New model of PIRADS and adjusted prostatespecific antigen density of peripheral zone improves the detection rate of initial prostate biopsy: a diagnostic study.

This study explored a new model of Prostate Imaging Reporting and Data System (PIRADS) and adjusted prostate-specific antigen density of peripheral zone (aPSADPZ) for predicting the occurrence of prostate cancer (PCa) and clinically significant prostate cancer (csPCa). The demographic and clinical characteristics of 853 patients were recorded. Prostate-specific antigen (PSA), PSA density (PSAD), PSAD of peripheral zone (PSADPZ), aPSADPZ, and peripheral zone volume ratio (PZ-ratio) were calculated and subjected to receiver operating characteristic (ROC) curve analysis. The calibration and discrimination abilities of new nomograms were verified with the calibration curve and area under the ROC curve (AUC). The clinical benefits of these models were evaluated by decision curve analysis and clinical impact curves. The AUCs of PSA, PSAD, PSADPZ, aPSADPZ, and PZ-ratio were 0.669, 0.762, 0.659, 0.812, and 0.748 for PCa diagnosis, while 0.713, 0.788, 0.694, 0.828, and 0.735 for csPCa diagnosis, respectively. All nomograms displayed higher net benefit and better overall calibration than the scenarios for predicting the occurrence of PCa or csPCa. The new model significantly improved the diagnostic accuracy of PCa (0.945 vs 0.830, P < 0.01) and csPCa (0.937 vs 0.845, P < 0.01) compared with the base model. In addition, the number of patients with PCa and csPCa predicted by the new model was in good agreement with the actual number of patients with PCa and csPCa in high-risk threshold. This study demonstrates that aPSADPZ has a higher predictive accuracy for PCa diagnosis than the conventional indicators. Combining aPSADPZ with PIRADS can improve PCa diagnosis and avoid unnecessary biopsies.

Effect of silencing VDR gene in kidney on renal epithelial calcium transporter proteins and urinary calcium excretion in genetic hypercalciuric stone-forming rats.

OBJECTIVE: To address the molecular mechanisms that the vitamin D receptor (VDR) in the kidney might contribute to decreased renal calcium reabsorption in idiopathic hypercalciuria using genetic hypercalciuric stone-forming (GHS) rats. METHODS: We silenced the VDR gene in the GHS and normal control (NC) rat kidney in vivo using adenovirus vector-delivered microRNA targeting VDR through renal venous transduction. On days 3-21 after injection with adenovirus, the expression levels of the VDR, calcium-sensing receptor, and epithelial calcium transporters in the kidney were detected. The urine calcium and serum calcium, phosphorus, 1,25(OH)(2)D(3), and parathyroid hormone levels were measured. RESULTS: The basal expression levels in the kidney tissues of VDR, calbindin-D(28k), and calcium-sensing receptor were significantly greater in the GHS rats than in the NC rats, and the basal expression levels of transient receptor potential vanilloid receptor subtype 5, transient receptor potential vanilloid receptor subtype 6, calbindin-D(9k), and plasma membrane calcium-adenosine triphosphatase were significantly lower in the GHS rats than in the NC rats. VDR knockdown in the kidney caused significant increase in renal transient receptor potential vanilloid receptor subtype 5, sodium/calcium exchanger, and calbindin-D(9k) expression levels in the GHS rats. The GHS rats excreted significantly more urine calcium after VDR knockdown. The serum calcium, phosphorus, parathyroid hormone, and 1,25(OH)(2)D(3) levels were not altered during the study period in the GHS and NC rats. CONCLUSION: Our findings suggest that VDR knockdown in the kidney can upregulate the expression of transient receptor potential vanilloid receptor subtype 5 in GHS rats. However, VDR depletion results in an increase in urine calcium excretion. The role of VDR in the hypercalciuric formation needs to be elucidated further.

[The role of CD4+CD25+ regulatory T cells in the pathogenesis of chronic abacterial prostatitis/chronic pelvic pain syndrome].

OBJECTIVE: To explore the role of CD4+CD25+ regulatory T cells in the pathogenesis of chronic abacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS). METHODS: Peripheral blood samples were collected from 45 CAP/CPPS patients and 18 healthy age-matched male persons. Peripheral blood mononuclear cells (PBMCs) were isolated. The percentages of CD4+CD25+ and CD4+CD25high regulatory T cells were detected by flow cytometry. PCR was used to examine the mRNA expression of Foxp3, a transcription factor expressed in the CD4+CD25+ cells. ELISA was used to examine the plasma level of tumor growth factor (TGF)-beta1. RESULTS: There were no significant differences in the percentages of peripheral blood CD4+CD25+ and CD4+CD25highT cells between the CAP/CPPS patients and normal control group (both P>0.05). The Foxp3 mRNA in the PBMCs of the CAP/CPPS IIIA and CAP/CPPS IIIB patients were (0.69+/-0.23) and (0.44+/-0.18) respectively, both significantly lower than that of the control group [(1.37+/-0.19), P<0.05]. The serum TGF-beta1 levels of the CAP/CPPS IIIA and CAP/CPPS IIIB patients were (18.09+/-10.45) pg/ml and (14.06+/-6.22) pg/ml respectively, both significantly lower than that of the control group [(27.01+/-13.29) pg/ml, both P<0.05]. CONCLUSION: Not the number of peripheral blood CD4+CD25+ regulatory T cells, but its defective function participates in the pathogenesis of CAP/CPPS. The Foxp3 gene and TGF-beta1 play important roles in the process of pathogenesis of CAP/CPPS too.

[Expression of calbindin-D28k in genetic hypercalciuric stone-forming rats kidney and its role in pathogenesis of idiopathic hypercalciuria].

OBJECTIVE: To study the expression level of calbindin-D28k, a kind of calcium binding protein, in the kidneys of genetic hypercalciuric stone-forming (GHS) rats and to investigate its role in idiopathic hypercalciuria (IH). METHODS: Kidneys were taken out from 16 GHS rats and 6 normal control (NC) rats. Western blotting and real time quantitative PCR were used to detect the protein and mRNA expression levels of calbindin-D28k respectively. RESULTS: Western blotting showed that the A value of calbindin-D28k of the GHS rats was 0.49 +/- 0.02, significantly higher than that of the NC rats (0.20 +/- 0.01, P < 0.05). The 2(-(delta delta CT)) value of mRNA of calbindin-D28k of the GHS rats was 1.21, remarkably higher than that of the NC rats [with the of 2(-(delta delta CT)) value of 1.0]. There was not significant difference in the delta CT value between the two groups (P > 0.05). CONCLUSION: The up-regulation of calbindin-D28k in the GHS rats is possibly caused by hyperexpression of VDR and hypercalcinuria, and plays an important role in urine calcium reabsorption; however, it is not the key protein that results in IH.