Temperature changes of renal calyx during high-power flexible ureteroscopic Moses holmium laser lithotripsy: a case analysis study.

PURPOSE: The risk of thermal damage increases with the introduction of high-power lasers during holmium laser lithotripsy. This study aimed to quantitatively evaluate the temperature change of renal calyx in the human body and the 3D printed model during high-power flexible ureteroscopic holmium laser lithotripsy and map out the temperature curve. METHODS: The temperature was continuously measured by a medical temperature sensor secured to a flexible ureteroscope. Between December 2021 and December 2022, willing patients with kidney stones undergoing flexible ureteroscopic holmium laser lithotripsy were enrolled. High frequency and high-power settings (24 W, 80 Hz/0.3 J and 32 W, 80 Hz/0.4 J) were performed for each patient with room temperature (25 °C) irrigation. In the 3D printed model, we studied more holmium laser settings (24 W, 80 Hz/0.3 J, 32 W, 80 Hz/0.4 J and 40 W, 80 Hz/0.4 J) with warmed (37 °C) and room temperature (25 °C) irrigation. RESULTS: Twenty-two patients were enrolled in our study. With 30 ml/min or 60 ml/min irrigation, the local temperature of the renal calyx did not reach 43 °C in any patient under 25 °C irrigation after 60 s laser activation. There were similar temperature changes in the 3D printed model with the human body under the irrigation of 25 °C. Under the irrigation of 37 °C, the temperature rise slowed down, but the temperature in the renal calyces was close to or even exceeded the 43 °C at the setting of 32 W, 30 ml/min and 40 W, 30 ml/min after continuing laser activation. CONCLUSION: In the irrigation of 60 ml/min, the temperature in the renal calyces can still be maintained within a safe range after continuous activation of a holmium laser up to 40 W. However, continuous activation of 32 W or higher power holmium laser in the renal calyces for more than 60 s in the limited irrigation of 30 ml/min can cause excessive local temperature, in such situation room temperature perfusion at 25 ℃ may be a relatively safer option.

Exosomal circKDM4A Induces CUL4B to Promote Prostate Cancer Cell Malignancy in a miR-338-3p-Dependent Manner.

Circular RNA lysine demethylase 4A (circKDM4A) is also named circ_0012098 and its abnormal expression has been confirmed in serum exosomes of prostate cancer (PC) patients. However, whether PC progression involves the exosomal circ_0012098 remains unknown. RNA expression of circKDM4A, microRNA-338-3p (miR-338-3p) and cullin 4B (CUL4B) was detected by quantitative real-time polymerase chain reaction. Protein expression was checked by Western blot. The positive expression rate of nuclear proliferation marker (ki-67) was analyzed by immunohistochemistry assay. Dual-luciferase reporter assay and RNA immunoprecipitation assay were used to identify the interaction between miR-338-3p and circKDM4A or CUL4B. Mouse model assay was performed to determine the effect of exosomal circKDM4A on tumorigenesis in vivo. CircKDM4A expression was significantly upregulated in the serum exosomes from PC patients compared with the exosomes from healthy volunteers. Exosomes treatment promoted the proliferation, migration and invasion of PC cells but inhibited apoptosis; however, these effects were attenuated after circKDM4A knockdown. Meanwhile, circKDM4A depletion restored exosome-increased circKDM4A expression. Additionally, circKDM4A acted as a miR-338-3p sponge, and miR-338-3p bound to CUL4B in PC cells. CircKDM4A regulated the effect of exosome-induced PC cell malignancy by interacting with miR-338-3p and CUL4B. Moreover, circKDM4A silencing relieved exosome-induced tumor growth in vivo. Exosomal circKDM4A promoted PC malignant progression by the miR-338-3p/CUL4B axis, providing a therapeutic target for PC.

Bone marrow mesenchymal stem cell-derived extracellular vesicles containing miR-181d protect rats against renal fibrosis by inhibiting KLF6 and the NF-κB signaling pathway.

Recent studies have investigated the ability of extracellular vesicles (EVs) in regulating neighboring cells by transferring signaling molecules, such as microRNAs (miRs) in renal fibrosis. EVs released by bone marrow mesenchymal stem cells (BMSCs) contain miR-181d, which may represent a potential therapy for renal fibrosis. miR-181d has been speculated to regulate Krüppel-like factor 6 (KLF6), which activates the nuclear factor-kappa B (NF-κB) signaling pathway. Luciferase assays were performed to confirm the relationship between miR-181d and KLF6. Gain- and loss-of-function studies in vivo and in vitro were performed to assess the effect of BMSC-derived EVs (BMSC-EVs), which contained miR-181d, on KLF6, NF-κB, and renal fibrosis. Transforming growth factor-ß (TGF-ß)-induced renal tubular epithelial HK-2 cells were treated with EVs derived from BMSCs followed by evaluation of collagen type IV α1 (Col4α1), Collagen I and α-smooth muscle actin (α-SMA) as indicators of the extent of renal fibrosis. Renal fibrosis was induced in rats by unilateral ureteral obstruction (UUO) followed by the subsequent analysis of fibrotic markers. BMSC-EVs had higher miR-181d expression. Overexpression of miR-181d correlated with a decrease in KLF6 expression as well as the levels of IκBα phosphorylation, α-SMA, Col4α1, TGF-ßR1 and collagen I in HK-2 cells. In vivo, treatment with miR-181d-containing BMSC-derived EVs was able to restrict the progression of fibrosis in UUO-induced rats. Together, BMSC-EVs suppress fibrosis in vitro and in vivo by delivering miR-181d to neighboring cells, where it targets KLF6 and inhibits the NF-κB signaling pathway.