EPDR1 levels and tumor budding predict and affect the prognosis of bladder carcinoma.

Background: Bladder carcinoma is a common malignancy of the urinary system. The previous study showed that EPDR1 expression was significantly related to the carcinogenesis and progression of bladder carcinoma. Methods: We retrospectively reviewed the records of 621 patients who were newly diagnosed with bladder carcinoma between January 2018 and August 2020 at The Affiliated Hospital of Zunyi Medical University. We conducted immunohistochemistry of EPDR1 in tumor tissues. Meanwhile, tumor budding evaluation was also carried out by 2 independent experienced pathologists. Results: 80 patients were included in this study with a median age of 66 years (range; 42-88 years). 45% of the patients (36/80) were non-muscle-invasive bladder carcinoma patients, while 55% of muscle-invasive bladder carcinoma(44/80). The follow-up time was from 6 months to 36 months. We found that there were significant differences in expression of EPDR1 in the tumor pT stages(p<0.05), pM stages(p<0.05), and pN stages(p<0.05). Meanwhile, a higher expression of EPDR1 indicated a worse outcome for the patient(p<0.05). A tendency toward a worse status of the patient was accompanied by a high positive rate (p<0.001). Moreover, the IOD of EPDR1 had a positive relationship with TB (p<0.05). Furthermore, we found that EPDR1 and tumor budding could be crucial factors for affecting the prognosis of bladder carcinoma, even better than pTMN(Riskscore=(0.724)* pT_stage +(4.960) *EPDR1+(4.312)*TB). Conclusion: In conclusion, bladder cancer patients with higher expression levels of EPDR1 had worse survival outcomes. The combination of TB and EPDR1 levels could predict the prognosis for muscle-invasive bladder cancer patients.

5α-Reductase Inhibitors Could Prevent the Clinical and Pathological Progression of Prostate Cancer: A Meta-analysis.

PURPOSE: To explore the efficacy of 5-ARIs in PCA (Prostate Cancer). METHODS: Searching through the major medical databases such as PubMed, Science Citation Index, EMBASE, Medline, Web of Science, Cochrane Library for all published studies in English until 2018. The following search terms were used: "Finasteride", "dutasteride", "5α reductase inhibitors", "5-ARIs", "prostate cancer", "prostate neoplasm" and the additional related studies were manually searched. Newcastle-Ottawa Scale (NOS) assessed the qualities of studies, and the outcome measures were observed by RR or OR with 95% CIs. RESULTS: We included 9 eligible studies for analyses from 2011 to 2017. We found that 5-ARIs group may have fewer progression (OR = 0.48 95%CI: 0.37-0.61 P < 0.00001, I2=4% p = 0.39) and lower pathological progression (OR = 0.46; 95%CI: 0.29-0.73; p = 0.001, I2=0% p = 0.45), compared with control groups. However, the OS did not show significant difference between two groups (OR=1.10; 95%CI:0.90-1.35; P = 0.35, I2 = 93% P < .00001 ). CONCLUSION: The use of 5-ARIs could prevent progression in PCA patients both clinical and pathological.

EPDR1 is related to stages and metastasize in bladder cancer and can be used as a prognostic biomarker.

BACKGROUND: Bladder cancer (BLCA) is a malignant urothelial carcinoma and has a high mortality rate. EPDR1 (ependymin related 1) is a type II transmembrane protein and related to calcium-dependent cell adhesion. METHODS: We explored the potential oncogenic roles of EPDR1 in BLCA basing on the multiple public datasets. RESULTS: We found that EPDR1 expression had a significant difference in BLCA and adjacent normal bladder tissues, and the level of EPDR1was up-regulated with advanced tumor stage and metastasis in BLCA. Meanwhile, the high expression group of EPDR1 had a shorter OS compared to the low or medium expression-group. Furthermore, EPDR1 expression was associated with tumor-infiltrating immune cells (TIICs), including NK cells, CD8 + T cells, CD4 + T cells, Macrophages cells, and so on. Moreover, EPDR1 also involved in several signaling pathways as well as PI3K/AKT pathway, Cytokine receptor interaction, and apoptosis. CONCLUSION: EPDR1 can be used as a novel prognostic biomarker as well as an effective target for diagnosis and treatment in BLCA.

