[Construction and validation of a risk nomogram for sepsis-associated acute kidney injury in intensive care unit].

OBJECTIVE: To construct and validate a nomogram model for predicting sepsis-associated acute kidney injury (SA-AKI) risk in intensive care unit (ICU) patients. METHODS: A retrospective cohort study was conducted. Adult sepsis patients admitted to the department of ICU of the 940th Hospital of Joint Logistic Support Force of PLA from January 2017 to December 2022 were enrolled. Demographic characteristics, clinical data within 24 hours after admission to ICU diagnosis, and clinical outcomes were collected. Patients were divided into training set and validation set according to a 7 : 3 ratio. According to the consensus report of the 28th Acute Disease Quality Initiative Working Group (ADQI 28), the data were analyzed with serum creatinine as the parameter and AKI occurrence 7 days after sepsis diagnosis as the outcome. Lasso regression analysis and univariate and multivariate Logistic regression analysis were performed to construct the nomogram prediction model for SA-AKI. The discrimination and accuracy of the model were evaluated by the Hosmer-Lemeshow test, receiver operator characteristic curve (ROC curve), decision curve analysis (DCA), and clinical impact curve (CIC). RESULTS: A total of 247 sepsis patients were enrolled, 184 patients developed SA-AKI (74.49%). The number of AKI patients in the training and validation sets were 130 (75.58%) and 54 (72.00%), respectively. After Lasso regression analysis and univariate and multivariate Logistic regression analysis, four independent predictive factors related to the occurrence of SA-AKI were selected, namely procalcitonin (PCT), prothrombin activity (PTA), platelet distribution width (PDW), and uric acid (UA) were significantly associated with the onset of SA-AKI, the odds ratio (OR) and 95% confidence interval (95%CI) was 1.03 (1.01-1.05), 0.97 (0.55-0.99), 2.68 (1.21-5.96), 1.01 (1.00-1.01), all P < 0.05, respectively. A nomogram model was constructed using the above four variables. ROC curve analysis showed that the area under the curve (AUC) was 0.869 (95%CI was 0.870-0.930) in the training set and 0.710 (95%CI was 0.588-0.832) in the validation set. The P-values of the Hosmer-Lemeshow test were 0.384 and 0.294, respectively. In the training set, with an optimal cut-off value of 0.760, a sensitivity of 77.5% and specificity of 88.1% were achieved. Both DCA and CIC plots demonstrated the model's good clinical utility. CONCLUSIONS: A nomogram model based on clinical indicators of sepsis patients admitted to the ICU within 24 hours could be used to predict the risk of SA-AKI, which would be beneficial for early identification and treatment on SA-AKI.

miR-152-3p Inhibits Proliferation, Invasion and Autophagy in UMUC3 and TCCSUP Bladder Cancer Cell Lines via Suppressing HMGA2 Expression.

OBJECTIVE: MicroRNAs have been reported to be involved in the regulation of tumor progression. This study investigated the role of miR-152-3p in bladder cancer development. METHODS: A total of 67 bladder cancer cases were enrolled. miR-152-3p expression in bladder cancer tissues and cells were detected using quantitative reverse transcriptase polymerase chain reaction. Bladder cancer cells were transfected by miR-152-3p mimic and inhibitor to up-regulate and down-regulate miR-152-3p expression. After transfection, cell counting kit-8 assay, flow cytometry, Brdu staining assay, transwell experiment and wound healing assay were conducted to research the effect of miR-152-3p up-regulation/down-regulation on bladder cancer cell viability, apoptosis, proliferation, invasion and migration abilities. The expression of high-mobility group protein A2 (HMGA2) and autophagy-related proteins was researched using Western blot. The interaction between miR-152-3p and HMGA2 was explored by dual luciferase reporter gene assay. RESULTS: Low miR-152-3p expression in tumor tissues bladder cancer patients was associated with poor prognosis. miR-152-3p expression was abnormally down-regulated in bladder cancer cells. miR-152-3p up-regulation inhibited viability, proliferation, invasion, migration but promoted apoptosis of bladder cancer cells. miR-152-3p down-regulation showed the opposite effects. miR-152-3p up-regulation suppressed the expression of Beclin 1 and LC3II/LC3I proteins in bladder cancer cells, but miR-152-3p down-regulation increased them. HMGA2 was target of miR-152-3p, which could be directly inhibited by miR-152-3p. HMGA2 up-regulation reversed the inhibitory effect of miR-152-3p on bladder cancer cell malignant phenotype. CONCLUSION: miR-152-3p inhibited malignant phenotype of bladder cancer cell lines via suppressing HMGA2 expression.

circ3323 Motivates Host Gene to Promote the Aggressiveness of Bladder Cancer.

Bladder cancer (BCa) is the most common cancer in the urinary system with high recurrence rate and poor prognosis. Circular RNA (circRNA) is a novel subclass of noncoding-RNA which participate in progression of BCa. Here, we identified a novel circRNA-circ3323 and aimed to investigate the role of circ3323 in progression of BCa. Public data of RNA sequencing was used to identify significant circRNA related to BCa. The role of circRNAs in progression of BCa was assessed in cytotoxicity assay, transwell assay and flow cytometry. Biotin-coupled RNA pull-down and fluorescence in situ hybridization were performed to evaluate the interaction between circRNAs and miRNAs. The expression of circ3323 was higher in BCa tissues and cells than in normal samples. Experiments in vitro showed that the knockdown of circ3323 inhibited cell proliferation and impeded the metastasis of BCa cells. Mechanistically, we demonstrated that circ3323 acts as a sponge for miR-186-5p and promotes host gene APP's expression. Clinically, circ3323 predicts worse overall survival of BCa patients, indicating its prognostic value. Our study identified that circ3323 modulates metastasis of BCa through miR-186-5p/APP axis and may serve as a promising prognostic biomarker for BCa, which provides novel insights into treatment of BCa.

[Tadalafil for ED after transurethral resection of the prostate: a report of 113 cases].

OBJECTIVE: To evaluate the efficacy of tadalafil in the treatment of ED after transurethral resection of the prostate (TURP). METHODS: A total of 113 patients with ED after TURP received 3 months of tadalafil treatment and were followed up for 6 months. The IIEF-5 scores of the patients and the number of successful penile intromissions and sustained penile erections in the patients' sexual life diary were compared before and after the treatment. RESULTS: The IIEF-5 scores were 9.83 +/- 3.96 before the medication, 20.23 +/- 3.25 after it, and 17.28 +/- 3.03 at 6 months after drug withdrawal, with statistically significant differences between pre- and post-treatment (P < 0.05). The patients' success rates of penile intromission and sexual intercourse were increased from 44.8% and 7.5% before the medication to 81.7% and 63.2% after it. CONCLUSION: Tadalafil can be used as a first-line drug for the treatment of ED after TURP.