ecologies, along with one vespertilionid species (Myotis lavali). OPN1LW genes appear intact for all species, and predicted spectral tuning of long-wavelength opsins varied among lineages. OPN1SW genes appear intact and under purifying selection for Myotis lavali and most phyllostomid bats, with two exceptions: (a) We found evidence of ancient OPN1SW pseudogenization in the vampire bat lineage, and loss-of-function mutations in all three species of extant vampire bats; (b) we additionally found a recent, independently derived OPN1SW pseudogene in Lonchophylla mordax, a cave-roosting species. These mutations in leaf-nosed bats are independent of the OPN1SW pseudogenization events previously reported in Yinpterochiropterans. Therefore, the evolution of monochromacy (complete colour blindness) has occurred in both suborders of bats and under various evolutionary drivers; we find independent support for the hypothesis that obligate cave roosting drives colour vision loss. We additionally suggest that haematophagous dietary specialization and corresponding selection on nonvisual senses led to loss of colour vision through evolutionary sensory trade-off. Our results underscore the evolutionary plasticity of opsins among nocturnal mammals.

Color blind is a type of Color Vision Deficiency, which is the inability that a person could not realize the differences between some colors. There are three types of color blindness: Monochromacy, Dichromacy, and Anomalous Trichromacy. Color blind cannot be cured. Today, technology gets up with solutions to help people with color blindness to see the image and distinguish between the different colors using some algorithms. This paper presents a smartphone based experimental comparison of color correction algorithms for all Dichromacy color-blind viewers: Protanopia, Duteranopia, and Tritanopia. This comparison includes LMS Daltonization algorithm, Color-blind Filter Service (CBFS) algorithm, LAB color corrector algorithm, and the shifting color algorithm. The LMS algorithm is implemented for all the three types of Dichromacy. While CBFS, LAB adjustment, and Shifting color algorithms are applied to correct colors for Protanopia, Duteranopia, and Tritanopia respectively. The results show that the processing time for LMS algorithm is slow compared to other algorithms. For Protanopia people, the LMS algorithm is better than CBFS algorithm as the LMS algorithm only changes color of con-fused areas with no change in the brightness. For Duteranopia people, the LAB color correction is better than the LMS algorithm. For Tritanopia people, both the shifting color algorithm and the LMS algorithm may produce a new confu-sion in the proceed images. An application interface is implemented to enable the user to choose the algorithm that gives the most appropriate results.

Colour vision in the marine environment is on average simpler than in terrestrial environments with simple or no colour vision through monochromacy or dichromacy. Monochromacy is found in marine mammals and elasmobranchs, including whales and sharks, but not some rays. Conversely, there is also a greater diversity of colour vision in the ocean than on land, examples being the polyspectral stomatopods and the many colour vision solutions found among reef fish. Recent advances in sequencing reveal more opsin (visual pigment) types than functionally useful at any one time. This diversity arises through opsin duplication and conversion. Such mechanisms allow pick-and-mix adaptation that tunes colour vision on a variety of very short non-evolutionary timescales. At least some of the diversity in marine colour vision is best explained as unconventional colour vision or as neutral drift.

This paper proposes a recoloring algorithm that when applied to images and videos, recolors them such that the color vision deficient users are able to see things that they previously couldn't. We compare the performances of two other prominent recoloring algorithms and prove how the proposed contrast enhancement color compensation technique is the most efficacious. Our previous paper [7] discusses color blindness, its causes and effects, the research that had been done previously on mitigating it, their outcomes and the various approaches adopted by some of the eminent researchers in this field. Color blindness is the inability of its victim to differentiate between the objects whose colors lie in a specific range of wavelengths, specific for each and every type of color blindness. Its three types are monochromacy, dichromacy and trichromacy. Our work focuses on anomalous trichromacy (especially on deuteranomaly and tritanomaly). While there is no medical cure for it yet, defective vision can be assuaged by certain techniques which many researchers have come up with. The merits and demerits of the various author's approaches were discussed in our previous [5] publication. Most of the research work that had been done never accounted for videos. We implement the previously invented algorithms on videos as well, thereby making a significant breakthrough. Apart from that, we propose a novel recoloring algorithm that is also applicable on both.

