Association between serum ferritin and bone turnover marker levels in type 2 diabetes mellitus patients with non-alcoholic fatty liver disease.

OBJECTIVE: To investigate the correlation between serum ferritin (SF) and bone turnover markers in type 2 diabetes mellitus (T2DM) patients with non-alcoholic fatty liver disease (NAFLD). METHODS: Seven hundred and forty-two people with T2DM were selected. Serum bone turnover markers: osteocalcin (OC), type I procollagen N-terminal peptide (PINP), ß-I type collagen carboxy-terminal peptide (ß-CTx), and 25-hydroxyvitamin D3 (25-[OH]-D) levels were detected. High SF (HF) was defined as the indicated SF levels above 400 ng/mL in males and more than 150 ng/mL in females. Patients were divided into four groups: T2DM+normal SF (non-HF); T2DM+high SF (HF); T2DM+NAFLD+non-HF; andT2DM+NAFLD+HF. Relationships between SF and bone turnover markers were analyzed. RESULTS: Compared with the T2DM+non-HF group, ß-CTx levels were higher in the T2DM+HFgroup. Compared with the T2DM+NAFLD+non-HF group, ß-CTx levels were increased and 25-(OH)-D levels decreased in the T2DM+NAFLD+HF group (all p < 0.05). SF was positively correlated with ß-CTx [ß = 0.074; 95% CI (0.003, 0.205)] and negatively correlated with 25-(OH)-D [ß=-0.108; 95%CI (-0.006, -0.001)]. Compared with the T2DM+non-HF group, an independent positive correlation was found between ß-CTx and SF in the T2DM+NAFLD+HF group [OR = 1.002; 95% CI (1.001, 1.004)]. Among males, SF was positively correlatedwith ß-CTx [ß = 0.114; 95% CI (0.031, 0.266)]. SF was negatively correlated with 25-(OH)-D levels in both male and female patients [ß=-0.124; 95% CI (0.007,0.001) and ß=-0.168; 95% CI (-0.012, -0.002)]. Among those >50 years of age and postmenopausal females, SF was negatively correlated with 25-(OH)-D levels [ß=-0.117; 95% CI (-0.007, -0.001) and ß=-0.003; 95% CI (-0.013, -0.003)]. CONCLUSION: SF level was positively correlated with ß-CTx in T2DM patients with NAFLD, which may promote bone resorption and increase the risk of bone loss.

Efficacy and safety of the Latarjet procedure for the treatment of athletes with glenoid bone defects ≥ 20%: a single-arm meta-analysis.

BACKGROUND: The shoulder joint is the most commonly dislocated joint in the human body, and the recurrence rate exceeds 50% after nonsurgical treatment. Although surgical treatment reduces the recurrence rate, there is controversy regarding the optimal surgical approach. Previous studies suggest that the Latarjet procedure yields favourable outcomes for specific populations at risk of recurrence, such as competitive athletes with significant glenoid defects. However, most of the existing related research consists of nonrandomized controlled trials with small sample sizes, and there is a lack of strong evidence regarding the efficacy and safety of the Latarjet procedure. METHODS: The PubMed, Embase, Cochrane Library, and Web of Science databases were systematically searched. Athletes with ≥ 20% glenoid defects were selected for inclusion. The following data were extracted: general patient information, instability rates, return to sports (RTS) rates, imaging features (graft positioning rate and graft healing rate), functional assessments [Rowe score, Athletic Shoulder Outcome Scoring System(ASOSS), visual analogue scale (VAS), forward flexion function, and external rotation function], and complications. RESULTS: After excluding suspected duplicate cases, a total of 5 studies were included in this meta-analysis. The studies involved a total of 255 patients, including 237 males (93%) and 18 females (7%). The average age at the time of surgery was 25.4 ± 8.5 years. All the studies had a minimum follow-up period of 2 years, with an average follow-up time of 48.7 ± 18.9 months. The pooled rate of return to sport (RTS) was 94.3% (95% CI: 87.3%, 98.8%), and 86.1% (95% CI: 78.2%, 92.5%) of patients returned to their preoperative level of activity. The pooled redislocation rate was 1.1% (95% CI: 0%, 3.8%). Regarding the imaging results, the combined graft retention rate was 92.1% (95% CI: 88.1%, 95.5%), and the graft healing rate was 92.1% (95% CI: 88%, 95.4%). Postoperative functional evaluation revealed that the combined Rowe score, ASOSS score, and VAS score were 93.7 ± 6.5 points, 88.5 ± 4.4 points, and 1.1 ± 10 points, respectively. The forward flexion and external rotation angles were 170.9 ± 6.9 degrees and 65.6 ± 4.5 degrees, respectively. After excluding one study with unclear complications, the combined complication rate was 9.4% (95% CI: 1.0%, 23.6%). CONCLUSION: For athletes with shoulder instability and a total of ≥ 20% glenoid bone defects, the Latarjet procedure can achieve excellent functional outcomes, with the majority of patients returning to preoperative levels of sports activity. This procedure also leads to a low recurrence rate. Therefore, the Latarjet procedure has been proven to be a safe and effective treatment.

