Multivariate analyses on male factors and construction of a nomogram for predicting low in vitro fertilization rate.

Low fertilization rate (LFR) and total fertilization failure (TFF) are often encountered in routine in vitro fertilization (IVF) procedure. To solve this problem, multivariate analyses on the relationship between male factors and in vitro fertilization rate were performed, and a nomogram for prediction of LFR was constructed. This retrospective study contained 2011 couples who received IVF treatment from January 2017 to December 2021. Man factors and in vitro fertilization rate were collected. Among these couples, 1347 cases had in vitro fertilization rates ≥30 % (control group), and 664 cases had in vitro fertilization rates <30 % (LFR group). Univariate analyses of male factors found that between the two groups there were significant differences (p < 0.05) in sperm progressive motility (SPR), sperm concentration (SC), total sperm number, normal sperm morphology rate (NSMR), DNA fragmentation index (DFI), sperm acrosin activity (SAA) and the clinical diagnosis of primary or secondary infertility. Multivariate logistic regression analyses showed that SPR, SAA, and SC were independent risk factors for LFR. An algorithm and a correspondent nomogram for predicting high LFR risk were constructed using data from the training cohort. The LFR nomogram exhibited an excellent discrimination power and a high fitting degree in both the training cohort (AUC = 0.90, 95 % CI: 0.88-0.92), (H-L: x2 = 5.43, p = 0.71) and validation cohort (AUC = 0.89, 95 % CI:0.87-0.92), (H-L: x2 = 7.85, p = 0.45), respectively. The decision curve analysis (DCA) demonstrated a high efficiency of the LFR nomogram for clinical utility. SPR, SAA, and SC are independent risk factors for LFR. The LFR nomogram established based on these factors could be a useful tool to predict high risk of LFR, and patients with high risk of LFR can be guided to direct ICSI procedure. Clinical application of the LFR nomogram may increase the in vitro fertilization rate by facilitating the decision making in IVF service.

Identification of an anaplastic subtype of prostate cancer amenable to therapies targeting SP1 or translation elongation.

Histopathological heterogeneity is a hallmark of prostate cancer (PCa). Using spatial and parallel single-nucleus transcriptomics, we report an androgen receptor (AR)-positive but neuroendocrine-null primary PCa subtype with morphologic and molecular characteristics of small cell carcinoma. Such small cell-like PCa (SCLPC) is clinically aggressive with low AR, but high stemness and proliferation, activity. Molecular characterization prioritizes protein translation, represented by up-regulation of many ribosomal protein genes, and SP1, a transcriptional factor that drives SCLPC phenotype and overexpresses in castration-resistant PCa (CRPC), as two potential therapeutic targets in AR-indifferent CRPC. An SP1-specific inhibitor, plicamycin, effectively suppresses CRPC growth in vivo. Homoharringtonine, a Food And Drug Administration-approved translation elongation inhibitor, impedes CRPC progression in preclinical models and patients with CRPC. We construct an SCLPC-specific signature capable of stratifying patients for drug selectivity. Our studies reveal the existence of SCLPC in admixed PCa pathology, which may mediate tumor relapse, and establish SP1 and translation elongation as actionable therapeutic targets for CRPC.

Comprehensiveness cuproptosis related genes study for prognosis and medication sensitiveness across cancers, and validation in prostate cancer.

Cuproptosis-related genes (CRGs) are important for tumor development. However, the functions of CRGs across cancers remain obscure. We performed a pan-cancer investigation to reveal the roles of CRGs across cancers. In an analysis of 26 cancers, 12 CRGs were differentially expressed, and those CRGs were found to have prognostic value across different cancer types. The expression of CRGs exhibited varied among tumors of 6 immune subtypes and were significantly correlated with the 16 sensitivities of drugs. The expression of CRGs were highly correlated with immunological subtype and tumor microenvironment (TME) of prostate cancer. We also established CRGs-related prognostic signatures that closely correlated with prognosis and drug sensitivity of prostate cancer patients. Single-cell RNA-seq revealed that several CRGs were enriched in the cancer cells. Finally, an in vitro experiment showed that elesclomol, a cuproptosis inducer, targets ferredoxin 1 and suppress cell viability in prostate cancer cells. In conclusion, we carried out a comprehensive investigation for determining CRGs in differential expression, prognosis, immunological subtype, TME, and cancer treatment sensitivity across 26 malignancies; and validated the results in prostate cancer. Our research improves pan-cancer knowledge of CRGs and identifies more effective immunotherapy strategies.

