Primary testicular neuroendocrine tumor with liver lymph node metastasis: A case report and review of the literature.

BACKGROUND: Primary testicular neuroendocrine tumors (TNETs) are sporadic, accounting for only 0.23% of all testicular tumors. Few cases have been reported in the literature, and no uniform treatment protocol exists. We report a case of a primary TNET with liver lymph node metastasis diagnosed at the age of 24 years and discuss its clinicopathological features, diagnosis, differential diagnosis, treatment, and prognosis. CASE SUMMARY: We report the case of a 24-year-old patient with a primary TNET with liver lymph node metastasis. The patient was found to have a right testicular swelling of about 3 cm × 4 cm in size with unclear borders and no testicular pressure pain seven years ago without any examination or treatment. One month ago, an ultrasound examination was performed for persistent enlargement of the right testis, which showed an occupying lesion of the right testis approximately 110 mm × 102 mm × 82 mm in size. Magnetic resonance imaging scan of the testis (plain scan) showed that the right testis was an occupying lesion with inhomogeneous density and mixed signal, the boundary was still clear, and the possibility of seminoma was considered; chest X-ray and computed tomography did not show any apparent abnormalities. The patient underwent radical orchiectomy, and the pathological examination suggested a right TNET with a typical carcinoid tumor histological type. One month after the surgery, the patient received nine cycles of lanreotide chemotherapy at a dose of 90 mg/mo without adverse effects. No distant lymph node or other organ metastases were detected at follow-up. He is in good physical condition and attends regular follow-up visits. CONCLUSION: Neuroendocrine tumors are rare in clinical practice, and the diagnosis mainly relies on the characteristics of microscopic tumor cells and immunohistochemical features. Treatment involves radical orchiectomy. If it is accompanied by distant lymph node metastasis and the metastatic lesion can be resected, it should be surgically removed; if it cannot be resected, growth inhibitor analog octreotide or lanreotide chemotherapy can be administered to obtain good results, with close postoperative follow-up to prevent recurrence and metastasis.

Down-regulation of lncRNA MEG3 promotes endothelial differentiation of bone marrow derived mesenchymal stem cells in repairing erectile dysfunction.

AIMS: In the treatment of diabetes mellitus associated erectile dysfunction (DMED), the intracavernous and periprostatic implantations of bone marrow derived mesenchymal stem cells (BM-MSCs) represent the new therapeutic approaches with great applied prospect. However, the specific mechanisms of BM-MSCs protecting erectile function remain largely unknown. MATERIALS AND METHODS: The DMED rats were induced and the erectile function was assessed in the models with or without BM-MSCs implantation using intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio. The differentiation of BM-MSCs toward endothelial cells (ECs) was induced by exogenous vascular endothelial growth factor (VEGF) in vitro. RNA pull-down and RIP assays were performed to explore the interaction between MEG3 and FOXM1 protein. KEY FINDINGS: Intracavernous implantation of BM-MSCs effectively improved the erectile function of DMED rats, which was accompanied by a significant decrease in the expression of MEG3 in the corpus cavernosum tissues. Also, our study revealed that MEG3 expression was significantly down-regulated during the endothelial differentiation of BM-MSCs in vitro. The down-regulation of MEG3 was further confirmed to be conducive to the differentiation of BM-MSCs toward ECs. More importantly, MEG3 promoted the degradation of FOXM1 protein via facilitating FOXM1 ubiquitination, thereby decreasing VEGF expression, which ultimately regulated the endothelial differentiation of BM-MSCs. SIGNIFICANCE: Taken together, our findings presented the vital role of MEG3 in the repairing processes of BM-MSCs for erectile function and provided new mechanistic insights into the BM-MSCs-mediated DMED repairing.

The Effect of microRNA-328 antagomir on erectile dysfunction in streptozotocin-induced diabetic rats.

The study aimed at exploring the effect of microRNA-328 (miR-328) antagomir on erectile dysfunction (ED) in streptozotocin (STZ)-induced diabetic rats. A total of 120 male Sprague-Dawley (SD) rats were selected for this study. Fifteen rats were assigned as the diabetic control group and 75 out of the remaining rats (105 diabetic rat models) were divided into five groups with 15 rats in each group: diabetic ED, diabetic ED+negative control (NC), diabetic ED+miR-328 antagomir, diabetic ED+sildenafil and diabetic ED+miR-328 antagomir+sildenafil groups. The cGMP/AGEs production levels were measured using enzyme-linked immunosorbent assay (ELISA) test. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were conducted for testing the expression level of miR-328, transcription and protein levels of endothelial nitric oxide synthase (eNOS) and dickkopf-3 (DKK3). The diabetic ED+miR-328 antagomir group had better erectile function, lower cGMP production level, transcription and protein levels of eNOS and DKK3 but higher AGEs production level than the diabetic control group. The diabetic control group showed higher cGMP production level transcription and protein levels of eNOS and DKK3 and lower production levels of AGEs and miR-328 than the diabetic ED and diabetic ED+NC groups. Our results indicated that miR-328 antagomir could improve ED in STZ-induced diabetic rats by regulating cGMP and AGEs.

B Cell Lymphoma-2-Modified Bone Marrow-Derived Mesenchymal Stem Cells Transplantation for the Treatment of Diabetes Mellitus-Induced Erectile Dysfunction in a Rat Model.

OBJECTIVE: The study aimed to explore the effects of B cell lymphoma-2 (Bcl-2)-modified bone marrow-derived mesenchymal stem cells (BMSCs) transplantation for the treatment of diabetes mellitus-induced erectile dysfunction (DMED) in a rat model. METHODS: The DMED rat model was successfully established. Thirty-six DMED rats were assigned into the Bcl-2-BMSCs, null-BMSCs, BMSCs and phosphate buffered saline (PBS) groups. Meanwhile, 9 normal rats injected with PBS were taken as the normal control group. RESULTS: In the Bcl-2-BMSCs group, the average times of erection, rate of erection, peak intra-cavernous pressure (ICP) and peak ICP/mean arterial pressure were higher than those in the null-BMSCs, BMSCs and PBS groups, but were lower than those in the normal control group. In the Bcl-2-BMSCs group, capillary vessels and Bcl-2 mRNA and protein expressions were similar to those in the normal control group, while they were higher than those in other groups. CONCLUSION: These findings indicate that Bcl-2-modified BMSC transplantation could improve erectile function in DMED rats.