Methylation of AcGST1 Is Associated with Anthocyanin Accumulation in the Kiwifruit Outer Pericarp.

Most red-fleshed kiwifruit cultivars, such as Hongyang, only accumulate anthocyanins in the inner pericarp; the trait of full red flesh becomes the goal pursued by breeders. In this study, we identified a mutant "H-16" showing a red color in both the inner and outer pericarps, and the underlying mechanism was explored. Through transcriptome analysis, a key differentially expressed gene AcGST1 was screened out, which was positively correlated with anthocyanin accumulation in the outer pericarp. The result of McrBC-PCR and bisulfite sequencing revealed that the SG3 region (-292 to -597 bp) of AcGST1 promoter in "H-16" had a significantly lower CHH cytosine methylation level than that in Hongyang, accompanied by low expression of methyltransferase genes (MET1 and CMT2) and high expression of demethylase genes (ROS1 and DML1). Transient calli transformation confirmed that demethylase gene DML1 can activate transcription of AcGST1 to enhance its expression. Overexpression of AcGST1 enhanced the anthocyanin accumulation in the fruit flesh and leaves of the transgenic lines. These results suggested that a decrease in the methylation level of the AcGST1 promoter may contribute to accumulation of anthocyanin in the outer pericarp of "H-16".

Didymin alleviates metabolic dysfunction-associated fatty liver disease (MAFLD) via the stimulation of Sirt1-mediated lipophagy and mitochondrial biogenesis.

BACKGROUND: Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the most prevalent metabolic syndromes worldwide. However, no approved pharmacological treatments are available for MAFLD. Chenpi, one kind of dried peel of citrus fruits, has traditionally been utilized as a medicinal herb for liver diseases. Didymin is a newly identified oral bioactive dietary flavonoid glycoside derived from Chenpi. In this study, we investigated the therapeutic potential of Didymin as an anti-MAFLD drug and elucidated its underlying mechanisms. METHODS: High-fat diet (HFD)-induced MAFLD mice and alpha mouse liver 12 (AML12) cells were utilized to evaluate the effects and mechanisms of Didymin in the treatment of MAFLD. Liver weight, serum biochemical parameters, and liver morphology were examined to demonstrate the therapeutic efficacy of Didymin in MAFLD treatment. RNA-seq analysis was performed to identify potential pathways that could be affected by Didymin. The impact of Didymin on Sirt1 was corroborated through western blot, molecular docking analysis, microscale thermophoresis (MST), and deacetylase activity assay. Then, a Sirt1 inhibitor (EX-527) was utilized to confirm that Didymin alleviates MAFLD via Sirt1. Western blot and additional assays were used to investigate the underlying mechanisms. RESULTS: Our results suggested that Didymin may possess therapeutic potential against MAFLD in vitro and in vivo. By promoting Sirt1 expression as well as directly binding to and activating Sirt1, Didymin triggers downstream pathways that enhance mitochondrial biogenesis and function while reducing apoptosis and enhancing lipophagy. CONCLUSIONS: These suggest that Didymin could be a promising medication for MAFLD treatment. Furthermore, its therapeutic effects are mediated by Sirt1.