Color Blindness which can be also referred as Color Vision Deficiency (CVD) is one of the biggest scaling defect in humans which is still under the research for its accurate detection and cure measures & strategies. Color Blindness is the decreased ability to sight the distinctive colors instantly under normal lighting conditions. There are approximately 250 million individuals who suffer from Color Blindness. So it is need of an hour to understand all the important aspects of the Problem CVD and take the necessary measures to help the People who are knowingly or unknowingly suffering from CVD. In this paper we are going to put light on how exactly color blindness is genetically transferred to children, types in color vision deficiency i.e. Anomalous Trichromacy (protanomaly, deuteranomaly, tritanomaly), Monochromacy and how exactly person sees the normal image under respective CVD and finally put light on few algorithms and strategies which with the help of re-coloring and wavelength shifting actually help the color vision deficient to view and sight all the colors of the actual image distinctively.

Regressive evolution involves the degeneration of formerly useful structures in a lineage over time, and may be accompanied by the molecular decay of phenotype-specific genes. The mammalian eye has repeatedly undergone degeneration in taxa that occupy dim-light environments including subterranean habitats. Here we assess whether a decrease in the amount of light that reaches the retina is associated with increased regression of retinal genes, whether the phototransduction and visual cycle pathways degrade in a predictable pattern, and if the timing of retinal gene loss is associated with the entrance of mammalian lineages into subterranean environments. Sequence data were obtained from the publically available genomes of the Cape golden mole (Chrysochloris asiatica), naked mole-rat (Heterocephalus glaber) and star-nosed mole (Condylura cristata) for 65 genes associated with phototransduction, the visual cycle, and other retinal functions. Gene sequences were inspected for inactivating mutations and, when present, pseudogene sequences were compared to sequences from subaerial outgroup species. To test whether retinal degeneration is correlated with historical entrances into subterranean environments, estimated dates of retinal gene inactivation were compared to the fossil record and phylogenetic inferences of ancestral fossoriality. Our results show that (1) lower levels of light available to the retina correspond with an increase in the number of retinal pseudogenes, (2) retinal protein networks generally degrade in a predictable manner, although the extensive loss of cone phototransduction genes in Heterocephalus raises further questions regarding SWS1-cone monochromacy versus functional rod monochromacy in this species, and (3) inactivation dates of retinal genes usually post-date inferred entrances into subterranean habitats.

Human X-linked blue-cone monochromacy (BCM), a disabling congenital visual disorder of cone photoreceptors, is a candidate disease for gene augmentation therapy. BCM is caused by either mutations in the red (OPN1LW) and green (OPN1MW) cone photoreceptor opsin gene array or large deletions encompassing portions of the gene array and upstream regulatory sequences that would predict a lack of red or green opsin expression. The fate of opsin-deficient cone cells is unknown. We know that rod opsin null mutant mice show rapid postnatal death of rod photoreceptors. Using in vivo histology with high-resolution retinal imaging, we studied a cohort of 20 BCM patients (age range 5-58) with large deletions in the red/green opsin gene array. Already in the first years of life, retinal structure was not normal: there was partial loss of photoreceptors across the central retina. Remaining cone cells had detectable outer segments that were abnormally shortened. Adaptive optics imaging confirmed the existence of inner segments at a spatial density greater than that expected for the residual blue cones. The evidence indicates that human cones in patients with deletions in the red/green opsin gene array can survive in reduced numbers with limited outer segment material, suggesting potential value of gene therapy for BCM.

We established a protocol using a well-established LED stimulator to measure temporal contrast sensitivities driven by sine-wave modulation of L- and M-cones in the perifovea using triple silent substitution. The stimulus was presented in an annular field (2° inner diameter, 13° outer diameter). We validated this technique by studying the contrast sensitivity of three color normal observers at 10 different temporal frequencies (between 1 and 28 Hz) over a large range of retinal illuminances (between 0.07 and 587 phot Td), spanning the complete mesopic range. In one subject, sensitivities to counterphase modulation of L- and M-cones and in-phase modulation of L, M, and S-cones were additionally measured, which putatively reflected the parvo- and magnocellular retinogeniculate pathways, respectively. Furthermore, we performed measurements of temporal contrast sensitivities as a function of frequency at 294 phot Td in two protanopes, in two deuteranopes, and in one subject with S-cone monochromacy. Quality of isolation was satisfactory and we were able to reproduce known physiological patterns of temporal vision, such as the typical temporal contrast sensitivity functions of the L- and M-cone, the parvo- and magnocellular retinogeniculate pathways, as well as the light adaptation curves. These results will help determine optimal stimulus conditions in future studies. Results from the dichromats and the S-cone monochromat also support the quality of isolation of our protocol and underpin its potential clinical value.

