Autophagy has been shown to be activated in neuronal cells in response to injury and suggested to have a cell-protective role in neurodegenerative diseases. In this study, we investigated the activation of autophagy in retinal ganglion cells (RGCs) following optic nerve transection (ONT) and evaluated its effect on RGC survival. Expression of several autophagy-related genes, including Atg5, Atg7, and Atg12, and autophagy markers microtubule-associated protein 1 light chain 3-II (LC3-II) and beclin-1 were analyzed at the transcriptional or protein level 1, 3, and 7 days after ONT. Transcription of the Atg5, Atg7, and Atg12 genes was upregulated 1.5-to 1.8-fold in the retina 3 days after ONT compared with that in the controls. Expression of Atg12 mRNA was increased 1.6-fold 1 day after ONT. Seven days after ONT, expression of Atg5, Atg7, and Atg12 mRNA was comparable to that in the untreated retinas. Western blot analysis of proteins isolated from RGCs showed 1.6-, 2.7-, and 1.7-fold increases in LC3-II level 1, 3, and 7 days after ONT, respectively, compared with those in the controls. Expression of beclin-1 was 1.7-fold higher 1 day after RGCs were axotomized, but 3 and 7 days after ONT it was comparable to that of the control. Inhibition of autophagy with bafilomycin A1, 3-methyladenine, and Wortmannin in RGC-5 cells under serum-deprived conditions decreased cell viability by approximately 40%. These results suggest possible activation of autophagy in RGCs after optic nerve transection and demonstrate its protective role in RGC-5 cells maintained under conditions of serum deprivation. V V C 2008 Wiley-Liss, Inc.

We investigated the neuroprotective effect of thioredoxin 1 (Trx1) and thioredoxin 2 (Trx2) which play critical roles in the regulation of oxidative stress on retinal ganglion cells (RGCs) in a rat glaucoma model. Expression of Trx1 and Trx2 and Trx-interacting protein (Txnip) was observed in the RGC layer (GCL), nerve fiber layer and inner nuclear layer. Txnip-, Trx1-and Trx2-expressing cells in the GCL were primarily colocalized with RGCs. The increased Txnip protein level was observed 2 and 5 weeks after glaucoma induction. Trx1 level decreased 2 weeks after glaucoma induction and more prominently after 5 weeks. No change in Trx2 levels was detected. The effects of Trx1 and Trx2 overexpression on RGC survival were evaluated 5 weeks after glaucoma induction. In nontransfected and EGFP-transfected (used as a negative control) retinas, RGC loss was approximately 27% compared with control. The loss of RGCs in Trx1-and Trx2-transfected retinas was approximately 15 and 17%, respectively. Thus, Trx1 and Trx2 preserved 45 and 37% of cells, respectively that were destined to die in glaucomatous retinas. The results of this study provide evidence for the involvement of oxidative stress in RGC degeneration in experimental glaucoma and point to potential strategies to reduce its impact.

Virtual cystoscopy of the contrast material-filled bladder is useful for the evaluation of the bladder in patients with gross hematuria.

Nerve compression syndromes commonly involve the nerves in the upper extremity. High-resolution ultrasonography (US) can satisfactorily assess these nerves and may detect the morphological changes of the nerves. US can also reveal the causes of nerve compression when structural abnormalities or space-occupying lesions are present. The most common US finding of compression neuropathy is nerve swelling proximal to the compression site. This article reviews the normal anatomic location and US appearances of the median, ulnar, and radial nerves. Common nerve compression syndromes in the upper extremity and their US findings are also reviewed.