Modified Ileal Conduit for Pelvic Lipomatosis: Technique Description and Outcome.

INTRODUCTION: To present the surgical technique and clinical outcomes of modified ileal conduit for pelvic lipomatosis (PL). METHODS: From 2020 to 2022, we prospectively enrolled 9 patients with PL undergoing modified ileal conduit. The patient characteristics, perioperative variables, and follow-up outcomes as well as the description of surgical technique were reported. RESULTS: All 9 patients successfully completed the operation. Two patients had perioperative complications of Clavien-Dindo grade I. The mean operation time and bleeding volumes were 253±51.4 min and 238.9±196.9 ml, with a mean postoperative follow-up time of 13.0±5.6 months. The postoperative 3-month and 1-year creatinine values were significantly decreased versus the preoperative (P=0.006 and P=0.024). The postoperative 3-month and 1-year eGFR values were significantly increased comapred with those before operation (P=0.0002 and P=0.018). The separation value of left renal pelvis collection system after operation were significantly reduced compared with preoperative evaluation (P=0.023 at 3 month and P=0.042 at 1 year) and so was the right side (P=0.019 and P=0.023). CONCLUSION: Modified ileal conduit is safe and feasible for PL. A large sample cohort with long-term follow-up is needed to evaluate the clinical outcomes of PL.

[Retracted] Human HLA­F adjacent transcript 10 promotes the formation of cancer initiating cells and cisplatin resistance in bladder cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the cellular morphological data in Fig. 1C, the immunofluorescence data shown in Fig. 1E, and certain of the scratch­wound assay data shown in Fig. 2A were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 308­314, 2018; DOI: 10.3892/mmr.2018.9005].

Impact of coexisting type 2 diabetes mellitus on the urinary microbiota of kidney stone patients.

Objectives: Type 2 diabetes mellitus (T2DM) commonly complicates kidney stone disease (KSD). Our objective is to investigate the variations in the urinary microbiota between individuals with KSD alone and those with KSD plus T2DM. This exploration could have implications for disease diagnosis and treatment strategies. Methods: During lithotripsy, a ureterscope was employed, and 1 mL of urine was collected from the renal pelvis after bladder disinfection. Sequencing targeting the V3-V4 hypervariable region was performed using the 16S rRNA and Illumina Novaseq platform. Results: The Shannon index showed a significant decrease in the KSD plus T2DM group compared to the KSD-only group (false discovery rate = 0.041). Principal Coordinate Analysis (PCoA) demonstrated a distinct bacterial community in the KSD plus T2DM group compared to the KSD-only group (false discovery rate = 0.027). The abundance of Sphingomonas, Corynebacterium, and Lactobacillus was significantly higher in the KSD plus T2DM group than in the KSD-only group (false discovery rate < 0.05). Furthermore, Enhydrobacter, Chryseobacterium, and Allobaculum were positively correlated with fasting blood glucose and HbA1c values (P < 0.05). Conclusions: The urinary microbiota in the renal pelvis exhibits differences between patients with KSD plus T2DM and those with KSD alone. Further studies employing animal models are necessary to validate these distinctions, potentially paving the way for therapeutic developments based on the urinary microbiota.

Effects of miR-214 on adenosine A2A receptor and carboxymethyl chitosan nanoparticles on the function of keloid fibroblasts and their mechanisms.

