Ae index is an independent predictor of kidney stone recurrence in overweight and obese patients.

BACKGROUND: Finding some convenient and economical indicators to initially screen overweight and obese patients at high risk of kidney stone recurrence can help them prevent stone recurrence with lower medical cost. The purpose of this article is to determine the clinical value of Ae index (Apo B × 1000/eGFR) as an independent predictor for kidney stone recurrence in overweight and obese populations. METHODS: We queried the electronic medical records of patients with kidney stone operated at our hospital from March 2016 to March 2022, and selected BMI ≥ 25 kg/m2 as the study population and divided the patients into stone recurrence group and non-recurrence group. Relevant parameters of routine blood and biochemical test, glycated serum protein (GSP), and history of hypertension and hyperglycemia were collected. Then the Chi-square test, independent samples t-test or Wilcoxon rank-sum test were used to calculate the differences between the two groups of data. Next, we performed univariate and multivariate logistic regression analysis to screen out the most significant variables Apo B and eGFR, and then we calculated the Ae index using the formula Apo B × 1000/eGFR, and analyzed the relationship between Ae index and kidney stone recurrence. RESULTS: Univariate analysis found that Apo B (OR:8.376,95%CI:3.093-22.680), Creatinine (OR:1.012,95%CI:1.003-1.021), Cystatin C(OR:2.747,95%CI:1.369-5.508), LDL-C (OR:1.588,95%CI:1.182-2.134), TC (OR:1.543,95%CI:1.198-1.988) were positively associated, eGFR (OR:0.980,95%CI:0.970-0.991) was negatively associated with kidney stone recurrence. And multivariate logistic regression analysis suggested that Apo B (OR:11.028, 95%CI:3.917-31.047) and eGFR (OR:0.976, 95%CI:0.965-0.988) were the most significant factors. Then we calculated Ae index and analyzed it, the sensitivity was 74.26% and the specificity was 60.00%, higher than either individual variable. Its smoothed curve revealed a non-linear relationship between them with the inflection point of 9.16. And the OR on the left side of the inflection point was 1.574 (95% CI: 1.228-2.018), whereas the OR on the right side of the inflection point was 1.088 (95% CI: 1.007-1.177). CONCLUSIONS: Ae index is an easily calculated and obtained index that has some predictive value for kidney stone recurrence in overweight and obese patients, which is of interest.

Establishment of a new predictive model for the recurrence of upper urinary tract stones.

PURPOSE: To construct a nomogram for evaluation of the recurrence risk of upper urinary tract stones in patients. METHODS: We retrospectively reviewed the clinical data of 657 patients with upper urinary tract stones and divided them into stone recurrence group and non-recurrence group. Blood routine, urine routine, biochemical, and urological CT examinations were searched from the electronic medical record, relevant clinical data were collected, including age, BMI, stones number and location, maximum diameter, hyperglycemia, hypertension, and relevant blood and urine parameters. The Wilcoxon rank-sum test, independent sample t test, and Chi-square test were used to preliminarily analyze the data of the two groups, then LASSO and logistic regression analysis were used to find out the significant difference indicators. Finally, R software was used to draw a nomogram to construct the model, and ROC curve was drawn to evaluate the sensitivity and specificity. RESULTS: The results showed that multiple stones (OR: 1.832, 95% CI 1.240-2.706), bilateral stones (OR: 1.779, 95% CI 1.226-2.582), kidney stones (OR: 3.268, 95% CI 1.638-6.518), and kidney ureteral stones (OR: 3.375, 95% CI 1.649-6.906) were high risk factors. And the stone recurrence risk was positively correlated with creatinine (OR: 1.012, 95% CI 1.006-1.018), urine pH (OR: 1.967, 95% CI 1.343-2.883), Apo B (OR: 4.189, 95% CI 1.985-8.841) and negatively correlated with serum phosphorus (OR: 0.282, 95% CI 0.109-0.728). In addition, the sensitivity and specificity of the prediction model were 73.08% and 61.25%, diagnosis values were greater than any single variable. CONCLUSION: The nomogram model can effectively evaluate the recurrence risk of upper urinary stones, especially suitable for stone postoperative patients, to help reduce the possibility of postoperative stone recurrence.

Surface modification of ureteral stents: development history, classification, function, and future developments.