All-inside versus complete tibial tunnel techniques in anterior cruciate ligament reconstruction: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: All-inside anterior cruciate ligament reconstruction (ACLR) is a novel technique that has gained attention due to its minimally invasive. However, evidence surrounding the efficacy and safety between all-inside and complete tibial tunnel ACLR are lacking. Present work was aimed to compare clinical outcome for ACLR performed with an all-inside versus a complete tibial tunnel technique. METHODS: Systematic searches were conducted of published literature on PubMed, Embase, and Cochrane for studies according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines up to May 10, 2022. The outcomes included KT-1000 arthrometer ligament laxity test, International Knee Documentation Committee (IKDC) subjective score, Lysholm score, Tegner activity scale, and Knee Society Score (KSS) Scale, and tibial tunnel widening. Complications of interest extracted were graft re-ruptures and evaluated the graft re-rupture rate. Data from published RCTs meeting inclusion criteria were extracted and analyzed, and all the extracted data are pooled and analyzed by RevMan 5.3. RESULTS: A total of 8 randomized controlled trials involving 544 patients (consisting of 272 all-inside and 272 complete tibial tunnel patients) were included in the meta-analysis. We found clinical outcomes (International Knee Documentation Committee [IKDC] subjective score: mean difference [MD], 2.22; 95% CI, 0.23-4.22; p = 0.03; Lysholm score: MD, 1.09; 95% CI, 0.25-1.93; p = 0.01; Tegner activity scale: MD, 0.41; 95% CI, 0.11-0.71; p < 0.01; Tibial Tunnel Widening: MD = - 1.92; 95% CI, - 3.58 to - 0.25; p = 0.02; knee laxity: MD = 0.66; 95% CI, 0.12-1.20; p = 0.02; and graft re-rupture rate: RR, 1.97;95% CI, 0.50-7.74; P = 0.33) in the all-inside and complete tibial tunnel group. The findings also indicated that all-inside may be more advantageous in tibial tunnel healing. CONCLUSION: Our meta-analysis indicated that the all-inside ACLR was superior to complete tibial tunnel ACLR in functional outcomes and tibial tunnel widening. However, the all-inside ACLR was not entirely superior to complete tibial tunnel ACLR in knee laxity measured, and graft re-rupture rate.

HWJMSC-derived extracellular vesicles ameliorate IL-1ß-induced chondrocyte injury through regulation of the BMP2/RUNX2 axis via up-regulation TFRC.