This work prepared and investigated the impact of carboxymethyl chitosan nanoparticles (MC-NPs) on the proliferative capability of keloid fibroblasts (KFBs) while analyzing the mechanistic roles of miR-214 and adenosine A2A receptor (A2AR) in fibroblasts within hypertrophic scars. MC-NPs were synthesized through ion cross-linking, were characterized using transmission electron microscopy (TEM) and laser particle size scattering. The influence of MC-NPs on the proliferation capacity of KFBs was assessed using the MTT method. Changes in the expression levels of miR-214 and A2AR in KFBs, normal skin fibroblasts (NFBs), hypertrophic scar tissue, and normal skin tissue were analyzed. KFBs were categorized into anti-miR-214, anti-miR-NC, miR-214 mimics, miR-NC, si-A2AR, si-con, anti-miR-214+ si-con, and anti-miR-214+ si-A2AR groups. Bioinformatics target prediction was conducted to explore the interaction between miR-214 and A2AR. Real-time quantitative PCR and immunoblotting (WB) were employed to detect the expression levels of miR-214, A2AR, apoptotic protein Bax, and TGF-ß in different cells. Cell counting kit-8 (CCK8) and flow cytometry were employed to assess cell proliferation activity and apoptosis. The results indicated that MC-NPs exhibited spherical particles with an average diameter of 236.47 ± 4.98 nm. The cell OD value in the MC-NPs group was lower than that in KFBs (P < 0.05). The mRNA levels of miR-214 in KFBs and hypertrophic scar tissue were lower than those in NFBs and normal tissue (P < 0.001), while the mRNA and protein levels of A2AR were significantly elevated (P < 0.05). Compared to the control group and anti-miR-NC, the anti-miR-214 group showed significantly increased cell OD values and Bcl-2 protein expression (P < 0.001), decreased levels of apoptotic gene Bax protein, TGF-ß gene mRNA, and protein expression (P < 0.001). Continuous complementary binding sites were identified between miR-214 and A2AR. Compared to the control group, the si-A2AR group exhibited a significant decrease in A2AR gene mRNA and protein expression levels (P < 0.001), reduced cell viability (P < 0.001), increased apoptosis rate (P < 0.001), and a significant elevation in TGF-ß protein expression (P < 0.001). miR-214 targetedly regulated the expression of A2AR, inducing changes in TGF-ß content, promoting the proliferation of keloid fibroblasts, and inhibiting cell apoptosis.

Decanoylcarnitine Inhibits Triple-Negative Breast Cancer Progression via Mmp9 in an Intermittent Fasting Obesity Mouse.

Purpose: Treatment of triple-negative breast cancer (TNBC) remains challenging. Intermittent fasting (IF) has emerged as a promising approach to improve metabolic health of various metabolic disorders. Clinical studies indicate IF is essential for TNBC progression. However, the molecular mechanisms underlying metabolic remodeling in regulating IF and TNBC progression are still unclear. Methods: In this study, we utilized a robust mouse model of TNBC and exposed subjects to a high-fat diet (HFD) with IF to explore its impact on the metabolic reprogramming linked to cancer progression. To identify crucial serum metabolites and signaling events, we utilized targeted metabolomics and RNA sequencing (RNA-seq). Furthermore, we conducted immunoblotting, real-time quantitative polymerase chain reaction (RT-qPCR), cell migration assays, lentivirus-mediated Mmp9 overexpression, and Mmp9 inhibitor experiments to elucidate the role of decanoylcarnitine/Mmp9 in TNBC cell migration. Results: Our observations indicate that IF exerts notable inhibitory effects on both the proliferation and cancer metastasis. Utilizing targeted metabolomics and RNA-seq, we initially identified pivotal serum metabolites and signaling events in the progression of TNBC. Among the 349 serum metabolites identified, decanoylcarnitine was picked out to inhibit TNBC cell proliferation and migration. RNA-seq analysis of TNBC cells treated with decanoylcarnitine revealed its suppressive effects on extracellular matrix-related protein components, with a notable reduction observed in Mmp9. Further investigations confirmed that decanoylcarnitine could inhibit Mmp9 expression in TNBC cells, primary tumors, lung, and liver metastasis tissues. Mmp9 overexpression abolished the inhibitory effect of decanoylcarnitine on cell migration. Conclusion: This study pioneers the exploration of IF intervention and the role of decanoylcarnitine/Mmp9 in the progression of TNBC in obese mice, enhancing our comprehension of the potential roles of various dietary patterns in the process of cancer treatment.