INTRODUCTION: Ureteral stents are commonly used in urology but are frequently associated with hematuria, abdominal discomfort, urinary tract infection, stent displacement, and stent encrustation. Surface modification of ureteral stents is beneficial to solve the problem, and these can be divided into coated stents and drug-eluting stents according to the modification method. Coated stents can be divided into hydrophilic coatings, antibacterial coatings, and anti-encrustation coatings. Drug-eluting stents can be divided into antimicrobial drug-eluting, antispasmodic analgesic drug-eluting, anti-ureteral stricture drug-eluting, and anti-tumor drug-eluting. Surface modification of ureteral stents can not only reduce complications related to ureteral stents but also strengthen the treatment of certain urologic diseases, which has a high clinical application value. AREAS COVERED: This review focuses on highlighting and summarizing the latest research progress about surface modification of ureteral stents, ureteral stent development history, classification, functions, and future development prospects. EXPERT OPINION: The purpose of this article is to discuss surface modification of ureteral stents to reduce stent-related complications and potential research directions for the treatment of urinary tract tumors are also briefly discussed, to help guide further innovation in ureteral stent coatings, which contribute to the future progress of ureteral stents surface modification.

piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2.

Background: PIWI-interacting RNAs (piRNAs) are a class of noncoding RNAs originally reported in the reproductive system of mammals and later found to be aberrantly expressed in tumors. However, the function and mechanism of piRNAs in testicular cancer are not very clear. Methods: The expression level and distribution of piR-36249 were detected by RT-qPCR and immunofluorescence staining assay. Testicular cancer cell (NT2) progression was measured by CCK8 assay, colony formation assay and wound healing assay. Cell apoptosis was assessed by flow cytometry and western blot. RNA sequencing and dual-luciferase reporter assay were conducted to identify the potential targets of piR-36249. The relationship between piR-36249 and OAS2 or DHX36 was confirmed using overexpression assay, knockdown assay, pull-down assay and RIP assay. Results: piR-36249 is significantly downregulated in testicular cancer tissues compared to tumor-adjacent tissues. Functional studies demonstrate that piR-36249 inhibits testicular cancer cell proliferation, migration and activates the cell apoptosis pathway. Mechanically, we identify that piR-36249 binds to the 3'UTR of 2'-5'-oligoadenylate synthetase 2 (OAS2) mRNA. OAS2 has been shown in the literature to be a tumor suppressor modulating the occurrence and development of some tumors. Here, we show that OAS2 knockdown also promotes testicular cancer cell proliferation and migration. Furthermore, piR-36249 interacts with DHX36, which has been reported to promote translation. DHX36 can also bind to OAS2 mRNA, and knockdown of DHX36 increases OAS2 mRNA but downregulates its protein, indicating the enhancing effect of DHX36 on OAS2 protein expression. Conclusion: All these data suggest that piR-36249, together with DHX36, functions in inhibiting the malignant phenotype of testicular cancer cells by upregulating OAS2 protein and that piR-36249 may be used as a suppressor factor to regulate the development of testicular cancer.

Video Compressive Sensing Reconstruction Using Unfolded LSTM.

Video compression sensing can use a few measurements to obtain the original video by reconstruction algorithms. There is a natural correlation between video frames, and how to exploit this feature becomes the key to improving the reconstruction quality. More and more deep learning-based video compression sensing (VCS) methods are proposed. Some methods overlook interframe information, so they fail to achieve satisfactory reconstruction quality. Some use complex network structures to exploit the interframe information, but it increases the parameters and makes the training process more complicated. To overcome the limitations of existing VCS methods, we propose an efficient end-to-end VCS network, which integrates the measurement and reconstruction into one whole framework. In the measurement part, we train a measurement matrix rather than a pre-prepared random matrix, which fits the video reconstruction task better. An unfolded LSTM network is utilized in the reconstruction part, deeply fusing the intra- and interframe spatial-temporal information. The proposed method has higher reconstruction accuracy than existing video compression sensing networks and even performs well at measurement ratios as low as 0.01.

LncRNA-MALAT1 Regulates Cancer Glucose Metabolism in Prostate Cancer via MYBL2/mTOR Axis.

It is known that the long noncoding RNAs (lncRNA) MALAT1 is associated with tumorigenesis and progression in various cancers; however, its functions and mechanisms in prostate cancer (PCa) initiation and progression are still unknown. In the present study, our findings revealed that MALAT1 plays a critical part in regulating PCa proliferation and glucose metabolism. Knockdown of MALAT1 affects the protein and mRNA levels of MYBL2. In addition, MALAT1 enhances the phosphorylation level of mTOR pathway by upregulating MYBL2. Knockdown of MALAT1 or MYBL2 in PCa cell lines significantly inhibits their proliferation capacity. Silencing MALAT1/MYBL2/mTOR axis in PCa cell lines affects their glycolysis and lactate levels, and we verified these findings in mice. Furthermore, we explored the underlying tumorigenesis functions of MYBL2 in PCa and found that high expression of MYBL2 was positively associated with TNM stage, Gleason score, PSA level, and poor survival rate in PCa patients. Taken together, our research suggests that MALAT1 controls cancer glucose metabolism and progression by upregulating MYBL2-mTOR axis.