X-linked cone photoreceptor disorders caused by mutations in the OPN1LW (L) and OPN1MW (M) cone opsin genes on chromosome Xq28 include a range of conditions from mild stable red-green colour vision deficiencies to severe cone dystrophies causing progressive loss of vision and blindness. Advances in molecular genotyping and functional analyses of causative variants, combined with deep retinal phenotyping, are unravelling genetic mechanisms underlying the variability of cone opsin disorders.

Much is known regarding the evolution of colour vision in nearly every vertebrate class, with the notable exception of the elasmobranchs. While multiple spectrally distinct cone types are found in some rays, sharks appear to possess only a single class of cone and, therefore, may be colour blind. In this study, the visual opsin genes of two wobbegong species,Orectolobus maculatusandOrectolobus ornatus, were isolated to verify the molecular basis of their monochromacy. In both species, only two opsin genes are present,RH1(rod) andLWS(cone), which provide further evidence to support the concept that sharks possess only a single cone type. Examination of the coding sequences revealed substitutions that account for interspecific variation in the photopigment absorbance spectra, which may reflect the difference in visual ecology between these species.

Aim: The aim of this study was to describe an automated method for extracting quantitative measures of foveal morphology from optical coherence tomography (OCT) images of the human retina. Methods: We performed a methodological study and retrospective investigation of selected cases. Sixty-five human subjects were included: 61 healthy subjects and four female carriers of blue-cone monochromacy (BCM). Thickness data from B-scans traversing the foveal pit were fitted to a mathematical model designed to capture the contour of the foveal surface. From this model, various metrics of foveal morphology were extracted (pit depth, diameter and slope). Results: Mathematical descriptions of foveal morphology enabled quantitative and objective evaluation of foveal dimensions from archived OCT data sets. We found a large variation in all aspects of the foveal pit (depth, diameter and slope). In myopes and BCM carriers, foveal pits were slightly less deep and had a more shallow slope, although these differences were not significant. Conclusions: Offline analysis of OCT data sets enables quantitative assessment of foveal morphology. The algorithm works on the Stratus™ and Cirrus™ macular thickness protocols, as well as the Spectralis® and Bioptigen© radial-line scan protocols, and can be objectively applied to existing data sets. These metrics will be useful in following changes associated with diseases such as retinopathy of prematurity and high myopia, as well as in studying normal postnatal development of the human fovea.

Research conducted in recent years has documented the widespread presence of various forms of color vision in species from across the animal kingdom, helped to develop an understanding of the basic biological mechanisms that underlie this sensory capacity, and provided some insights into the utility of color vision in the natural world. This chapter draws information from all these various sources to reveal what has been learned about the evolution of color vision. In doing so, we examine the extent and nature of animal color vision, describe various structural features of eyes and photoreceptors that condition color vision, look at photopigment opsin genes and their color vision concomitants, and comment on specific cases where progress has been made toward understanding the functional utility of color vision. Although results from a wide range of different species are considered, we focus particular attention on issues relevant to the evolution of vertebrate color vision.

Aotus is a platyrrhine primate that has been classically considered to be nocturnal. Earlier research revealed that this animal lacks a color vision capacity because, unlike all other platyrrhine monkeys, Aotus has a defect in the opsin gene that is required to produce short‐wavelength sensitive (S) cone photopigment. Consequently, Aotus retains only a single type of cone photopigment. Other mammals have since been found to show similar losses and it has often been speculated that such change is in some fashion tied to nocturnality. Although most species of Aotus are indeed nocturnal, recent observations show that Aotus azarai, an owl monkey species native to portions of Argentina and Paraguay, displays a cathemeral activity pattern being active during daylight hours as frequently as during nighttime hours. We have sequenced portions of the S‐cone opsin gene in A. azarai and Aotus nancymaae, the latter a typically nocturnal species. The S‐cone opsin genes in both species contain the same fatal defects earlier detected for Aotus trivirgatus. On the basis of the phylogenetic relationships of these three species these results imply that Aotus must have lost a capacity for color vision early in its history and they also suggest that the absence of color vision is not compulsively linked to a nocturnal lifestyle. Fil: Levenson, David H.. University of California at San Diego. Scripps Institution of Oceanography; Estados Unidos Fil: Fernandez Duque, Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Nordeste. Centro de Ecología Aplicada del Litoral. Universidad Nacional del Nordeste. Centro de Ecología Aplicada del Litoral; Argentina. University of Pennsylvania; Estados Unidos Fil: Evans, Sian. Dumond Conservancy For Primates And Tropical Forests; Estados Unidos Fil: Jacobs, Gerald H.. University of California; Estados Unidos

