Activation of Autophagy in a Rat Model of Retinal Ischemia following High Intraocular Pressure

Acute primary open angle glaucoma is an optic neuropathy characterized by the elevation of intraocular pressure, which causes retinal ischemia and neuronal death. Rat ischemia/reperfusion enhances endocytosis of both horseradish peroxidase (HRP) or fluorescent dextran into ganglion cell layer (GCL) neurons 24 h after the insult. We investigated the activation of autophagy in GCL-neurons following ischemia/reperfusion, using acid phosphatase (AP) histochemistry and immunofluorescence against LC3 and LAMP1. Retinal I/R lead to the appearance of AP-positive granules and LAMP1-positive vesicles 12 and 24 h after the insult, and LC3 labelling at 24 h, and induced a consistent retinal neuron death. At 48 h the retina was negative for autophagic markers. In addition, Western Blot analysis revealed an increase of LC3 levels after damage: the increase in the conjugated, LC3-II isoform is suggestive of autophagic activity. Inhibition of autophagy by 3-methyladenine partially prevented death of neurons and reduces apoptotic markers, 24 h post-lesion. The number of neurons in the GCL decreased significantly following I/R (I/R 12.21±1.13 vs controls 19.23±1.12 cells/500 µm); this decrease was partially prevented by 3-methyladenine (17.08±1.42 cells/500 µm), which potently inhibits maturation of autophagosomes. Treatment also prevented the increase in glial fibrillary acid protein immunoreactivity elicited by I/R. Therefore, targeting autophagy could represent a novel and promising treatment for glaucoma and retinal ischemia

Advanced THz laser performance of shallow donors in axially stressed silicon crystal

Terahertz stimulated emission (4â��6 THz) from optically excited group-V donors (phosphor P, antimony Sb, arsenic As, bismuth Bi) in silicon crystal under compressive force has been studied. Measurements evidence that compressive force of 1â��1.5 kbar for P, Sb and of 2â��3 kbar for As, Bi applied along {100} crystallographic orientations results in the enhancement of the laser gain and enlarges the emission efficiency. At that laser threshold intensity can be decreased by two orders of magnitude. For As and Bi donors it is accompanied by the laser line switching while the 2p0 state turns out to be the upper laser state instead of the 2p�± one. The effect of the uniaxial stress on donor lasing originates from conduction band valley shift which split donor states changing their eigen-values and eigen-functions. According to the calculations of phonon-assisted relaxation rates appropriate donor modification increases the lifetime and makes pump efficiency of the upper laser states better

Influence of uniaxial stress on phonon-assisted relaxation in bismuth-doped silicon

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