Bone marrow mesenchymal stem cells therapy on bilateral pelvic nerve crush-induced voiding dysfunction in rats.

INTRODUCTION AND HYPOTHESIS: Neurogenic voiding dysfunction can be induced after radical pelvic surgery and severely affects patients' quality of life. This study aims to investigate the effects of bone marrow mesenchymal stem cells (BMSCs) on neurogenic voiding dysfunction in male rats and explore the underlying mechanisms. METHODS: Thirty 4-week-old male Sprague-Dawley rats were randomly divided into three groups: (1) sham-operated (sham, n = 10), (2) intrabladder wall injection of phosphate buffer solution (PBS) after bilateral pelvic nerve crush (BPNC+PBS, n = 10), and (3) intrabladder wall injection of BMSCs after bilateral pelvic nerve crush (BPNC+BMSCs, n = 10). Four weeks postoperatively, functional and morphological examinations were performed. RESULTS: Compared to the sham group, BPNC rats manifested significant augmentation in the frequency of non-voiding contractions and postvoid residual and bladder capacity, and they had decreases in intravesical pressure and voiding efficiency. However, they were markedly improved after BMSC injection. Masson's trichrome staining showed that the ratio of collagen area in bladder wall tissue significantly increased in the BPNC+PBS group but was reduced following BMSC injection. BPNC increased the protein expression of TGF-ß1, Smad2/3, and collagen I/III but decreased the expression of α-SMA. BMSC injection stimulated higher expression levels of α-SMA and lower expression levels of the other target proteins. The expression levels of vesicular acetylcholine transporters were reduced at 4 weeks post-BPNC, whereas injection of BMSCs boosted the expression quantity. CONCLUSIONS: BMSC therapy suppressed detrusor fibrosis, improved intravesical pressure and voiding efficiency, and partially restored voiding function in male rats after BPNC.

The Association of Urine Creatinine With Kidney Stone Prevalence in US Adults: Data From NHANES 2009-2018.

Background: The primary objective of this project is to explore the association of urine creatinine (UCR) with the prevalence rate of kidney stones. Method: The National Health and Nutrition Examination Survey (NHANES) database was employed to conduct a cross-sectional study. The analysis samples included adults aged ≥20 years from five consecutive cycles of the NHANES 2009-2018. The association between UCR and kidney stones was detected using univariate and multivariate logistic regression analyses. Further, subgroup analyses were performed to evaluate the subgroup effects. Results: After adjustment for all confounders, multiple logistic regression analysis revealed a weak positive relationship between UCR and kidney stone (OR = 1.015, 95% CI: 1.008-1.021). In the subgroup analysis stratified by sex, age, or race, the risk further increased in men (OR = 1.014, 95% CI: 1.005-1.023), women (OR = 1.015, 95% CI: 1.005-1.025), white race (OR = 1.022, 95% CI: 1.013-1.030), aged 40-59 years (OR = 1.017, 95% CI: 1.006-1.028), and aged 60-80 years (OR = 1.017, 95% CI: 1.006-1.028). Conclusions: Our results confirmed a moderately increased risk of kidney stone formation attributed to high levels of UCR, especially in middle-aged and older adults and the white race. However, because of the cross-sectional design of the study, causal inferences cannot be made.

LncRNA NEAT1-associated aerobic glycolysis blunts tumor immunosurveillance by T cells in prostate cancer.

