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      Lighting and discomfort in the classroom

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      Journal of Environmental Psychology
      Elsevier BV

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          Photochemical damage of the retina.

          Visual perception occurs when radiation with a wavelength between 400 and 760 nm reaches the retina. The retina has evolved to capture photons efficiently and initiate visual transduction. The retina, however, is vulnerable to damage by light, a vulnerability that has long been recognized. Photochemical damage has been widely studied, because it can cause retinal damage within the intensity range of natural light. Photochemical lesions are primarily located in the outer layers at the central region of the retina. Two classes of photochemical damage have been recognized: Class I damage, which is characterized by the rhodopsin action spectrum, is believed to be mediated by visual pigments, with the primary lesions located in the photoreceptors; whereas Class II damage is generally confined to the retinal pigment epithelium. The action spectrum peaks in the short wavelength region, providing the basis for the concept of blue light hazard. Several factors can modify the susceptibility of the retina to photochemical damage. Photochemical mechanisms, in particular mechanisms that arise from illumination with blue light, are responsible for solar retinitis and for iatrogenic retinal insult from ophthalmological instruments. Further, blue light may play a role in the pathogenesis of age-related macular degeneration. Laboratory studies have suggested that photochemical damage includes oxidative events. Retinal cells die by apoptosis in response to photic injury, and the process of cell death is operated by diverse damaging mechanisms. Modern molecular biology techniques help to study in-depth the basic mechanism of photochemical damage of the retina and to develop strategies of neuroprotection.
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            Photic- and pattern-induced seizures: a review for the Epilepsy Foundation of America Working Group.

            This report summarizes background material presented to a consensus conference on visually provoked seizures, convened by the Epilepsy Foundation of America. A comprehensive review of literature was performed. Photosensitivity, an abnormal EEG response to light or pattern stimulation, occurs in approximately 0.3-3% of the population. The estimated prevalence of seizures from light stimuli is approximately 1 per 10,000, or 1 per 4,000 individuals age 5-24 years. People with epilepsy have a 2-14% chance of having seizures precipitated by light or pattern. In the Pokemon cartoon incident in Japan, 685 children visited a hospital in reaction to red-blue flashes on broadcast television (TV). Only 24% who had a seizure during the cartoon had previously experienced a seizure. Photic or pattern stimulation can provoke seizures in predisposed individuals, but such stimulation is not known to increase the chance of subsequent epilepsy. Intensities of 0.2-1.5 million candlepower are in the range to trigger seizures. Frequencies of 15-25 Hz are most provocative, but the range is 1-65 Hz. Light-dark borders can induce pattern-sensitive seizures, and red color also is a factor. Seizures can be provoked by certain TV shows, movie screen images, video games, natural stimuli (e.g, sun on water), public displays, and many other sources. Recommendations on reducing risk of seizures have been developed by agencies in the United Kingdom, Japan, and the International Telecommunications Union, affiliated with the United Nations. The Epilepsy Foundation of America has developed a consensus of medical experts and scientists on this subject, reported in an accompanying work.
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              Occupant preferences and satisfaction with the luminous environment and control systems in daylit offices: a literature review

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                Author and article information

                Journal
                Journal of Environmental Psychology
                Journal of Environmental Psychology
                Elsevier BV
                02724944
                March 2009
                March 2009
                : 29
                : 1
                : 63-75
                Article
                10.1016/j.jenvp.2008.11.007
                ab348e66-0993-44aa-8fa0-51810a5a92aa
                © 2009

                http://www.elsevier.com/tdm/userlicense/1.0/

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