No abstract

Background Although there are different treatments for benign prostate hyperplasia, their efficacy and safety differ. We are currently exploring a new minimally invasive interventional therapy for benign prostatic hyperplasia (BPH). Purpose To determine the feasibility, effectiveness, and safety of ultrasound-guided transperineal laser ablation (US-TPLA) for the treatment of BPH. Material and Methods Twenty patients with BPH (mean age = 73.9 ± 9.2 years) who underwent US-TPLA from June 2018 to January 2020 with a subsequent six-month follow-up were retrospectively reviewed. After local anesthesia, a 21-G trocar was inserted into the prostate tissue under ultrasound monitoring, followed by 1064 nm diode laser irradiation. Changes in international prostate symptom score (IPSS), quality of life (QoL), maximum urinary flow rate (Qmax), postvoid residual (PVR), prostate volume, and complications were evaluated six months after surgery. Results All patients underwent the operation successfully without serious complications. After six months, the average IPSS improved from 22.7 ± 5.3 to 9.1 ± 3.2 ( P < 0.001), the QoL improved from 4.9 ± 1.7 to 2.3 ± 1.3 ( P < 0.001), the Qmax improved from 8.5 ± 3.0 to 15.2 ± 4.8 mL/s ( P < 0.001), the PVR increased from 78.7 ± 58.8 to 30.3 ± 34.2 ( P < 0.05), and the mean prostate volume ranged from 70.8 ± 23.8 to 54.7 ± 20.9 mL ( P < 0.05). Conclusion US-TPLA is safe and feasible for the treatment of BPH. An evaluation at the six-month follow-up is effective.

Diabetes is an inflammatory disease. Inflammation plays an important role in islet functions. However, the exact mechanisms by which inflammation affects islet functions remain unclear. In this study, we investigated the regulatory effects of miR-30a on inflammation and islet functions. The results indicate that miR-30a serves as an inflammation-resolving buffer factor by targeting interleukin 1a (IL-1α) in immune cells and in islet cells, which might play an important role in inflammation homeostasis. miR-30a ameliorates islet functions in an inflammatory micro-environment by targeting the IL-1α/nuclear factor kappa B (NFKB) p65 subunit (p65)/p62 (SQSTM1)/insulin axis, which can be developed into a novel antidiabetic approach. miR-30a serves as a promising inflammation-response biomarker in inflammatory diseases and is possibly activated by the toll-like receptor 4 (TLR4)/IL-1α/NFKB pathways. However, the exact molecular mechanisms by which miR-30a regulates inflammation and islet functions as well as the potential applications in transitional medicine require further elucidation.

No abstract