Long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) is nuclear-located and transcribed from chromatin 11. To date, little is known about the cellular functions and regulatory mechanisms of NEAT1 in prostate cancer (PCa). In this study, whole-genome RNA sequencing data were downloaded from TCGA and GEO databases. Biological information was used to analyze the different expressions of NEAT1. In situ hybridization (ISH) was performed to detect the expression of NEAT1 in PCa and paracarcinoma clinical samples. Then, NEAT1 was knocked down in PC3 cells through lentiviral infection with a plasmid construct. Bioinformatics and integrative analytical approaches were utilized to identify the relationships of NEAT1 with specific cancer-related gene sets. Cell proliferation assay and colony formation assay were performed to evaluate the cell proliferative ability. Glycolysis stress test, metabolism assay, and infiltrating T-cell function analysis were implemented to assess the changes in metabolism and immune microenvironment of PCa. We found that the expression of NEAT1 was higher in PCa than in non-neoplastic tissues. The cell proliferative capability of PCa cells was significantly reduced in the NEAT1 knockdown group. PCR array and bioinformatics analysis revealed that the enrichment of acidic substance-related gene sets was associated with NEAT1 expression. NEAT1 depletion inhibited PCa cell aerobic glycolysis accompanied by the reduction of lactate levels in the medium. Further, we found that lactate dehydrogenase A (LDHA) expression was positively regulated by NEAT1. At last, co-culture systems indicated that NEAT1 or LDHA knockdown promoted the secretion of CD8+ T-lymphocyte factors, including TNF-α, IFN-γ, and Granzyme B, and enhanced the antitumor effects.

Histone demethylase JMJD1C promotes the polarization of M1 macrophages to prevent glioma by upregulating miR-302a.

Glioma is regarded as an aggressive lethal primary brain tumor. Jumonji domain containing 1C (JMJD1C) is a H3K9 demethylase which participates in the progression of various tumors, but its specific function and underlying mechanism in glioma development remain undefined, which is the purpose of our work. We initially assessed JMJD1C expression in glioma tissues and cells using the assays of RT-qPCR and immunohistochemistry. Meanwhile, the H3K9 level at the microRNA (miR)-302a promoter region was measured by chromatin immunoprecipitation assay, while luciferase-based reporter assay was performed for validation of the binding affinity between miR-302a and methyltransferase-like 3 (METTL3). The effect of METTL3 on suppressor of cytokine signaling 2 (SOCS2) was subsequently analyzed by MeRIP-RT-qPCR. Finally, a xenograft tumor model was established in nude mice, followed by measurement of tumor-associated macrophages using flow cytometry. JMJD1C was poorly expressed in glioma tissues. Furthermore, JMJD1C increased miR-302a expression through promoting H3K9me1 demethylation at the miR-302a promoter region. miR-302a was identified to target METTL3, which could inhibit SOCS2 expression via m6A modification. JMJD1C promoted M1 macrophage polarization and suppressed the growth of glioma xenografts through the miR-302a/METTL3/SOCS2 axis both in vivo and in vitro. In conclusion, JMJD1C could enhance M1 macrophage polarization to inhibit the onset of glioma, bringing a new insight into the contribution of JMJD1C to the pathobiology of glioma, with possible implications for targeted therapeutic method.

LINC00511 knockdown suppresses glioma cell malignant progression through miR-15a-5p/AEBP1 axis.

BACKGROUND: A strong relationship between long intergenic non-protein coding RNA 511 (LINC00511) and glioma has been previously reported but the mechanism of LINC00511 in glioma is yet to be determined. This study examined the mechanism of LINC00511 in glioma. METHODS: The expression of LINC00511 in glioma was determined by bioinformatics analysis and real-time quantitative PCR (RT-qPCR) analysis. The target relationship between genes was predicted by starBase, TargetScan, and was verified by dual-luciferase. Subsequently, siRNA targeting LINC00511 (siLINC00511) and miR-15a-5p mimic were transfected into glioma cells to examine the effect on biological characteristics using cell counting kit-8, clone formation, flow cytometry, wound-healing, and transwell. MiR-15a-5p inhibitor and AEBP1 were used for in vitro rescue experiments, and tumorigenesis assay and immunohistochemical assays were performed for in vivo experiments. Epithelial-mesenchymal transition (EMT) and p65 phosphorylation were examined by Western blot. RESULTS: LINC00511 was predicted and verified to be up-regulated in glioma. SiLINC00511 suppressed cell viability, proliferation, migration and invasion, accelerated apoptosis of glioma cells. Mechanically, siLINC00511 promoted E-cadherin expression but suppressed N-cadherin and Snail expressions. MiR-15a-5p bound to LINC00511, and miR-15a-5p inhibitor partially reversed the effect and regulation of siLINC00511 on glioma cells. AEBP1, a target gene of miR-15a-5p, could activate p65 phosphorylation to promote EMT protein expression and partially reverse the inhibitory effect of miR-15a-5p mimic on the malignant phenotype of glioma cells. SiLINC00511 inhibited tumor growth, down-regulated miR-15a-5p expression and up-regulated AEBP1 and Ki67 expressions in vivo. CONCLUSION: LINC00511 knockdown inhibits glioma cell progression via miR-15a-5p/AEBP1 axis.

