Clinical Study on the Application of Preserved Urethral Mucosa at the Prostatic Apex in Transurethral Plasmakinetic Resection of the Prostate.

Objective: To explore the differences in the clinical efficacy, complications, and safety of transurethral plasmakinetic resection of the prostate (PKRP) by the conventional approach versus the approach preserving the urethral mucosa at the prostatic apex in the treatment of benign prostatic hyperplasia (BPH).

Methods: A total of 90 patients with PKRP admitted to the First Hospital of Qinhuangdao from December 2018 to March 2021 were selected and divided into a control group (conventional PKRP,  = 45) and an observation group (PKRP with preserved urethral mucosa at the prostatic apex,  = 45). The clinical efficacy, safety, and sexual function of the groups were evaluated using the patients' International Prostate Symptom Score (IPSS), quality of life (QoL), prostate volume, maximum flow rate (Qmax), post-void residual (PVR), blood loss, surgical resection efficiency, and surgical complication data.

Comparison of the Transurethral Resection of the Prostate by Traditional Versus Preserved Urethral Mucosa of the Prostatic Apex.

Benign prostatic hyperplasia (BPH) is a common disease in elderly men. Transurethral resection of the prostate (TURP) is still the standard treatment for BPH. However, postoperative urinary incontinence (UI) is still one of the complications.

Heat shock protein 70 binds caspase-activated DNase and enhances its activity in TCR-stimulated T cells.

DNA fragmentation is a hallmark of cells undergoing apoptosis and is mediated mainly by the caspase-activated DNase (CAD or DNA-fragmentation factor 40 [DFF40]), which is activated when released from its inhibitor protein (ICAD or DFF45) upon apoptosis signals. Here we analyzed the effect of heat shock protein 70 (Hsp70) on CAD activity in T-cell receptor (TCR)-induced apoptosis using a T-cell line (TAg-Jurkat). Overexpression of Hsp70 significantly augmented the apoptotic cell death as well as DNA fragmentation in CD3/CD28- or staurosporine-stimulated cells.