37 research outputs found

    Light pollution: The possible consequences of excessive illumination on retina

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    Light is the visible part of the electromagnetic radiation within a range of 380-780 nm; (400-700 on primates retina). In vertebrates, the retina is adapted to capturing light photons and transmitting this information to other structures in the central nervous system. In mammals, light acts directly on the retina to fulfill two important roles: (1) the visual function through rod and cone photoreceptor cells and (2) non-image forming tasks, such as the synchronization of circadian rhythms to a 24 h solar cycle, pineal melatonin suppression and pupil light reflexes. However, the excess of illumination may cause retinal degeneration or accelerate genetic retinal diseases. In the last century human society has increased its exposure to artificial illumination, producing changes in the Light/Dark cycle, as well as in light wavelengths and intensities. Although, the consequences of unnatural illumination or light pollution have been underestimated by modern society in its way of life, light pollution may have a strong impact on people's health. The effects of artificial light sources could have direct consequences on retinal health. Constant exposure to different wavelengths and intensities of light promoted by light pollution may produce retinal degeneration as a consequence of photoreceptor or retinal pigment epithelium cells death. In this review we summarize the different mechanisms of retinal damage related to the light exposure, which generates light pollution.Fil: Contin, Maria Ana. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - CĂłrdoba. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba. Universidad Nacional de CĂłrdoba. Facultad de Ciencias QuĂ­micas. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba; ArgentinaFil: Benedetto, MarĂ­a Mercedes. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - CĂłrdoba. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba. Universidad Nacional de CĂłrdoba. Facultad de Ciencias QuĂ­micas. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba; ArgentinaFil: Quinteros Quintana, MarĂ­a Luz. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - CĂłrdoba. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba. Universidad Nacional de CĂłrdoba. Facultad de Ciencias QuĂ­micas. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba; ArgentinaFil: Guido, Mario Eduardo. Consejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicas. Centro CientĂ­fico TecnolĂłgico Conicet - CĂłrdoba. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba. Universidad Nacional de CĂłrdoba. Facultad de Ciencias QuĂ­micas. Centro de Investigaciones en QuĂ­mica BiolĂłgica de CĂłrdoba; Argentin

    Quantitative modeling of the physiology of ascites in portal hypertension

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    Although the factors involved in cirrhotic ascites have been studied for a century, a number of observations are not understood, including the action of diuretics in the treatment of ascites and the ability of the plasma-ascitic albumin gradient to diagnose portal hypertension. This communication presents an explanation of ascites based solely on pathophysiological alterations within the peritoneal cavity. A quantitative model is described based on experimental vascular and intraperitoneal pressures, lymph flow, and peritoneal space compliance. The model's predictions accurately mimic clinical observations in ascites, including the magnitude and time course of changes observed following paracentesis or diuretic therapy
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