Matrix stiffness promotes glioma cell stemness by activating BCL9L/Wnt/ß-catenin signaling.

Matrix stiffness is a key physical characteristic of the tumor microenvironment and correlates tightly with tumor progression. Here, we explored the association between matrix stiffness and glioma development. Using atomic force microscopy, we observed higher matrix stiffness in highly malignant glioma tissues than in low-grade/innocent tissues. In vitro and in vivo analyses revealed that culturing glioma cells on stiff polyacrylamide hydrogels enhanced their proliferation, tumorigenesis and CD133 expression. Greater matrix stiffness could obviously up-regulated the expression of BCL9L, thereby promoting the activation of Wnt/ß-catenin signaling and ultimately increasing the stemness of glioma cells. Inhibiting Wnt/ß-catenin signaling using gigantol consistently improved the anticancer effects of chemotherapy and radiotherapy in mice with subcutaneous glioma tumors. These findings demonstrate that a stiffer matrix increases the stemness of glioma cells by activating BCL9L/Wnt/ß-catenin signaling. Moreover, we have provided a potential strategy for clinical glioma treatment by demonstrating that gigantol can improve the effectiveness of traditional chemotherapy/radiotherapy by suppressing Wnt/ß-catenin signaling.

Remodeling cancer stemness by collagen/fibronectin via the AKT and CDC42 signaling pathway crosstalk in glioma.

Cancer development is a complex set of proliferative progression, which arises in most cases via multistep pathways associated with various factors, including the tumor microenvironment and extracellular matrix. However, the underlying mechanisms of cancer development remain unclear and this study aimed to explore the role of extracellular matrix in glioma progression. Methods: The expression of type I collagen and fibronectin in tumor tissues from glioma patients was examined by immunofluorescence staining. The correlations between collagen/fibronectin and glioma progression were then analyzed. A 3D collagen/fibronectin cultured system was established for tumor cells culture in vitro. Quantitative, real-time PCR and western blot were used to detect PI3K/ATK and CDC42 signals associated proteins expression in glioma. We used in vitro Cell Counting Kit-8, colony formation, and tumorigenesis assays to investigate the function of PI3K/AKT and CDC42 signals associated proteins. A xenograft glioma mice model was also used to study the anticancer effects of integrin inhibitor in vivo. Results: Our study demonstrated that type I collagen and fibronectin collaborate to regulate glioma cell stemness and tumor growth. In a 3D collagen/fibronectin culture model, glioma cells acquired tumorigenic potential and revealed strengthened proliferative characteristics. More significantly, collagen/fibronectin could facilitate the activation of PI3K/AKT/SOX2 and CDC42/YAP-1/NUPR1/Nestin signaling pathways via integrin αvß3, eliciting sustained tumor growth and cancer relapse. Combination of the integrin signaling pathway inhibitor and the chemotherapeutic agent efficiently suppressed glioma cell proliferation and tumorigenic ability. Conclusion: We demonstrated that type I collagen and fibronectin could collaborate to promote glioma progression through PI3K/AKT/SOX2 and CDC42/YAP-1/NUPR1/Nestin signaling pathways. Blockade of the upstream molecular integrin αvß3 revealed improved outcome in glioma therapy, which provide new insights for eradicating tumors and reducing glioma cancer relapse.

Study on the Effect of Polymer Nano-Loaded Drug System on Bladder Cancer Perfusion.

Bladder tumor is a malignant tumor on bladder mucosa and the most common malignant tumor of urinary system. At present, bladder cancer is mainly treated by surgical resection and intravesical infusion of anticancer drugs. The high-molecular nano-drug-loading system has the advantages of direct focus of the drug in the treatment of cancer, reduced systemic toxicity and high local concentration. The purpose of this paper was to study the effect of polymer nano-drug loading system on bladder cancer perfusion. The synthesized polymer was applied to the establishedmouse bladder cancer model, the anticancer effect of polymer nano-drug loading system on mice in vivo was observed, and the health status of mice during administration was determined. It was found that a large number of drugs could adhere to the tumor tissue after perfusion of bladder cancer with polymer nano-drug loading system, and the effect of killing bladder cancer cells was better.

[Relationship of prostate volume and inflammatory cell infiltration with the positive rate of prostate biopsy].