Identification of PRDX5 as A Target for The Treatment of Castration-Resistant Prostate Cancer.

Treatment of castration-resistant prostate cancer (CRPC) is a long-standing clinical challenge. Traditionally, CRPC drugs work by either reducing dihydrotestosterone biosynthesis or blocking androgen receptor (AR) signaling. Here it is demonstrated that AR inhibitor treatment gives rise to a drug-tolerant persister (DTP) state. The thioredoxin/peroxiredoxin pathway is up-regulated in DTP cells. Peroxiredoxin 5 (PRDX5) promotes AR inhibitor resistance and CRPC development. Inhibition of PRDX5 suppresses DTP cell proliferation in culture, dampens CRPC development in animal models, and stabilizes PSA progression and metastatic lesions in patients. Therefore, the study provides a novel mechanism and potential target for the management of castration-resistant prostate cancer.

Identification and validation of obesity related genes signature based on microenvironment phenotypes in prostate adenocarcinoma.

BACKGROUND: The role of obesity related genes (ORGs) in the immune checkpoint inhibitors (ICIs) treatment of prostate adenocarcinoma (PRAD) has not yet been proved by research. METHODS: We comprehensively evaluated the ORGs patterns in PRAD based on tumor microenvironment (TME) phenotypes and immunotherapy efficacies. Then we constructed a ORGs risk score for prognosis and a ORGs signature for accurate prediction of TME phenotype and immunotherapy efficacy in order to evaluate individual patients. RESULTS: Two distinct ORGs patterns were generated. The two ORGs patterns were consistent with inflammatory and non-inflammatory TME phenotypes. ORGs patterns had an important role for predicting immunotherapy efficacies. Next, we constructed a ORGs risk score for predicting each patient's prognosis with high performance in TCGA-PRAD. The ORGs risk score could be well verified in the external cohorts including GSE70769 and GSE21034. Then, we developed a ORGs signature and found it was significantly positively correlated with tumor-infiltrating lymphocytes in TCGA-PRAD. We found that each patient in the high-risk ORGs signature group represented a non-inflamed TME phenotype on the single cell level. The patients with high ORGs signature had more sensitivity to immunotherapy. And those ORGs were verified. CONCLUSIONS: ORGs pattern depicts different TME phenotypes in PRAD. The ORGs risk score and ORGs signature have an important role for predicting prognosis and immunotherapy efficacies.

SETD4 inhibits prostate cancer development by promoting H3K27me3-mediated NUPR1 transcriptional repression and cell cycle arrest.

The suppressor of variegation enhancer of zeste-trithorax (SET) domain methyltransferases have been reported to function as key regulators in multiple tumor types by catalyzing histone lysine methylation. Nevertheless, our understanding on the role of these lysine methyltransferases, including SETD4, in prostate cancer (PCa) remains limited. Hence, the specific role of SETD4 in PCa was investigated in this study. The expression of SETD4 in PCa cells and tissue samples was downregulated in PCa cells and tissue specimens, and decreased SETD4 expression led to inferior clinicopathological characteristics in patients with PCa. knockdown of SETD4 facilitated the proliferation of PCa cells and accelerated cell cycle progression. Mechanistically, SETD4 repressed NUPR1 transcription by methylating H3K27 to generate H3K27me3, subsequently inactivated Akt pathway and impeded the tumorigenesis of PCa. Our results highlight that SETD4 prevents the development of PCa by catalyzing the methylation of H3K27 and suppressing NUPR1 transcription, subsequently inactivating the Akt signaling pathway. The findings suggest the potential application of SETD4 in PCa prognosis and therapeutics.

