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Objective: The aim of the analysis was to measure the pressure-flow urodynamic changes following GreenLight(™) laser vaporization of the prostate based on pressure-flow studies., Material and Methods: Sixty-two patients suffering from voiding dysfunction due to lower urinary tract symptoms underwent potassium titanyl phosphate (KTP) laser vaporization. A pressure-flow study was performed at baseline and at 3 months postoperatively. Symptoms and quality of life (QoL) were assessed using the International Prostate Symptom Score (IPSS) and questions regarding sexuality were assessed using the International Index of Erectile Function (IIEF)., Results: IPSS and QoL scores changed from 24 and 5 at baseline to 6 and 2 at 3 months, respectively. The initial median prostate volume was 35 ml (range 16-60 ml), the median maximum uroflow (Q max) was 9.2 ml/s (4-14.9 ml/s) and the median postvoiding residual urine was 80 ml (20-400 ml) (95% confidence interval 89.14, 135.44). The median IPSS and QoL score were significantly improved (p < 0.001). There was a significant decrease in median detrusor pressure at Q max from 83.1 to 40.45 cmH2O, and the median obstruction grade according to Schäfer's classification was also decreased significantly, from 4 to 1 postoperatively., Conclusion: This study showed that significant deobstruction can be demonstrated using a pressure-flow study at 3 months postoperatively.

Objective: The angiogenic phenotype is an effect of a net balance of angiogenic and anti-angiogenic factors. Endostatin is one of a group of recently described matrix-derived inhibitors of tumour angiogenesis that have acquired increasing significance for tumour treatment. Endostatin's anti-angiogenic mechanism and the causes of its heterogenic influence on various tissue types have not yet been defined., Methods: We investigated the variations in endostatin's binding behaviour to vessels in benign prostatic hyperplasia (BPH) compared to endostatin binding to vessels in normal prostate tissue. Biotinylated endostatin was used and was detected using Extravidin CY3., Results: In BPH 89.12% +/- 10.72% of vessels showed endostatin binding. This was significantly more than observed for vessels in normal prostate tissue (1.66% +/- 1.66%)., Conclusion: The strongly proliferative tissue of BPH may be a growth-limited cause of significantly more endostatin binding sites. The investigation indicates endostatin as a possible new target for BPH treatment.

To define the anti-angiogenic mechanism and causes of the heterogeneous influence of endostatin, one of a group of matrix-derived inhibitors of tumour angiogenesis of increasing significance in tumour treatment, on various tissue types.Variations in the binding behaviour of endostatin with vessels were assessed in different tumours (bladder, prostate and kidney) and compared with benign tissue vessels. Biotinylated endostatin was used and detected using extravidin CY3 and extravidin-gold immunolabelling.There were significant differences in the number of vessels showing endostatin binding among benign and malignant bladder, prostate and kidney tissues. While there was distinct endostatin binding on a mean (sd) of 94.2 (3.0)% bladder and 73.8 (19.5)% prostate tumour vessels, there was less binding, at 11.32 (3.9)%, on kidney tumour vessels. There was less binding to vessels of benign bladder, prostate and kidney tissue, at 2.0 (1.5), 1.7 (1.7) and 1.5 (1.7)%, respectively. At the ultrastructural level, different binding sites were detected both inside and outside the endothelial cells.Endostatin binds more to all tumour tissues than to benign tissue, but the degree of binding in malignant kidney tissue was significantly less than that in malignant prostate and bladder tissues. These divergent vascular endostatin-binding patterns could be responsible for a tumour type-dependent anti-angiogenic effect attributable to endostatin. Such selective behaviour would have therapeutic consequences for future anti-angiogenic therapy, in which different kinds of tumours could be further classified into those responding to endostatin or not. [ABSTRACT FROM AUTHOR]