Mice of the DBA/2J strain spontaneously develop complex ocular abnormalities, including glaucomatous loss of retinal ganglion cells (RGC). In the present study ultrastructural features of retinal neurodegeneration in DBA/2J mice of different age (3, 6, 8 and 11 months) are described. By 3 months, RGC apoptosis characterized by electron-dense karioplasm and cytoplasm of ganglion cells was observed. The occurrence of apoptotic ganglion cells peaked at the age of 6 months. Past this age, necrosis characterized by swelling and electron-rare cytoplasm appeared to be the prevailing form of cell death. Müller glia activation increased with age, but there were no signs of leukocyte infiltration. At 8 and 11 months, signs of neoangiogenesis were found both at the ultrastructural level and in clinical examinations. In these older animals myelin-like bodies, most probably representing the intracellular aggregates of phospholipids in irreversibly injured cells, were also seen. Photoreceptor cells were not affected at any age. Our observations suggest that retinal degeneration in the DBA/2J mice does not involve recruitment of blood-borne inflammatory/phagocytosing cells, and that apoptosis is gradually replaced by necrosis as the predominant pathway of RGC death. Retinal degeneration in 3- to 11-month-old DBA/2J mice partially resembles human pigment dispersion syndrome and pigmentary glaucoma with characteristic anterior segment changes and elevation of intraocular pressure. However, neovasculogenesis and myelin-like bodies are observed during aging. Therefore, the DBA/2J model requires judicious interpretation as a glaucoma model.

Trauma is an important cause of ocular morbidity in Greece. Risk factors include young age, male gender, Albanian ethnic background, and workplace. General safety precautions and behavior modification are indicated.

The results of this study indicated that functional alterations in the retina develop rapidly after the onset of diabetes. Analysis of each electroretinogram component may be useful in further investigating the development mechanisms of diabetic retinopathy.

It is known that the eye's scotopic photodetectors, rhodopsin molecules and their associated phototransduction mechanism leading to light perception, are efficient single photon counters. We here use the photon counting principles of human rod vision to propose a secure quantum biometric identification based on the quantum-statistical properties of retinal photon detection. The photon path along the human eye until its detection by rod cells is modeled as a filter having a specific transmission coefficient. Precisely determining its value from the photodetection statistics registered by the conscious observer is a quantum parameter estimation problem that leads to a quantum secure identification method. The probabilities for false positive and false negative identification of this biometric technique can readily approach 10 −10 and 10 −4 , respectively. The security of the biometric method can be further quantified by the physics of quantum measurements. An impostor must be able to perform quantum thermometry and quantum magnetometry with energy resolution better than 10 −9 , in order to foil the device by non-invasively monitoring the biometric activity of a user.