Identification of the H3K36me3 reader LEDGF/p75 in the pancancer landscape and functional exploration in clear cell renal cell carcinoma.

Lens epithelium-derived growth factor (LEDGF/p75) is a reader of epigenetic marks and a potential target for therapeutic intervention. Its involvement in human immunodeficiency virus (HIV) integration and the development of leukemia driven by MLL (also known as KMT2A) gene fusion make it an attractive candidate for drug development. However, exploration of LEDGF/p75 as an epigenetic reader of H3K36me3 in tumors is limited. Here, for the first time, we analyze the role of LEDGF/p75 in multiple cancers via multiple online databases and in vitro experiments. We used pancancer bulk sequencing data and online tools to analyze correlations of LEDGF/p75 with prognosis, genomic instability, DNA damage repair, prognostic alternative splicing, protein interactions, and tumor immunity. In summary, the present study identified that LEDGF/p75 may serve as a prognostic predictor for tumors such as adrenocortical carcinoma, kidney chromophobe, liver hepatocellular carcinoma, pancreatic adenocarcinoma, skin cutaneous melanoma, and clear cell renal cell carcinoma (ccRCC). In addition, in vitro experiments and gene microarray sequencing were performed to explore the function of LEDGF/p75 in ccRCC, providing new insights into the pathogenesis of the nonmutated SETD2 ccRCC subtype.

An electrochemical biosensor based on network-like DNA nanoprobes for detection of mesenchymal circulating tumor cells.

The identification and detection of mesenchymal circulating tumor cells （mCTCs） is important for early warning of tumor metastasis. The majority of conventional detection methods for CTCs rely on the recognition of epithelial biomarkers, which is technically challenging for detecting CTCs with epithelial-mesenchymal transition (EMT)-induced phenotypic alteration. In this work, we have constructed a label-free biosensor for sensitive electrochemical assay of mCTCs. In our design, the capture probe can recognize the vimentin overexpressed on the surface of mCTCs with high specificity. Meantime, the network-like DNA nanoprobes with multiple G-quadruplex/hemin complexes and multiple cholesterol molecules can be grafted to the cell surface based on the high affinity between cholesterol molecules and cell membrane. Owing to the mimic horseradish peroxidase of G-quadruplex/hemin complexes, strong electrochemical responses will be obtained for sensitive quantification of mCTCs with a detection limit of 8 cell mL-1. Moreover, the biosensor can effectively overcome the interference of vimentin negative cells or secretory vimentin, and realize the recovery tests in whole blood with high accuracy, thereby may further promoting the diagnosis and personalized treatment of cancer in clinic.

Cis-monounsaturated fatty acids inhibit ferroptosis through downregulation of transferrin receptor 1.

Ferroptosis, a form of cell death mediated by lipid peroxidation, is implicated in various pathological processes. Although monounsaturated fatty acids (MUFAs) can inhibit ferroptotic lipid peroxidation, the underlying structural mechanism of this antagonistic effect remains poorly understood. We hypothesized that MUFAs with different structures (including chain length, conformation, and double bond position) may affect their regulatory effect on ferroptosis. In this study, 11 MUFAs with varying structures were screened to identify those with an inhibitory effect on ferroptosis. Results from 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazoliumbromide assays indicated that only exogenous MUFAs with cis-conformation and centered double bond could inhibit ferroptosis. Meanwhile, it was found that suppressing the expression of SCD1 and SCD5 genes could sensitize cells to ferroptosis indicating the protective role of endogenous MUFA against ferroptosis. Additionally, western blot analysis revealed that cis-MUFAs with centered double bond downregulated the protein levels of transferrin receptor 1. Flow cytometry confirmed that these MUFAs led to decreases in intracellular iron, reactive oxygen species, and lipid peroxides. It was also found that SCD1 inhibitor could enhance ferroptosis inducer-mediated tumor suppression both in vivo and in vitro. Overall, these findings shed light on the particular structural features of MUFAs that contribute to their ferroptosis-resistant properties and suggest the potential therapeutic relevance of natural MUFAs in a range of ferroptosis-related diseases.