OBJECTIVE: To investigate the factors influencing the positive rate of prostate biopsy and its relationship with the prostate volume and inflammatory cell infiltration (ICI). METHODS: We retrospectively analyzed the clinical data on 230 cases of double-plane transrectal ultrasound-guided prostate biopsy in our Department of Urology, including the patients' age, body mass index (BMI), serum total prostate-specific antigen (tPSA), PSA density (PSAD), prostate volume, and ICI in the prostate tissue. We also investigated the relationship of the above factors with the pathological results of prostate biopsy by binary logistic regression analysis. RESULTS: The positive rate of prostate biopsy was 38.7% (89/230) in the total number of cases, 28.57% (n = 56) in the 196 cases with tPSA < 100 µg/L, and 97.06% (n = 33) in the 34 cases with tPSA ≥ 100 µg/L. Binary logistic regression analysis showed that the positive rate of prostate biopsy in those with tPSA < 100 µg/L was correlated positively with age (P < 0.01, OR = 1.09), tPSA (P < 0.01, OR = 1.04) and PSAD (P < 0.01, OR = 10.04), negatively with the prostate volume (P < 0.01, OR = 0.98) and ICI (P < 0.01, OR = 0.22), but not with BMI (P > 0.05). As a predictor of positive prostate biopsy, tPSA > 10 µg/L exhibited a sensitivity of 82.14% and a specificity of 35.71%, while PSAD > 0.26 showed a sensitivity of 78.57% and a specificity of 71.43%. CONCLUSIONS: Non-specific elevation of the tPSA level induced by increased prostate volume and inflammatory cell infiltration may lead to unnecessary biopsies in some patients. As a predictor of positive prostate biopsy, PSAD > 0.26 has a higher clinical application value than tPSA > 10 µg/L.

Establishing a novel prediction model for improving the positive rate of prostate biopsy.

BACKGROUND: At present, prostate-specific antigen (PSA) is the primary evaluation index for judging the necessity of prostate cancer (PCa) biopsy. However, there is a high false-positive rate and a low predictive value due to many interference factors. In this study, we tried to find a novel prediction model that could improve the positive rate of prostate biopsy and reduce unnecessary biopsy. METHODS: We retrospectively studied 237 patients, including their age, body mass index (BMI), PSA, prostate volume (PV), prostate imaging-reporting and data system (PI-RADS) v2 score, neutrophil-lymphocyte ratio (NLR), biopsy Gleason score (BGS), and other information. The univariate and multivariate logistic analyses were used to screen out indicators related to PCa. After establishing a prediction formula model, we used receiver operating characteristic (ROC) curves to assess its prediction performance. RESULTS: Our study found that age, PSA, PI-RADS v2 score, and diabetes significantly correlated with PCa. Based on multivariate logistic regression analysis results, we created the following prediction formula: Y = 2.599 × PI-RADS v2 score + 1.766 × diabetes + 0.052 × age + 1.005 × PSAD - 9.119. ROC curves showed the formula's threshold was 0.3543. The composite formula had an excellent capacity to detect PCa with the area under the curve (AUC) of 0.91. In addition, the composite formula also achieved significantly better sensitivity, specificity, and diagnostic accuracy than PSA, PSA density (PSAD), and PI-RADS v2 score alone. CONCLUSIONS: Our predictive formula predicted performance better than PSA, PSAD, and PI-RADS v2 score. It can thus contribute to the diagnosis of PCa and be used as an indicator for prostate biopsy, thereby reducing unnecessary biopsy.

Multi-syphilitic gummas in pituitary and cerebellopontine angle in a patient.

PURPOSE: Multi-syphilitic gummas in pituitary and cerebellopontine angle (CPA) are extremely rare and easily misdiagnosed especially in patients with antibiotic abuse. We write this paper for clinicians to better understanding of cerebral gumma. METHODS: We report a patient with syphilitic gummas in pituitary and left CPA. The definite diagnosis is made by histopathology after surgery. RESULTS: A 49-years-old woman suffered from headaches with tinnitus and hypoacusis in left ear. She was diagnosed with syphilis but untreated. There were no chancre and rashes in the course of disease. Syphilis serological tests were positive. Brain MRI found two masses located in the left CPA and hypophysial fossa. The two masses were removed successively. We found a large number of Treponemapallidum in paraffin-embedded specimens by immunohistochemical staining. CONCLUSIONS: Syphilitic gummas in pituitary and CPA are similar to benign or malignant brain tumors, easily leading to misdiagnosis. Gumma should be considered in differential diagnosis when a patient has unexplained nervous system symptoms or signs and imaging findings suggest intracranial mass in syphilis seropositive patients.