In recent years, great advances have been made in our understanding of the molecular basis of colour vision defects, as well as of the patterns of genetic variation in individuals with normal colour vision. Molecular genetic analyses have explained the diversity of types and degrees of severity in colour vision anomalies, their frequencies, pronounced individual variations in test results, etc. New techniques have even enabled the determination of John Dalton?s real colour vision defect, 150 years after his death. Inherited colour vision deficiencies most often result from the mutations of genes that encode cone opsins. Cone opsin genes are linked to chromosomes 7 (the S or ?blue? gene) and X (the L or ?red? gene and the M or ?green? gene). The L and M genes are located on the q arm of the X chromosome in a head-to-tail array, composed of 2 to 6 (typically 3) genes - a single L is followed by one or more M genes. Only the first two genes of the array are expressed and contribute to the colour vision phenotype. The high degree of homology (96%) between the L and M genes predisposes them to unequal recombination, leading to gene deletion or the formation of hybrid genes (comprising portions of both the L and M genes), explaining the majority of the common red-green colour vision deficiencies. The severity of any deficiency is influenced by the difference in spectral sensitivity between the opsins encoded by the first two genes of the array. A rare defect, S monochromacy, is caused either by the deletion of the regulatory region of the array or by mutations that inactivate the L and M genes. Most recent research concerns the molecular basis of complete achromatopsia, a rare disorder that involves the complete loss of all cone function. This is not caused by mutations in opsin genes, but in other genes that encode cone-specific proteins, e.g. channel proteins and transducin.

Computed tomographic images of soft materials are obtained using differential attenuation and transmission method with a tube source of X-rays, for samples like walnut, brew tooth and peaches in order to know the interior properties of the material at optimum energy in terms of attenuation coefficient. At optimum energy it is possible to calculate the three-dimensional representation of inner and outer surfaces of the object. The interior of the soft material is visualized using the novel soft ware in order to know the distribution of attenuation coefficient in terms of density. The results for walnut, brew tooth and peaches are presented as a set of images from the internal parts of the sample.

In the Human eye there are two types of image receptor cells cones and rods. Rods are helpful for seeing the image in low light or in the dark whereas the cones work for seeing the image in different colours. Both the receptors cells are found in retina of human eye. They contain three colour pigments Red (Large Bandwidth), Green (Medium Bandwidth) and Blue (Small Bandwidth) by which we are trichromats (tri =3 chromats =colour) and able to see any object in the world because of all objects are viewable by these colour hues. Mostly the colour blindness is the genetic mutation and not to be cured. It can also get place when there is a problem related to pigments in certain nerve cells (cone) of the eye or when there would be a trauma in mind or the chemical accident by which those receptor cells got affect. In the Human vision there are different stages which describe what type of colour vision deficiency the people have. Monochromacy (1%): Total colour blinded Dichromacy (10%): Partial colour blinded (i) red-green colour blindness (ii) blue-yellow colour blindness. Trichromacy: Normal colour vision. The Dichromacy, this type of colour blindness mostly people have. So correcting it, a new filter is developed in the image processing on the basis of Ishihara colour test. It works successfully as per tested it many time. In this filter adjusting, contrast stretching and inverting function are used for providing better result and it does. By applying this new filter the normal and as well colour vision deficient people easily recognise the objects whether they are of any of shape, number or alphabets.