Articular osteochondral injury is a common and frequently occurring disease in orthopedics that is caused by aging, disease, and trauma. The cytokine interleukin-1ß (IL-1ß) is a crucial mediator of the inflammatory response, which exacerbates damage during chronic disease and acute tissue injury. Human Wharton's jelly mesenchymal stem cell (HWJMSC) extracellular vesicles (HWJMSC-EVs) have been shown to promote cartilage regeneration. The study aimed to investigate the influence and mechanisms of HWJMSC-EVs on the viability, apoptosis, and cell cycle of IL-1ß-induced chondrocytes. HWJMSC-EVs were isolated by Ribo™ Exosome Isolation Reagent kit. Nanoparticle tracking analysis was used to determine the size and concentration of HWJMSC-EVs. We characterized HWJMSC-EVs by western blot and transmission electron microscope. The differentiation, viability, and protein level of chondrocytes were measured by Alcian blue staining, Cell Counting Kit-8, and western blot, respectively. Flow cytometer was used to determine apoptosis and cell cycle of chondrocytes. The results showed that HWJMSCs relieved IL-1ß-induced chondrocyte injury by inhibiting apoptosis and elevating viability and cell cycle of chondrocyte, which was reversed with exosome inhibitor (GW4869). HWJMSC-EVs were successfully extracted and proven to be uptake by chondrocytes. HWJMSC-EVs ameliorate IL-1ß-induced chondrocyte injury by inhibiting cell apoptosis and elevating viability and cycle of cell, but these effects were effectively reversed by knockdown of transferrin receptor (TFRC). Notably, using bone morphogenetic protein 2 (BMP2) pathway agonist and inhibitor suggested that HWJMSC-EVs ameliorate IL-1ß-induced chondrocyte injury through activating the BMP2 pathway via up-regulation TFRC. Furthermore, over-expression of runt-related transcription factor 2 (RUNX2) reversed the effects of BMP2 pathway inhibitor promotion of IL-1ß-induced chondrocyte injury. These results suggested that HWJMSC-EVs ameliorate IL-1ß-induced chondrocyte injury by regulating the BMP2/RUNX2 axis via up-regulation TFRC. HWJMSC-EVs may play a new insight for early medical interventions in patients with articular osteochondral injury.

Indexes of ferroptosis and iron metabolism were associated with the severity of diabetic nephropathy in patients with type 2 diabetes mellitus: a cross-sectional study.

Objective: To explore the correlations between diabetic nephropathy (DN) and serum levels of glutathione peroxidase 4 (GPX4), acyl-CoA synthetase long-chain family member 4 (ACSL4), iron, transferrin (Tf), and ferritin in patients with type 2 diabetes mellitus (T2DM). Methods: According to the urinary albumin excretion rate(UAER) or estimated glomerular filtration rate (eGFR) levels, a total of 123 patients with T2DM were separately divided into normoalbuminuria (NO), microalbuminuria (MI), macroalbuminuria (MA) groups, and G1 (eGFR ≥ 90 mL/min), G2 (eGFR ≤ 60 mL/min to < 90 mL/min), and G3 groups (eGFR< 60 mL/min), with 33 healthy participants as the control (HC). The differences in serum GPX4, ACSL4, iron, Tf, and ferritin levels between groups were compared, and the relationships between these levels were analysed. The independent correlations between UAER or DN severity and serum GPX4, ACSL4, iron, Tf, and ferritin levels were analysed by multiple linear and multinomial logistic regression, respectively. Results: To the patients with T2DM, with the increase in UAER levels, GPX4, iron, and Tf levels gradually decreased, whereas ACSL4 levels increased, meanwhile with the decrease in eGFR levels, GPX4 and Tf levels gradually decreased, whereas ACSL4 levels increased. UAER were independently and positively correlated with ACSL4 [ß = 17.53, 95% confidence interval (CI; 11.94, 23.13)] and negatively correlated with GPX4 [ß = -1.633, 95% CI (-2.77, -0.496)] and Tf [ß = -52.94, 95% CI (-95.78, -10.11)].The NO and MI groups were considered as reference groups, respectively. The severity of DN was negatively correlated with serum GPX4 [odds ratio (OR) = 0.925 and 0.902, p =0.015 and 0.001], and Tf (OR = 0.109 and 0.119, p =0.043 and 0.034), and positively correlated with ACSL4 (OR = 1.952 and 1.865, both p <0.001) in the MA group. Conclusion: DN severity was negatively correlated with serum GPX4 and Tf levels and positively correlated with serum ACSL4 levels in patients with T2DM.

Preparation of biodegradable carboxymethyl cellulose/dopamine/Ag NPs cryogel for rapid hemostasis and bacteria-infected wound repair.