Can antibiotics for enteritis or for urinary tract infection disrupt the urinary microbiota in rats?

Background: To establish antibiotic preregimes and administration routes for studies on urinary microbiota. Methods and materials: Antibiotics for enteritis (Abx-enteritis) and UTIs (Abx-UTI) were administered via gavage and/or urinary catheterisation (UC) for 1 and/or 2 weeks. The effects of these Abx on the urinary microbiota of rats were examined via 16S rRNA sequencing and urine culture, including anaerobic and aerobic culture. Additionally, the safety of the Abx was examined. Results: Abx-enteritis/Abx-UTI (0.5 g/L and 1 g/L) administered via gavage did not alter the microbial community and bacterial diversity in the urine of rats (FDR > 0.05); however, Abx-UTI (1 g/L) administered via UC for 1 and 2 weeks altered the urinary microbial community (FDR < 0.05). Rats administered Abx-UTI (1 g/L) via UC for 1 week demonstrated a distinct urinary microbiota in culture. Abx-enteritis/Abx-UTI administered via gavage disrupted the microbial community and reduced bacterial diversity in the faeces of rats (FDR < 0.05), and Abx-UTI administered via UC for 2 weeks (FDR < 0.05) altered the fecal microbiota. Abx-UTI (1 g/L) administered via UC did not alter safety considerations. In addition, we noticed that UC did not induce infections and injuries to the bladder and kidney tissues. Conclusions: Administration of Abx-UTI via UC for 1 week can be considered a pre-treatment option while investigating the urinary microbiota.

Iodide-Enhanced Perovskite Nanozyme-Based Colorimetric Platform for Detection of Urinary Nuclear Matrix Protein 22.

In the last decade, perovskite nanocrystals (PNCs) have brought extensive thinking owing to their excellent optical properties. Recently, we have uncovered the peroxidase-like activity of PNCs and used this for detecting many small molecules; however, the low enzymatic activity makes them unsuitable for fluorescence analysis, which is easily disturbed by the autofluorescence of biological media. This greatly limits their application in bioanalysis. Thus, the development of a method to facilely modulate the activity of PNCs for the instrument-free colorimetric detection is highly desirable. Herein, we demonstrated an iodide-enhanced perovskite nanozyme-based colorimetric platform for the visual assay of urinary nuclear matrix protein 22 (NMP22), a typical biomarker for the diagnosis of bladder cancer. We discovered that halogen could regulate the activity of perovskite nanozymes through a simple anion replacement reaction. Experimental analysis suggested that CsPbI3 nanocrystals (NCs) displayed 24-fold higher catalytic efficiency than classical CsPbBr3 NCs. As a proof-of-concept assay, the CsPbI3 NCs could be explored into an immunoassay for the detection of NMP22 in clinical urine specimens, resulting in a low detection limit of 0.03 U/mL. This iodide-enhanced immunoassay deepens our understanding of perovskite nanozymes and also provides great potential for bioanalysis.

AF9 targets acetyl-modified STAT6 to diminish purine metabolism and accelerate cell apoptosis during metastasis.

Cell migration and invasion are two important steps for tumour metastasis, and involved the behaviors including metabolism remodeling and anti-apoptosis. However, it's still elusive that cancer cells how to antagonize apoptosis during tumour metastasis. In this study, we observed that super elongation complex (SEC) subunit AF9 depletion exacerbated cell migration and invasion but reduced the apoptosis during invasive migration. Mechanically, AF9 targeted acetyl (Ac)-STAT6 at lysine (K) 284 and blocked STAT6 transactivation on the promoter of such genes involved in regulating purine metabolism and metastasis, in turn induced apoptosis of suspended cells. Of note, AcSTAT6-K284 was not induced by IL4 signaling but decreased by limited nutrition which triggered SIRT6 to remove acetyl group at STAT6-K284. The functional experiments proved that AcSTAT6-K284 attenuated cell migration and invasion depending on AF9 expression level. Animal metastatic study further confirmed the AF9/AcSTAT6-K284 axis existed and blocked kidney renal clear cell carcinoma (KIRC) metastasis. In clinical, both AF9 expression and AcSTAT6-K284 were decreased accompanied by the advanced tumour grade and positively correlated with KIRC patients' survival. Conclusively, we explored an inhibitory axis which not only suppressed tumour metastasis but also could be utilized for drug development to hamper KIRC metastasis.

