[Trabeculotomy Combined with Cataract Surgery in Glaucoma: Outcome in a Rural Setting]. / Trabekulotomie kombiniert mit Phakoemulsifikation als operative Glaukomtherapie: Ergebnisse im ländlichen Versorgungsbereich.

Purpose: Intensive postoperative care is essential for the outcome of trabeculectomy. However, in a rural setting, repeated visits to the operating theatre are often not requested or possible. The objective of this study was to examine the outcome of trabeculotomy combined with cataract surgery in patients with glaucoma. Patients and Methods: 142 patients with glaucoma and cataract were included in a retrospective clinical study. All patients were operated on from November 2005 to December 2008 by a single surgeon and with a minimum follow-up of 2 months. Intraocular pressure (IOP), number of antiglaucomatous medications and surgical success rate were assessed at 2 months and at the longest follow-up (at least 1 year). Results: IOP was significantly reduced from 24.1 ± 8.3 mmHg preoperatively to 14.9 ± 3.3 mmHg at 2 months (p < 0.0001) and to 15.1 ± 3 mmHg at the longest follow-up (3.71 ± 1.5 years). The number of IOP-lowering medications was lowered from 1.35 ± 1 preoperatively to 0.73 ± 1 at the longest follow-up. Complete surgical success (no IOP-lowering medications, longest follow-up) was achieved in 51.3 % (IOP < 22 mmHg) and 47.5 % (IOP < 19 mmHg) of patients, respectively. Conclusions: Trabeculotomy combined with cataract surgery is a safe and effective surgical option to treat combined cataract and glaucoma without the need of intensified postoperative treatment.

Comprehensive identification of genes driven by ERV9-LTRs reveals TNFRSF10B as a re-activatable mediator of testicular cancer cell death.

The long terminal repeat (LTR) of human endogenous retrovirus type 9 (ERV9) acts as a germline-specific promoter that induces the expression of a proapoptotic isoform of the tumor suppressor homologue p63, GTAp63, in male germline cells. Testicular cancer cells silence this promoter, but inhibitors of histone deacetylases (HDACs) restore GTAp63 expression and give rise to apoptosis. We show here that numerous additional transcripts throughout the genome are driven by related ERV9-LTRs. 3' Rapid amplification of cDNA ends (3'RACE) was combined with next-generation sequencing to establish a large set of such mRNAs. HDAC inhibitors induce these ERV9-LTR-driven genes but not the LTRs from other ERVs. In particular, a transcript encoding the death receptor DR5 originates from an ERV9-LTR inserted upstream of the protein coding regions of the TNFRSF10B gene, and it shows an expression pattern similar to GTAp63. When treating testicular cancer cells with HDAC inhibitors as well as the death ligand TNF-related apoptosis-inducing ligand (TRAIL), rapid cell death was observed, which depended on TNFRSF10B expression. HDAC inhibitors also cooperate with cisplatin (cDDP) to promote apoptosis in testicular cancer cells. ERV9-LTRs not only drive a large set of human transcripts, but a subset of them acts in a proapoptotic manner. We propose that this avoids the survival of damaged germ cells. HDAC inhibition represents a strategy of restoring the expression of a class of ERV9-LTR-mediated genes in testicular cancer cells, thereby re-enabling tumor suppression.