Massive hemorrhage caused by accident or surgery is a major factor in accidental death. In addition, bacterial infection is also an important threat after bleeding. Cryogels with interpenetrating macroporous structures pose great application prospects in rapid hemostasis and infected wound repair. In this study, cryogels with different pore size are prepared by carboxymethyl cellulose (CMC) and dopamine (DA). The CMC grafted with different DA amounts is crosslinked by free DA through oxidative polymerization at low temperatures to form cryogels with different pore sizes. And the CMC/DA-3 cryogel is chosen as the optimal group for its high porosity, suitable mechanical, and good hemostatic ability. CMC/DA-3 cryogel is loaded with silver nanoparticles (Ag NPs) to prepare hemostatic cryogel with antibacterial properties. Antibacterial tests and animal hemostasis experiments confirm that the CMC/DA-3/Ag cryogel has good antibacterial properties and can finish rapid hemostasis. In the S. aureus infection skin defect model, the wound healing is significantly improved compared with commercial gelatin sponge. In summary, the novel cryogel has great potential in rapid hemostasis and infected wound healing.

Design and tuning of ionic liquid-based HNO donor through intramolecular hydrogen bond for efficient inhibition of tumor growth.

Developing ionic liquid (IL) drugs broaden new horizons in pharmaceuticals. The tunable nature endows ILs with capacity to delivery active ingredients. However, the tunability is limited to screen ionic components, and none realizes the kinetic tuning of drug release, which is a key challenge in the design of IL drugs. Here, a series of ILs are developed using biocompatible ionic components, which realizes absorption of gaseous NO to yield IL-NONOates. These IL-NONOates serve as HNO donors to release active ingredient. The release kinetics can be tuned through configuring the geometric construction of ILs (release half-lives, 4.2 to 1061 min). Mechanism research indicates that the tunability depends on the strength of intramolecular hydrogen bond. Furthermore, the IL-based HNO donors exert pharmacological potential to inhibit tumor progression by regulating intratumoral redox state. Coupled with biosafety, these IL-based HNO donors with facile preparation and tunable functionalization can be promising candidates for pharmaceutical application.

17ß-Estradiol via Orai1 activates calcium mobilization to induce cell proliferation in epithelial ovarian cancer.

Epithelial ovarian cancer (EOC) is the most lethal estrogen-sensitive gynecological cancer. Studies have reported that estrogen induces rapid cellular calcium mobilization in cells and can determine the fate of a cell. We found that estrogen increased the calcium release-activated calcium channel modulator 1 (Orai1) protein expression levels in SK-OV-3 cells. However, to date, there has been no research on the functional relationship and molecular mechanism of estrogen-regulating Orai1 during EOC development. In our study, Orai1 had a high expression level in high-grade serous ovarian tumor tissues and SK-OV-3 cells. Estrogen promoted cell proliferation and migration while inhibiting cell apoptosis in SK-OV-3 cells. Orai1 silencing suppressed estrogen-induced cell migration and proliferation. Overexpression of Orai1, however, enhanced the ability of 17ß-estradiol (E2) to exert its function. Estrogen induced rapid calcium influx in SK-OV-3 cells. Knockdown of Orai1 in SK-OV-3 cells blocked E2-induced stored-operated Ca2+ influx. The messenger RNA expression of caspase 3, matrix metallopeptidase 1, and cyclin-dependent kinase 6 were regulated via Orai1 under E2 treatment. Our results suggest that estrogen, by regulating Orai1, induced calcium influx to determine cell fate.

A Novel Splice-Site Mutation in MSH2 Is Associated With the Development of Lynch Syndrome.

