Ultrasound-guided percutaneous nephrolithotomy without indwelling ureteral catheter in older adults with upper urinary calculi: A retrospective study.

Retention of ureteral catheter to establish artificial hydronephrosis is a routine step of percutaneous nephrolithotomy procedure, which can improve the success rate of puncture, but it can prolong the procedure time and increase the risk of postoperative infection, especially for immunocompromised elderly patients. Therefore, this study aims to investigate the safety and effectiveness of ultrasound-guided percutaneous nephrolithotomy without indwelling ureteral catheter for older patients with upper urinary calculi. The clinical data of 119 older patients admitted to the Affiliated Hospital of Jining Medical University for percutaneous nephrolithotomy from January 2019 to December 2021 were retrospectively analyzed. The patients were divided into study and control groups according to whether the physician decided to use ureteral catheter during the procedure, and the differences in the success rate of one-time puncture, operative time, single-stage stone removal rate, postoperative hospital stay, and complication rate were compared between the 2 groups. There were no significant differences in the success rate of one-time puncture and single-stage stone removal rate between the 2 groups (P > .05). The operation time were significantly shorter in the study group [(30.0-61.0) minute vs (54.8-106.8) minute, P = .00], and the intraoperative bleeding was less in the study group [(5-20) mL vs (10-30) mL, P = .03]. The postoperative hospital stay was shorter in the study group [(2.5-4.0) days vs (3.0-5.0) days, P = .00], and the medical expenses were lower in the study group [(17,309.5-22,652.7) yuan vs (19,148.0-24,407.6) yuan, P = .02]. The incidence of systemic inflammatory response syndrome was lower in the study group (3.5% vs 19.4%, P = .007). There were no statistically significant differences in complications such as postoperative fever, renal artery embolism and blood transfusion between the two groups (P > .05). Ultrasound-guided percutaneous nephrolithotomy without indwelling ureteral catheter for elderly patients with upper urinary stones is safe and feasible.

Long noncoding RNA MAGI2-AS3 inhibits bladder cancer progression through MAGI2/PTEN/epithelial-mesenchymal transition (EMT) axis.

BACKGROUND: Long noncoding RNA (lncRNA) are critical regulators of tumor progression. OBJECTIVE: To determine how the lncRNA membrane associated guanylate kinase, WW and PDZ domain-containing 2 (MAG12) antisense RNA 3 (MAGI2-AS3) and the phosphatase and tensin homolog (PTEN) gene function in regulating bladder cancer (Bca) progression. METHODS: Total RNA from 80 Bca tissues and 30 paired para-cancerous tissues from patients was sequentially extracted, quantified, purified, and reverse transcribed using RT-PCR. A library was constructed and sequenced. Four Bca cell lines and a normal urothelial cell line were transfected with lentiviral plasmids, and cell migration and invasion were assayed in vitro. An orthotopic mouse model of Bca was created for in vivo studies. RESULTS: MAGI2-AS3 expression was significantly downregulated in Bca, compared with normal tissues, and negatively associated with tumor stage and a poor prognosis. MAGI2-AS3 and its sense RNA MAGI2 showed significant and positive correlation. The expression of MAGI2 and its downstream gene, PTEN, increased in Bca cells overexpressing MAGI2-AS3, and interference by MAGI2 expression reversed the migration and invasion inhibited by MAGI2-AS3 overexpression. CONCLUSION: MAGI2-AS3 overexpression inhibited Bca cell progression by regulating the MAGI2/PTEN/epithelial-mesenchymal transition, offering novel insights into the mechanism of Bca progression.

LncRNA-SNHG16 predicts poor prognosis and promotes tumor proliferation through epigenetically silencing p21 in bladder cancer.

More and more evidences have ensured the crucial functions of long non-coding RNAs (lncRNAs) in multiple tumors. It has been discovered that lncRNA-SNHG16 is involved in many tumors. Even so, it is still necessary to study SNHG16 comprehensively in bladder cancer. In terms of our study, the level of SNHG16 both in the tumor tissues and cell lines was measured and the relationship among SNHG16, clinicopathological traits and prognosis was explored. Interference assays were applied to determine the biological functions of SNHG16. It was discovered that the level of SNHG16 was evidently enhanced both in tissues and cell lines of bladder cancer. Patients with highly expressed SNHG16 suffered from poor overall survival. Multivariable Cox proportional hazards regression analysis implied that highly expressed SNHG16 could be used as an independent prognostic marker. It could be known from functional assays that silenced SNHG16 impaired cell proliferation, owing to the effects of SNHG16 on cell cycle and apoptosis. Finally, mechanism experiments revealed that SNHG16 could epigenetically silence the expression of p21. The facts above pointed out that lncRNA-SNHG16 might be quite vital for the diagnosis and development of bladder cancer, and could even become an important therapeutic target for bladder cancer.

Potential role of CXCR3 in proliferation and invasion of prostate cancer cells.

AIM: To investigate the potential role of CXCR3 expression on prostate cancer cell proliferation and invasion and to illustrate its mechanism. METHODS: Human PC-3 cells were transfected with siRNA-CXCR3A and siRNA-CXCR3B plasmids respectively. The mRNA expressions of CXCR3A and CXCR3B in PC-3 cells from each group were analyzed using RT-PCR. Besides, cell proliferation ability and cell invasion ability of PC-3 cells in each group were analyzed using MTT assay and Matrige assay respectively. Additionally, expressions of CXCR3 downstream proteins were detected using Western blotting. RESULTS: mRNA level of CXCR3A was decreased while CXCR3B mRNA level was increased in PC-3 cells (P<0.05). Compared with the controls, down-regulation of CXCR3A but up-regulation of CXCR3B significantly inhibited PC-3 cell proliferation and cell invasion ability (P<0.05). Besides, aberrant CXCR3 expression significantly increased expressions of phospholipase C (PLCß), matrix metallo proteinase (MMP-1), and MMP-3 except MMP-7 in PC-3 cells (P<0.05). CONCLUSION: The data presented in our study suggested that aberrant CXCR3 expression may play crucial roles in suppressing PC metastasis via inhibiting cell proliferation and invasion ability through the PCLß signaling pathway.