Imidazole-stabilized gold nanoparticles induce neuronal apoptosis: an in vitro and in vivo study.

Gold nanoparticles are increasingly being employed in innovative biological applications thanks to their advantages of material- and size-dependent physics and chemical interactions with the cellular systems. On the other hand, growing concern has emerged on the toxicity which would render gold-based nanoparticles harmful to cell cultures, animals, and humans. Emerging attention is focused on the interaction of gold nanoparticles with nervous system, especially regarding the ability to overcome the blood-brain barrier (BBB) which represents the major impediment to the delivery of therapeutics into the brain. We synthesized highly stable 2-mercapto-1-methylimidazole-stabilized gold-nanoparticles (AuNPs)-mmi to investigate their entry, accumulation, and toxicity in vitro (SH-SY5Y human neuroblastoma cells) and in vivo (brain of C57BL/6 mice) through optical and electron microscopy. After incubation in the cell culture medium at the lowest dose of 0.1 mg/mL the (AuNPs)-mmi nanoparticles were found compacted and recruited into endosome/lysosomes (1 h) before their fusion (2 h) and the onset of neuronal death by apoptosis (4 h) as proved by terminal-transferase-mediated dUTP nick end labeling assay and caspase-3 immunoreactivity. The ability of (AuNPs)-mmi to cross the BBB was assessed by injection in the caudal vein of C57BL/6 mice. Among different brain regions, the nanoparticles were found in the CaudatoPutamen area, mainly in the striatal neurons 4 h after injection. These neurons showed the typical hallmarks of apoptosis. Our findings provide, for the first time, the dynamic of 2-mercapto-1-methylimidazole nanogold uptake. The molecular mechanism which underlies the nanogold-driven apoptotic event is analyzed and discussed in order to take into account when designing nanomaterials to interface with biological structures.

Technical improvements in photorefractive keratectomy for correction of high myopia.

PURPOSE: To evaluate the effects of hardware and software improvements in photorefractive keratectomy (PRK) for the treatment of highly myopic eyes. METHODS: A retrospective study was carried out in 554 patients (582 eyes) with myopia between -7.00 and -17.00 D (mean -11.20 +/- 3.60 D) who had undergone PRK using the Aesculap Meditec laser. Group 1 with a 5-mm-diameter single ablation zone; Group 2 with a 5-mm-diameter single zone surrounded by a 2-mm tapered transitional zone; Group 3 and Group 4, same as Group 2 but with the laser upgraded with a smoke aspiration control system (Group 3), and with a computer-controlled fluence (Group 4). RESULTS: In Group 1 at 2 years after PRK (50 eyes), 10 eyes (20%) were within +/-1.00 D of attempted correction and 13 eyes (26%) were within +/-2.00 D. In Group 2 at 2 years (118 eyes), 42 eyes (36%) were within +/-1.00 D of attempted correction and 65 eyes (55%) were within +/-2.00 D. In Group 3 at 2 years (43 eyes), 18 eyes (42%) were within +/-1.00 D of attempted correction and 28 eyes (65%) were within +/-2.00 D. In Group 4 at 2 years (47 eyes), 25 eyes (53%) were within +/-1.00 D of attempted correction and 29 eyes (62%) were within +/-2.00 D. CONCLUSIONS: Software and hardware improvements facilitated PRK correction of high myopia with reasonable predictability, especially if a tapered transition zone was used. At 12 and 24-month follow-up, only the use of a tapered transition zone was associated with a statistically significant improvement in predictability.

[Neuroendocrine features of prostatic tumors: state of the art]. / Aspetti neuroendocrini del tumore della prostata: stato dell'arte.

Neuroendocrine (NE) differentiation in prostate cancer has received much attention recently because it has been found to be associated with androgen independence and shortened patient survival in some studies. The present review focuses on morphogenics origins of NE cells, growth properties and the androgen receptor status and relationship between NE-secreted products and regulation of angiogenesis and apoptosis.