Lynch syndrome (LS) is an inherited autosomal dominant disorder caused by germline mutations of mismatch repair (MMR) genes, including MSH2, MSH6, PMS2, and MLH1. This study aimed to analyze the molecular defects and clinical manifestations of an affected family and propose appropriate individual prevention strategies for all mutation carriers. A novel splicing mutation (c.1661+2 T>G) was identified in the MSH2 gene, which was found to co-segregate among affected family members by Whole exome sequencing (WES). RT-PCR analysis confirmed that c.1661+2 T>G could produce 3 transcripts, including 1 normal transcript and 2 aberrant transcripts. The 2 aberrant transcripts resulted in premature termination at the 6th nucleotide codon of MSH2 exon 11, so that the predicted products of the mutant MSH2 mRNAs were truncated proteins of 505 amino acids (with all of exon 10 deleted) and 528 amino acids (with a deletion of 82-nucleotides in exon 10), resulting in the loss of the interaction domain, the ATP domain and post-translationally modified residues. Quantitative RT-PCR (qRT-PCR) analysis showed that MSH2 mRNA levels in all patients were reduced to only 1/4 of the control levels. Our study reveals that a novel splicing mutation (c.1661+2 T>G) in the MSH2 gene causes LS and reaffirms the importance of genetic testing for LS.

Estrogen regulates forkhead transcription factor 2 to promote apoptosis of human ovarian granulosa-like tumor cells.

Granulosa cell tumors of the ovary (GCTs) are the predominant form of ovarian stromal tumors and can lead to abnormally secreted estrogen hormones. Studies have reported that forkhead transcription factor 2 (FOXL2) inhibits estrogen synthesis and its gene mutation can lead to GCTs. We unexpected found that estrogen also regulates the expression level of FOXL2. High-dose estrogen increased the expression of FOXL2 in ovarian-like granulosa (KGN) cells at both the mRNA and protein levels. However, no research has reported on the molecular regulatory mechanism and function between estrogen and FOXL2 in the development of GCTs. In this research, FOXL2 was highly expressed in KGN cells and ovarian stromal tumor tissues. Deletion of FOXL2 increased the estrogen secretion in KGN cells. In turn, high-dose estrogen increased the FOXL2 expression levels. FOXL2 was phosphorylated by GPR30 (G protein coupled receptor)-Protein kinase C (PKC) signaling pathway upon estrogen stimulation. Estrogen inhibited cell migration and proliferation, while promoting cell apoptosis. Deletion of FOXL2 inhibited the influence of estrogen on cell proliferation, migration, and apoptosis. Results suggest that estrogen via regulating FOXL2 suppresses cell proliferation and induces cell apoptosis.

Combination of 68Ga-PSMA PET/CT and Multiparametric MRI Improves the Detection of Clinically Significant Prostate Cancer: A Lesion-by-Lesion Analysis.

Our purpose was to explore whether 68Ga-PSMA PET/CT alone (PET/CT) or in combination with multiparametric MRI (PET/MRI) can improve the detection of clinically significant prostate cancer (PCa). Methods: We retrospectively enrolled 54 patients who underwent both MRI and PET/CT before radical prostatectomy. Regions of interest on MR images, PET/CT images, and pathologic images were marked. A lesion was defined as a region of interest marked on images obtained with any of the 3 modalities. All lesions were characterized using the prostate imaging reporting and data system (PI-RADS), the molecular imaging PSMA expression score, and the pathologic results and analyzed. Diagnostic performance was analyzed by receiver-operating-characteristic analysis. Specific improvement for lesions with different PI-RADS scores was analyzed using the net reclassification index (NRI). Results: In total, 90 lesions from 54 patients were analyzed, among which 66 lesions represented clinically significant PCa. Receiver-operating-characteristic analysis showed PET/MRI to perform better than MRI in detecting clinically significant PCa (change in area under the curve, 0.06; 95% confidence interval, 0.01-0.12; P < 0.05). With the calculated cutoff, PET/MRI performed significantly better than MRI (NRI, 21.9%; P < 0.01), with an improvement in sensitivity (89% vs. 76%, P < 0.01) at no sacrifice of specificity (96% vs. 88%, P > 0.05). Improvement in diagnosing clinically significant PCa occurred for lesions classified as PI-RADS 3 (NRI, 66.7%; P < 0.01). Conclusion: PET/MRI improves the detection of clinically significant PCa for PI-RADS 3 lesions.

miR34a/GOLPH3 Axis abrogates Urothelial Bladder Cancer Chemoresistance via Reduced Cancer Stemness.