Complete achromatopsia is a rare autosomal recessive disease associated with CNGA3, CNGB3, GNAT2 and PDE6C mutations. This retinal disorder is characterized by complete loss of color discrimination due to the absence or alteration of the cones function. The purpose of the present study was the clinical and the genetic characterization of achromatopsia in a large consanguineous Tunisian family. Ophthalmic evaluation included a full clinical examination, color vision testing and electroretinography. Linkage analysis using microsatellite markers flanking CNGA3, CNGB3, GNAT2 and PDE6C genes was performed. Mutations were screened by direct sequencing. A total of 12 individuals were diagnosed with congenital complete achromatopsia. They are members of six nuclear consanguineous families belonging to the same large consanguineous family. Linkage analysis revealed linkage to GNAT2. Mutational screening of GNAT2 revealed three intronic variations c.119-69G > C, c.161+66A > T and c.875 31G > C that co-segregated with a novel mutation p.R313X. An identical GNAT2 haplotype segregating with this mutation was identified, indicating a founder mutation. All patients were homozygous for the p.R313X mutation. This is the first report of the clinical and genetic investigation of complete achromatopsia in North Africa and the largest family with recessive achromatopsia involving GNAT2; thus, providing a unique opportunity for genotype-phenotype correlation for this extremely rare condition. Journal of Human Genetics (2011) 56, 22-28; doi:10.1038/jhg.2010.128; published online 25 November 2010

A patient from a large kindred with adrenoleukodystrophy showed profound disturbance of color ordering, color matching, increment thresholds, and luminosity. Except for color matching, his performance was similar to blue-cone "monochromacy," an X chromosome-linked recessive retinal dystrophy in which color vision is dichromatic, mediated by the visual pigments of rods and short-wave-sensitive cones. Color matching, however, indicated that an abnormal rudimentary visual pigment was also present. This may reflect the presence of a recombinant visual pigment protein or altered regulation of residual pigment genes, due to DNA changes--deletion of the long-wave pigment gene and reorganized sequences 5' to the pigment gene cluster--that segregate with the metabolic defect in this kindred.

Colour blindness is a genetic mutation that alters the colour vision of the subjects by decreasing the sensitivity to certain colour wavelengths, depending on the defect. There are many forms of colour blindness ranging from monochromacy (black-white) to the most common form, the “red-green” variation where reds or greens are weakened, the vibrant shades are easily seen and the dull shades are difficult to perceive. A filter was designed based on the Ishihara colour tests in order to correct the colour blind deficiencies. This was successful for seeing the hidden objects within the test plates but did not translate well for real world images. The filter was modified, removing the dullest/lightest shades and shifting all the shades to the darker vibrant shades. The original image was shown to colour blind and normal vision subjects with results varying among all the subjects. After the modified filter was applied to a natural image, the colour blind and normal vision subjects were all able to correctly identify the test colours.

The normal X-chromosome-linked color-vision gene array is composed of a single long-wave-sensitive (L-) pigment gene followed by one or more middle-wave-sensitive (M-) pigment genes. The expression of these genes to form L- or M-cones is controlled by the proximal promoter and by the locus control region. The high degree of homology between the L- and M-pigment genes predisposed them to unequal recombination, leading to gene deletion or the formation of L/M hybrid genes that explain the majority of the common red–green color-vision deficiencies. Hybrid genes encode a variety of L-like or M-like pigments. Analysis of the gene order in arrays of normal and deutan subjects indicates that only the two most proximal genes of the array contribute to the color-vision phenotype. This is supported by the observation that only the first two genes of the array are expressed in the human retina. The severity of the color-vision defect is roughly related to the difference in absorption maxima (λmax) between the photopigments encoded by the first two genes of the array. A single amino acid polymorphism (Ser180Ala) in the L pigment accounts for the subtle difference in normal color vision and influences the severity of red–green color-vision deficiency.Blue-cone monochromacy is a rare disorder that involves absence of L- and M-cone function. It is caused either by deletion of a critical region that regulates expression of the L/M gene array, or by mutations that inactivate the L- and M-pigment genes. Total color blindness is another rare disease that involves complete absence of all cone function. A number of mutants in the genes encoding the cone-specific α- and β-subunits of the cGMP-gated cation channel as well as in the α-subunit of transducin have been implicated in this disorder.

X-linked incomplete achromatopsia (XIA), also called blue-cone monochromacy (BCM), is a rare cone disorder that most commonly results either from one of two conditions.. The first condition is a deletion of the locus control region (LCR) which is a critical DNA element that lies upstream of the L and M photopigment gene array on the X-chromosome and is necessary for expression of the photopigment genes. The second condition is an inactivating point mutation within the coding sequence of the remaining photopigment gene in an array from which all but one gene has been deleted. Many previous studies have concluded that affected individuals either have only rods and S-cones (Blackwell & Blackwell, 1957, 1961; Daw & Enoch, 1973; Hess et al., 1989) or have rods, S-cones, and another cone type that contains the rod pigment (Pokorny et al., 1970; Alpern et al., 1971). However, Smith et al. (1983) described individuals with XIA who had residual L-cone function. Here we report results for a subject with XIA who appears to have residual M-cone function. Genetic analysis revealed that he had apparently normal genes for M-cone photopigment thus leaving open the possibility that he has a contribution to vision based on expression of these genes at a very low level.

