Fengbo Zhang

Thulium laser versus holmium laser transurethral enucleation of the prostate: 18-month follow-up data of a single center.

OBJECTIVE To compare the clinical outcomes between thulium laser transurethral enucleation of the prostate (ThuLEP) (70 W) and holmium laser transurethral enucleation of the prostate (HoLEP) (90 W) in a prospective randomized trial with 18 months of follow-up. Both ThuLEP and HoLEP effectively relieve the obstructive symptoms due to benign prostatic hyperplasia (BPH). METHODS A total of 133 consecutive patients with BPH were randomized to either ThuLEP (n = 71) or HoLEP (n = 62). An energy setting of 70 W and 90 W was used for the thulium and holmium laser in the enucleation procedure, respectively. The mushroom technique was used to fragment the enucleated lobes with the resection loop. The preoperative and postoperative parameters were compared. RESULTS ThuLEP required a longer operation time (72.4 vs 61.5 minutes, P = .034) but resulted in less blood loss than HoLEP (130.0 vs 166.6 mL, P = .045). The catheterization time was comparable. At 18 months, the lower urinary tract symptom indexes were improved significantly in both groups compared with the baseline values. The International Prostate Symptom Score decreased to 5.2 in the ThuLEP group and 6.2 in the HoLEP group. The quality of life score and peak urinary flow rate were similar between the 2 groups (1.3 vs 1.2 and 23.4 vs 24.2 mL/s) and the postvoid residual urine volume decreased by 82.50% and 81.73% in the ThuLEP and HoLEP groups, respectively. The mean prostate-specific antigen decrease after HoLEP and ThuLEP was 30.43% and 43.36%, respectively. No urethral or bladder neck stricture were found in either group. CONCLUSION Both ThuLEP (70 W) and HoLEP (90 W) relieve lower urinary tract symptoms equally with high efficacy and safety. ThuLEP was statistically superior to HoLEP in blood loss and inferior to HoLEP in operation time, although the differences were clinically negligible. The mushroom technique could be adequate, without an additional mechanical tissue morcellator.

Interleukin-22 suppresses the growth of A498 renal cell carcinoma cells via regulation of STAT1 pathway.

Background Renal cell carcinoma (RCC) is one of the most common kidney cancers and is highly resistant to chemotherapy. Accumulating evidence suggests that interleukin-22 (IL-22) may mediate host defense against varietal pathogens as a proinflammatory and anti-inflammatory cytokine. The purpose of this study is to assess the inhibitory effects of IL-22 on human RCC cell line A498 and to investigate the possible mechanisms underlying the anti-tumor effects of this cytokine. Methodology A498 cells, a RCC cell line, were used to assess the inhibitory growth effects of IL-22 using the MTT assay and flow cytometric analysis in vitro. BALB/C nude mice bearing A498 cell xenografts were used to examine the antitumor efficacy of IL-22 in vivo. Western blotting assay was performed to detect the regulation of the intracellular signaling pathway of IL-22. Principal Findings We found that IL-22 suppressed the growth of A498 cells in a dose-dependent manner and inhibited the growth of A498 xenografts. We also observed that IL-22 produced a dose-dependent inhibitory effect on A498 cells that involved the induction of G2/M cell cycle arrest without cell apoptosis. Moreover, we showed that the phosphorylation of STAT1 was increased and the phosphorylation of ERK1/2 was attenuated in A498 cells exposed to IL-22. The growth inhibition of A498 cells was partially revised after IL-22 treatment as the expression of STAT1 was knocked down. And inflammatory cytokines, interferon-α and tumor necrosis factor-α (TNF-α) were barely involved in the suppression of A498 cell xenografts treated with IL-22. Conclusions IL-22 dose-dependently suppresses RCC cell line A498 cells in vitro and induces growth inhibition of A498 cell-bearing mouse xenografts. These results suggest that the anti-RCC effects of IL-22 are at least partially mediated through regulation of STAT1 signaling pathways and G2/M cell cycle arrest, rather than by inducing apoptosis and inflammatory cytokines.

Interferon-α Induces G1 Cell-Cycle Arrest in Renal Cell Carcinoma Cells Via Activation of Jak-Stat Signaling

The purpose of this study was to clarify the mechanism of IFN-α resistance in RCC. The effects of IFN-α on induction of apoptosis and cell-cycle arrest were analyzed by flow cytometric analysis. Jak-Stat pathway components induced by IFN-α was evaluated using Western blotting. The results suggested that IFN-α caused growth inhibition of RCC cell lines via arrest in the G1 phase without inducing apoptosis. The resistance of RCC to IFN-α was associated with the low expression of Stat1. This study indicated that the Jak-Stat pathway should be considered a primary target for improving the response of RCC to IFN-α treatment.

AB084. Docetaxel therapy for hormone-sensitive prostate cancer—single center result

Background Androgen-deprivation therapy (ADT) has been the treatment for metastatic prostate cancer for more 75 years. We assessed whether concomitant treatment with ADT added to docetaxel would result in patients newly-diagnosed metastatic hormone-sensitive prostate cancer for longer overall survival. Methods and Materials Since August 2014, 14 patients with metastatic, hormone-sensitive prostate cancer received ADT plus docetaxel (at a dose of 75 mg per square meter of body-surface area every 3 weeks for six cycles). The primary objective was to test the hypothesis that the median overall survival would be more longer among patients receiving docetaxel added to ADT early during therapy. Results After six cycles of docetaxel added to ADT therapy, four patients PSA level reduced less than 0.2 ng/mL and observe the withdrawal; one patient PSA rise to 4 ng/mL received ADT treatment again; one patient had grade 3 blood toxicity. None grade 4 blood toxicity occurred. Conclusions Patients with hormone-sensitive metastatic prostate cancer overall survival prolonged significantly after ADT + D therapy; 6-cycle chemotherapy were recommended; the benefit for docetaxel therapy was found to be more apparent in the high-volume metastatic group.

The biomechanical alterations in the CD14+ monocytes of patients with living donor renal transplantation

Living-donor renal transplantation is an ideal treatment for patients with end stage renal disease because it affords earlier transplantation and better graft for long term survival. CD14+ monocytes are the predominant inflammatory cells in renal allograft intimal arteritis. The biomechanical alterations in CD14+ monocytes would affect the function of graft. The aim of the present study was to explore the changes in the biorheological properties of CD14+ monocytes before and after the living donor renal transplantation. We found that the viscoelastic properties of CD14+ monocytes were greatly decreased after renal transplantation. Confocal microscopy showed that the F-actin content was increased when the oral immunosuppressive agents started. We also found that two cytoskeletal regulatory proteins, cofilin1 and profilin1, changed. Our results suggest that the immunosuppressive agents could significantly change the biorheological characteristics of the CD14+ mononuclear cells and the biomechanical changes may greatly affects their function, which would play a critical role to gain longer immune-tolerance stage.