Rationale: Chemoresistance and subsequent recurrence of human urothelial bladder cancer (UBC) is partially driven by a subpopulation of tumor initiating cells, namely cancer stem cells (CSCs). However, the underlying molecular mechanism in chemotherapy-induced CSCs enrichment and following chemoresistance and recurrence remains largely unclear. Methods: Gemcitabine and cisplatin (GC) chemoresistant cell lines (T24 GC 3rd and 5637 GC 3rd cells) and the chemo-sensitive UBC cell lines T24 and 5637 were established in vivo for the investigation of acquired resistance mechanisms. The role of miR34a/GOLPH3 axis in regulating UBC chemoresistance and recurrence was evaluated in cell and animal models. The expression levels of miR34a/GOLPH3 axis and CSCs markers were assayed in specimens of UBC. The association of GOLPH3 with clinicopathologic features and prognosis was analysed. Results: RT-PCR and western blotting confirmed that the expression levels of miR34a were decreased and GOLPH3 were increased in GC chemoresistant UBC cell lines. Downregulation of miR34a resulted in the overexpression of GOLPH3, which is a target gene of miR34a confirmed by luciferase experiment. The ectopic expression of miR34a decreased the stem cell properties of chemoresistant UBC cells and re-sensitized these cells to GC treatment in vitro and in vivo. Moreover, miR34a/GOLPH3 axis has obvious clinical relevance with prognosis and recurrence in human UBC patients with standard GC chemotherapy. Conclusion: Our results suggest that miR34a/GOLPH3 axis exert key role in CSCs involved UBC drug resistance and recurrence and warrant further development as a promising therapeutic approach in treating drug-resistant UBC.

Comparison of 68Ga-PSMA-11 PET-CT with mpMRI for preoperative lymph node staging in patients with intermediate to high-risk prostate cancer.

BACKGROUND: To evaluate the diagnostic value of 68Ga-PSMA-11 PET-CT with multiparametric magnetic resonance imaging (mpMRI) for lymph node (LN) staging in patients with intermediate- to high-risk prostate cancer (PCa) undergoing radical prostatectomy (RP) with pelvic lymph node dissection (PLND). METHODS: We retrospectively identified 42 consecutive patients with intermediate- to high-risk PCa according to D'Amico and without concomitant cancer. Preoperative 68Ga-PSMA-11 PET-CT, pelvic mpMRI and subsequent robot assisted laparoscopic RP with PLND were performed in all patients. RESULTS: Among 42 patients assessed, the preoperative PSA value, Gleason score, pT stage and intraprostatic PCa volume of patients with LN metastases were all significantly higher than those without metastases (P = 0.029, 0.028, 0.004, respectively). The average maximum standardized uptake value (SUV) of 68Ga-PSMA-11 PET-CT positive PCa of patients with or without LN metastases were 13.10 (range 6.12-51.75) and 7.22 (range 5.4-11.2), respectively (P < 0.001). 68Ga-PSMA-11 PET-CT and pelvic mpMRI had the ability of succeed on preoperative definite accurate diagnosis and accurate localization of primary PCa in all 42 patients. Fifteen patients (35.71%) had a pN1 stage. 51 positive LN were found. Both 68Ga-PSMA-11 PET-CT and pelvic mpMRI displayed brillient patient-based and region-based sensitivity, specificity, negative predictive value and positive predictive value. There was no statistical difference for the detection of LNMs according to the diameter of the LNMs between 68Ga-PSMA-11 PET-CT and mpMRI in this study. CONCLUSIONS: Both 68Ga-PSMA-11 PET-CT and mpMRI performed great value for LN staging in patients with intermediate- to high-risk PCa undergoing RP with PLND. However, despite excellent performance of 68Ga-PSMA-11 PET-CT, it cannot replace mpMRI that remains excellent for lymph node staging.