Purpose: To describe the clinical phenotype, with emphasis on the electrophysiological findings, of patients with autosomal recessive rod monochromacy (RM) and defined mutations in the CNGA3/CNGB3 genes. Methods: RM patients from eight different families were included in the study. Their genotypes were determined by DNA sequencing and/or RFLP analysis of PCR-amplified genomic segments of the CNGA3 and CNGB3 genes. For comparison, we investigated one patient with blue-cone monochromacy (BCM). The clinical examination included best-corrected visual acuity, fundus examination, and full-field ERG. In six patients, the examination was complemented by multifocal ERG (MERG). Results: Three patients had three different CNG3A genotypes. Five patients were homozygous and one patient compound heterozygous for a 1-bp deletion (1148delC) in the CNGB3 gene. All patients examined presented with a visual acuity of 0.1-0.15. Small residual cone responses were noted in four young RM patients. The oldest patient examined (age 47 years) presented with pigmentary changes in the mid-peripheral retina and concentric constrictions of the visual fields. Conclusions: Patients with RM and mutations in the CNGA3/CNGB3 genes presented a similar clinical phenotype, confirming the essential function of both the alpha- and beta-subunits of the cGMP-gated cation channel in cone photoreceptor function. Small remaining cone responses in a few of the younger patients and mid-peripheral pigmentary degenerations in the oldest patient examined indicate that there could be some degree of progression in retinal dysfunction in at least some patients with RM. (Less)

Images of small plastic and food materials are obtained using a tomographic device based on image intensifier at optimum energy. The flux emitted by the x-ray tube is filtered using appropriate filters at the chosen optimum energy and reasonable monochromacy is achieved and the images are acceptably distinct.

Desert ants, Cataglyphis bicolor (Hymenoptera), navigate by using compass information provided by skylight polarization. In this study, electrophysiological recordings were made from polarization-sensitive interneurons (POL-neurons) in the optic lobe of Cataglyphis. The POL-neurons exhibit a characteristic polarization opponency. They receive monochromatic input from the UV receptors of the specialized dorsal rim area of the compound eye. Both polarization opponency and monochromacy are features also found in the POL-neurons of crickets (Orthoptera).

In this chapter we review the various genetic systems of color vision in primates, the origins and evolution of these systems, and the critical amino acid residues responsible for spectral sensitivity differences among primate photopigments (opsins). Much progress has been made on these topics in recent years, thanks to the application of molecular and biochemical techniques as well as the use of traditional approaches to color vision research. The progress has led to the revelation of some misconceptions and to several changes of view. We also discuss the interactions between lifestyle (nocturnal or diurnal) and color vision system, and the role of natural selection in the evolution of color vision in primates. Further, we review evidence of frequent gene conversion between X-linked opsin genes or alleles and describe how gene conversion has made it extremely difficult to infer the evolutionary history of the color vision systems in higher primates.

Many insects gain directional information from the polarization pattern of the sky. Polarization vision is mediated by the specialized ommatidia of the dorsal rim area of the compound eye, which contains highly polarization-sensitive photoreceptors. In crickets Gryllus campestris, polarized light information conveyed by the dorsal rim ommatidia was found to be processed by polarization-opponent interneurones (POL-neurones). In this study, a field-proof opto-electronic model of a POL-neurone was constructed that implements the physiological properties of cricket POL-neurones as measured by previous electrophysiological experiments in the laboratory. Using this model neurone, both the strength of the celestial polarization signal and the directional information available to POL-neurones were assessed under a variety of meteorological conditions. We show that the polarization signal as experienced by cricket POL-neurones is very robust, both because of the special filtering properties of these neurones (polarization-antagonism, spatial low-pass, monochromacy) and because of the relatively stable e-vector pattern of the sky.