Safety and Efficacy of Ultrasound-Guided Retrolaminar Block of Multiple Injections in Retroperitoneal Laparoscopic Nephrectomy: A Prospective Randomized Controlled Study.

PURPOSE: Ultrasound-guided retrolaminar block (RLB) has the potential to provide postoperative analgesia in retroperitoneal laparoscopic surgery. This study was conducted to evaluate the effects of RLB when compared with local infiltration analgesia (LIA) in retroperitoneal laparoscopic nephrectomy. PATIENTS AND METHODS: One hundred and fifteen patients scheduled for laparoscopic nephrectomy were divided into two groups: the RLB group (n = 57) received an ultrasound-guided RLB, while the LIA group (n = 58) received LIA. At 2, 4, 6, 24, and 48 hours after operation, the maximal visual analog score (VAS), sufentanil and rescue analgesia consumption, and the utilization of patient-controlled intravenous analgesia (PCIA) were assessed. The incidence rates of postoperative nausea and vomiting (PONV); time of leaving bed (at the first instance); and the levels of plasma ß-Endorphin (ß-EP), Interleukin-1ß (IL-1ß), and prostaglandin E2 (PEG2) 30 min after extubation were noted. RESULTS: Patients in the RLB group had significantly lower VAS scores; lower sufentanil cumulative consumption; lower manual addition frequency of PCIA; lower proportion of using rescue analgesia within 48 hours after operation; lower incidence rate of PONV; shorter resuscitation times; earlier time of leaving the bed; and lower ß-EP, IL-1 ß, and PEG2 levels. CONCLUSION: Ultrasound-guided RLB of multiple injections is both safe and controllable for postoperative analgesia after retroperitoneal laparoscopic nephrectomy. When compared with LIA, RLB has better and longer-lasting analgesic effect, lower incidence rates of PONV, and the potential to reduce the level of postoperative inflammatory factors. TRIAL REGISTRATION: China Clinical Trials Registration Center (http://www.chictr.org.cn, No. ChiCTR1800017526, Date of registration: 2018-08-02).

Effect of Hyperbaric Oxygen on Tissue Damage and Expression of Adhesion Molecules and C3 in a Rat Model of Renal Ischemia-Reperfusion Injury After Kidney Transplantation.

BACKGROUND The aim of this study was to investigate the protective effect and mechanism of hyperbaric oxygen (HBO) in a rat model of renal ischemia-reperfusion injury following kidney transplantation. MATERIAL AND METHODS Sprague Dawley rats were randomly divided into 3 groups (n=18): sham group, kidney transplantation group, and HBO treatment group. Six rats in each group were sacrificed at 1, 3, and 5 hours after reperfusion, and serum and renal tissue were then collected. The serum creatinine levels and histopathological changes of the renal tissue were detected. ICAM-1, VCAM-1, and C3 expression levels were also detected by immunohistochemical staining or real-time polymerase chain reaction. RESULTS Renal function was damaged in the kidney transplantation group and the HBO treatment group compared with sham group (P<0.05). Renal histopathological changes, including tubular cell swelling, tubular dilatation, and hyaline casts, were remarkably reduced in the HBO treatment group compared to the kidney transplantation group. In the immunohistochemical examination, the expression levels of ICAM-1, VCAM-1, and C3 were obviously increased in the kidney transplantation group and the HBO treatment group; moreover, the levels in the HBO treatment group were significantly lower than in the kidney transplantation group (P<0.05). In addition, the ICAM-1 and C3 mRNA levels were increased in the kidney transplantation group and HBO treatment group, but the levels of in the HBO treatment group them were significantly decreased compared to the kidney transplantation group that at 3 and 5 hours after reperfusion (P<0.05). CONCLUSIONS HBO treatment exerted a protective effect on renal function through inhibition of adhesion molecule overexpression and complement system activation in a rat model of renal ischemia-reperfusion injury after kidney transplantation.