BackgroundSusceptibility weighted imaging (SWI) is a new MRI technique which has been proved very useful in the diagnosis of brain diseases, but few study was performed on its value in prostatic diseases. The aim of the present study was to investigate the value of SWI in distinguishing prostate cancer from benign prostatic hyperplasia and detecting prostatic calcification.Methodology/Principal Findings23 patients with prostate cancer and 53 patients with benign prostatic hyperplasia proved by prostate biopsy were scanned on a 3.0T MR and a 16-row CT scanner. High-resolution SWI, conventional MRI and CT were performed on all patients. The MRI and CT findings, especially SWI, were analyzed and compared. The analyses revealed that 19 out of 23 patients with prostate cancer presented hemorrhage within tumor area on SWI. However, in 53 patients with benign prostatic hyperplasia, hemorrhage was detected only in 1 patient in prostate by SWI. When comparing SWI, conventional MRI and CT in detecting prostate cancer hemorrhage, out of the 19 patients with prostate cancer who had prostatic hemorrhage detected by SWI, the prostatic hemorrhage was detected in only 7 patients by using conventional MRI, and none was detected by CT. In addition, CT demonstrated calcifications in 22 patients which were all detected by SWI whereas only 3 were detected by conventional MRI. Compared to CT, SWI showed 100% in the diagnostic sensitivity, specificity, accuracy, positive predictive value(PPV) and negative predictive value(NPV) in detecting calcifications in prostate but conventional MRI demonstrated 13.6% in sensitivity, 100% in specificity, 75% in accuracy, 100% in PPV and 74% in NPV.ConclusionsMore apparent prostate hemorrhages were detected on SWI than on conventional MRI or CT. SWI may provide valuable information for the differential diagnosis between prostate cancer and prostatic hyperplasia. Filtered phase images can identify prostatic calcifications as well as CT.

Abstract. The elucidation of the underlying molecular mechanisms regulating the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) is of great importance in improving the treatment of bone-associated diseases. MicroRNAs (miRNAs) have been proven to regulate the osteogenic differentiation of BMSCs. The present study investigated the role of miR-217 in the osteogenic differentiation of rat BMSCs. It was observed that miR-217 expression levels were downregulated during the process of osteogenic differentiation. Subsequently, a dual-luciferase reporter gene assay demonstrated that miR-217 targets a putative binding site in the 3'-untranslated region of the runt related transcription factor 2 (Runx2) gene, which is a key transcription factor for osteogenesis. It was then demonstrated that overexpression of miR-217 attenuated the osteogenesis of BMSCs and downregulated the expression of Runx2, whereas inhibition of miR-217 promoted osteoblastic differentiation and upregulated Runx2 expression. Furthermore, the extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) signaling pathways were investigated during osteogenic induction, and the data indicated that miR-217 may exert a negative effect on the osteogenic differentiation of BMSCs through alteration of ERK and p38 MAPK phosphorylation. The present study therefore concluded that miR-217 functions as a negative regulator of BMSC osteogenic differentiation via the inhibition of Runx2 expression, and the underlying molecular mechanisms may partially be attributed to mediation by the ERK and p38 MAPK signaling pathways.

Objectives: To explore the expression of aquaporin 1 (AQP 1 ) in bladder uroepithelium cell carcinoma (BUCC) and its relevance to recurrence. Materials and Methods: Tissue samples from 45 BUCC patients who underwent total cystectomy or transurethral resection of bladder tumor (TURBT) and from 40 patients with non-bladder cancers who underwent special detection or treatments were collected. The level of expression of AQP 1 in BUCC tissues and normal bladder tissues was assessed by immunohistochemistry so as to analyze the relevance to pathological patterns and time of recurrence in BUCC patients. Results: The expression levels of AQP 1 normal bladder tissues and BUCC tissues were 2.175±0.693 and 3.689±0.701, respectively, and the difference was significant (t=9.99, P<0.0001). Marked increase was noted with BUCC histological grade and pathological stage (P<0.01). Moreover, the expression of AQP 1 was evidently higher in cancerous tissues with lymph node metastasis than in those without (P<0.01). With short-term recurrence, the positive cell expression rate of AQP 1 was higher in primary tissues, which increased obviously after recurrence. Additionally, the recurrent time of BUCC was negatively associated with the positive cell expression rate of AQP 1 and the difference between the expression of AQP 1 before and after recurrence (r=-0.843, F=39.302, P=0.000; r=-0.829, F=35.191, P=0.000). Conclusions: AQP 1 , which reflects the grade, stage, lymph node metastasis and recurrence of BUCC, has potential guiding significance in the diagnosis and treatment of bladder cancarcinoma.

Background: Clear cell renal cell carcinoma (ccRCC) is the most common type of renal cell carcinoma (RCC). Immunotherapy, especially anti-PD-1, is becoming a pillar of ccRCC treatment. However, precise biomarkers and robust models are needed to select the proper patients for immunotherapy.Methods: A total of 831 ccRCC transcriptomic profiles were obtained from 6 datasets. Unsupervised clustering was performed to identify the immune subtypes among ccRCC samples based on immune cell enrichment scores. Weighted correlation network analysis (WGCNA) was used to identify hub genes distinguishing subtypes and related to prognosis. A machine learning model was established by a random forest (RF) algorithm and used on an open and free online website to predict the immune subtype.Results: In the identified immune subtypes, subtype2 was enriched in immune cell enrichment scores and immunotherapy biomarkers. WGCNA analysis identified four hub genes related to immune subtypes, CTLA4, FOXP3, IFNG, and CD19. The RF model was constructed by mRNA expression of these four hub genes, and the value of area under the receiver operating characteristic curve (AUC) was 0.78. Subtype2 patients in the independent validation cohort had a better drug response and prognosis for immunotherapy treatment. Moreover, an open and free website was developed by the RF model (https://immunotype. shinyapps.io/ISPRF/). Conclusions:The current study constructs a model and provides a free online website that could identify suitable ccRCC patients for immunotherapy, and it is an important step forward to personalized treatment.

Renal tubular epithelial cell apoptosis is the main mechanism of cisplatin-induced acute kidney injury. The role of microRNAs (miRNAs) in the apoptosis of renal tubular epithelial cells has been suggested, but the underlying mechanism has not been fully elucidated. We used microarray analysis to identify miR-142-5p involved in cisplatin-induced acute kidney injury. miR-142-5p was down-regulated in human renal tubular epithelial (HK-2) cells with cisplatin treatment. Notably, the overexpression of miR-142-5p attenuated the cisplatin-induced HK-2 cell apoptosis and inhibition of miR-142-5p aggravated cisplatin-induced HK-2 cell apoptosis. During cisplatin treatment, p53 was activated. The inhibition of p53 by pifithrin-α attenuated the cisplatin-induced kidney injury and up-regulated miR-142-5p expression. We also identified the Sirtuin7 (SIRT7) as a target of miR-142-5p. Furthermore, we demonstrated that the inhibition of SIRT7 prevented cisplatin-induced HK-2 cell apoptosis and decreased the expression of nuclear factor kappa B (NF-κB). Our data revealed that p53 inhibition could attenuate cisplatin-induced acute kidney injury by up-regulating miR-142-5p to repress SIRT7/NF-κB. These findings may provide a novel therapeutic target of cisplatin-induced acute kidney injury.