The owl monkey (Aotus tridrgutus) is the only nocturnal monkey. The photopigments of Aotus and the relationship between these photopigments and visual discrimination were examined through (1) an analysis of the tlicker photometric electroretinogram (ERG), (2) psychophysical tests of visual sensitivity and color vision, and (3) a search for the presence of the photopigment gene necessary for the production of a short-wavelength sensitive (SWS) photopigment. Roth electrophysiological and behavioral measurements indicate that in addition to a rod photopigment the retina of this primate contains only one other photopigment type-a cone pigment having a spectral peak cu 543 nm. Earlier results that suggested these monkeys can make crude color discriminations are interpreted as probably resulting from the joint exploitation of signals from rods and cones. Although Aotus has no functional SWS photopigment, hybridization analysis shows that A&us has a pigment gene that is highly homologous to the human SWS photopigment gene. Aotus trivirgatus Cone photopigments Monkey color vision Monochromacy Photopigment genes Evolution of color vision

Procyonids are small, New World carnivores distributed among some 6 genera. Electroretinogram (ERG) flicker photometry was used to measure the spectra of the cone photopigments for members of two nocturnal species, the raccoon (Procyon lotor) and the kinkajou (Potos flavus), and a diurnal species, the coati (Nasua nasua). Each of the 3 has a class of cone photopigment with maximum sensitivity in the middle to long wavelengths. The spectral positioning of this cone is different for the three. Whereas the raccoon and kinkajou are monochromatic, the diurnal coati is a dichromat having an additional class of cone photopigment with peak sensitivity close to 433 nm.

The sections in this article are: 1 Scope and Organization 2 Physiological Explanation in Visual Science: Three Classes of Perceptual Phenomena 3 Visual Acuity 3.1 Overview 3.2 The Retinal Image 3.3 Spatial Modulation Detection 3.4 Neural Limits of Visual Acuity 4 Color Vision 4.1 Scotopic Spectral Sensitivity 4.2 Monochromacy 4.3 Dichromacy 4.4 Trichromacy 4.5 Color Blindness 4.6 Seeing Colors 5 Visual Adaptation 5.1 Overview 5.2 Experimental Paradigms 5.3 Identifying Neural Substrates 5.4 Single- Variable Theories 5.5 Concluding Comment 6 Note Added in Proof

SummaryThe different varieties of congenital dyschromatopsias are inherited following different modes. The dyschromatopsias of the protan and deutan type, as well as the atypical achromatopsia (blue mono-cone monochromacy), are sex-linked recessive, the tritanopia probably autosomal dominant and the typical achromatopsia surely autosomal recessive. The mode of transmission of the tritanomalia is still dubious.Concerning the localisation of the genes on the X chromosome, the bilocular theory for the deutan and protan genes is accepted at the present time. These genes form a cluster with the genes of hemophilia A and G6PD deficiency. It is possible that this cluster is situated on the short arm of the X chromosome or on the long arm near the centromeric region. The exact situation will be known very soon, when the interpretation of the results of the cellular hybridisation, which are still discordant, will be well established.

Two blue cone monochromats and four rod monochromats have been studied by increment threshold measurements applying the Stiles' principle. Some rudimentary colour discrimination was reported by the blue cone monochromats. One patient showed good discrimination between short- and middle-wavelength lights in matching experiments using the Nagel II apparatus. His neutral band in the spectrum was at lambda = 485--495 nm. Dichromatic vision could not be proved in the other patient. The blue cone monochromats also had good responding blue mechanism in the periphery. Indication of cone activity other than blue cones is found in both kinds of monochromats; these cones being probably of the rhodopsin-cone type (pi0 cones). The conclusions are drawn that the inhibitory effect of the pi0 cones upon the rod mechanism may account for the differences shown by our two blue cone monochromats as to visual acuity, nystagmus and photophobia. Likewise, their differences regarding dichromatic vision may be explained by an unequal number of pi0 cones in their retinas rather than by differences in their blue mechanisms.

In 1960, Alpern, Falls, and Lee reviewed the extensive literature on congenital monochromatism and then described the visual characteristics of five patients with typical total monochromacy.1At the time these data were presented, one of us (H.F.F.) made a plea for eyes of this kind which might become available for histological examination. One such case has now been described, but the eyes were only obtained 40 hours after death, at which time considerable autolysis of the photoreceptor layer had already occurred.2In the case to be presented, the eye was fixed immediately after surgical enucleation. While we had no psychophysical measurements on this observer at that time, we have since obtained good measurements of the color vision and dark adaptation characteristics of her remaining eye. The present paper will describe the results of both the histological examination and the psychophysical measurements. Report of Case A 69-year-old white woman