Multiparametric Magnetic Resonance Imaging-based Prostate Specific Antigen Density and PI-RADSv2 score help identify Apical Prostate Cancer.

Objective: To investigate the potential roles of preoperative multiparametric magnetic resonance imaging (mpMRI) in identifying aggressive apical prostate cancer (APCa), thereby helping to facilitate patient counseling and surgical planning. Patients and Methods: We performed a retrospective analysis of 662 patients who underwent radical prostatectomy (RP) between January 2010 to October 2019. All patients underwent a preoperative biopsy and mpMRI of the prostate. APCa was defined as any malignant lesions in the prostatic apex. Clinical, pathological and mpMRI variables were retrieved. Univariate, multivariate, and receiver operating characteristic (ROC) analyses were performed. Results: A total of 214 (32.3%) patients had APCa. Patients presenting APCa were more likely to harbor adverse clinicopathological features (all p < 0.05). On univariable analysis, serum prostate-specific antigen (PSA) (p < 0.001), mpMRI-based PSA density (PSAD) (p < 0.001), Prostate Imaging Reporting and Data System version 2 (PI-RADSv2) score (p < 0.001), number of positive cores (p < 0.001), percentage of positive cores (p < 0.001), max core involvement (p < 0.001) and biopsy GG (p = 0.001) were significant predictors of APCa. On multivariable analysis, mpMRI-based PSAD ≥ 0.27 ng/ml/cm3 (odds ratio [OR]: 2.251, p = 0.003), PI-RADSv2 score > 4 (OR: 1.611, p = 0.023) and percentage of positive cores (OR: 2.333, p = 0.041) were independently predictive of APCa during RP. The AUC values of mpMRI-based PSAD and PI-RADSv2 score were 0.646 (95% Confidence Intervals [CI]: 0.608-0.682) and 0.612 (95% CI: 0.568-0.656), respectively. Conclusion: Preoperative mpMRI-based PSAD and PI-RADSv2 score help identify the presence of APCa and may be useful for surgical decision-making during RP.

Laparoscopic bilateral ileal ureter replacement for bilateral long-segment ureteral strictures: a case series of nine patients.

Background: The treatment of bilateral long segment ureteral strictures is challenging. Minimally invasive bilateral ileal ureter replacement has been presented with limited experience. This study presents the results of the largest known sample size of minimally invasive bilateral ileal ureter replacement as well as the very first experience of minimally invasive bilateral ileal ureter replacement. Case Description: From April 2021 to October 2022, nine cases of laparoscopic bilateral ileal ureter replacement for bilateral long-segment ureteral strictures were recruited from the database of RECUTTER. Patient characteristics, perioperative data and follow-up outcomes were gathered retrospectively. Success was defined as relieved hydronephrosis and a stable renal function without serious complications. All the nine patients underwent the procedure successfully without serious complications or conversion. The median stricture length of bilateral ureters was 15 cm (range, 8-20). The median length of the ileum used was 25 cm (range, 25-30). The median operative time was 360 minutes (range, 270-400). The median estimated blood loss was 100 mL (range, 50-300). The median postoperative hospital stay was 14 days (range, 9-25). At a median follow-up of 9 months (range, 6-17), all patients maintained stable renal function and showed improvement in hydronephrosis. Four postoperative complications were recorded, including three urinary tract infections and one incomplete bowel obstruction. No serious postoperative complications occurred. Conclusions: Laparoscopic bilateral ileal ureter replacement is safe and feasible for bilateral long-segment ureteral strictures. However, a large sample size with long-term follow-up is still needed to further demonstrate it as the preferred option.