Incidence and changes in endometrial-leiomyoma fistula following uterine artery embolization: a single-center retrospective analysis.

OBJECTIVES: To investigate whether the number and size of endometrial-leiomyoma fistulas (ELFs) change following uterine artery embolization (UAE) for leiomyoma and the correlation between ELFs and vaginal discharge (VD). MATERIALS & METHODS: This study was a retrospective analysis of 100 patients who underwent UAE at a single institution between May 2016 and March 2021. They all underwent MRI at baseline, 4 months, and 1 year after UAE. The number and size of the ELFs were compared with the MRI images each time. The ELF tumor characteristics and the correlation between the ELFs and VD were assessed. Additional gynecologic interventions due to VD associated with ELFs were evaluated. RESULTS: No ELF was observed at baseline. Ten ELFs were noted in nine patients at 4 months, and 35 ELFs were noted in 32 patients 1 year after UAE. The ELFs significantly increased over time (p = 0.004, baseline vs. 4 months; p < 0.001, 4 months vs. 1 year). The ELF size did not significantly change over time (p = 0.941). The tumors developing ELFs after UAE were mainly located at the submucosal or intramural area contacting the endometrium at baseline, with a mean size of 7.1 (2.6) cm. Nineteen patients (19%) had VD 1 year after UAE. There was no significant correlation between VD and the number of ELFs (p = 0.80). No patients underwent additional gynecologic interventions due to VD associated with ELFs. CONCLUSION: ELFs increased in number and did not disappear over time after UAE in most tumors. CLINICAL RELEVANCE STATEMENT: Despite the MR imaging findings, within the limited data of this study, ELFs were not seemingly associated with clinical symptoms, including VD. KEY POINTS: • Endometrial-leiomyoma fistula (ELF) is a complication of uterine artery embolization (UAE). • ELFs increased in number over time after UAE and did not disappear in most tumors. • Most tumors developing ELFs after UAE were located near/contacted the endometrium and were larger.

Hemoptysis due to a lung metastasis of renal cell carcinoma: A case report.

A 53-year-old man with a history of surgery for renal cancer was referred to our hospital due to massive hemoptysis. Contrast-enhanced CT revealed a well-enhanced pulmonary nodule suggestive of a tumor (diameter of 16 mm), which was considered a causal lesion. Bronchial artery embolization was successfully performed and subsequently hemoptysis disappeared. However, hemoptysis recurred 6 months later, and the tumor was surgically resected. Pathological examination revealed the resected tumor was a lung metastasis of renal cell carcinoma, which directly invaded into pulmonary bronchus. Hemoptysis secondary to lung metastasis of renal cell carcinoma has rarely been reported in the literature.

Sunitinib maleate administration before percutaneous CT-guided cryoablation for large renal cell carcinoma: A case report.

A 60-year-old woman taking anti-platelet drugs was referred to the hospital for the treatment of advanced renal cell carcinoma. CT revealed that the tumor had a diameter of 5 cm and hyper-vascularity. Percutaneous CT-guided cryoablation (CA) was indicated. Since preprocedural arterial embolization failed to provide sufficient embolic effects, sunitinib maleate was administered. It provided good tumor devascularization and volume reduction, which corresponded to downstage. Therefore, the administration contributed to successfully performing subsequent percutaneous CT-guided CA with no serious hemorrhagic complications. Sunitinib maleate may be an alternative to conventional treatments before CA for renal cell carcinoma.

Heparan sulfate regulates self-renewal and pluripotency of embryonic stem cells.

Embryonic stem (ES) cell self-renewal and pluripotency are maintained by several signaling cascades and by expression of intrinsic factors, such as Oct3/4 and Nanog. The signaling cascades are activated by extrinsic factors, such as leukemia inhibitory factor, bone morphogenic protein, and Wnt. However, the mechanism that regulates extrinsic signaling in ES cells is unknown. Heparan sulfate (HS) chains are ubiquitously present as the cell surface proteoglycans and are known to play crucial roles in regulating several signaling pathways. Here we investigated whether HS chains on ES cells are involved in regulating signaling pathways that are important for the maintenance of ES cells. RNA interference-mediated knockdown of HS chain elongation inhibited mouse ES cell self-renewal and induced spontaneous differentiation of the cells into extraembryonic endoderm. Furthermore, autocrine/paracrine Wnt/beta-catenin signaling through HS chains was found to be required for the regulation of Nanog expression. We propose that HS chains are important for the extrinsic signaling required for mouse ES cell self-renewal and pluripotency.

Heparin-II domain of fibronectin is a vascular endothelial growth factor-binding domain: enhancement of VEGF biological activity by a singular growth factor/matrix protein synergism.

We describe extracellular interactions between fibronectin (Fn) and vascular endothelial growth factor (VEGF) that influence integrin-growth factor receptor crosstalk and cellular responses. In previous work, we found that VEGF bound specifically to fibronectin (Fn) but not vitronectin or collagens. Herein we report that VEGF binds to the heparin-II domain of Fn and that the cell-binding and VEGF-binding domains of Fn, when physically linked, are necessary and sufficient to promote VEGF-induced endothelial cell proliferation, migration, and Erk activation. Using recombinant Fn domains, the C-terminal heparin-II domain of Fn (type III repeats 13 to 14) was identified as a key VEGF-binding site. Mutation of the heparin-binding residues on FnIII(13-14) abolished VEGF binding, and peptides corresponding to the heparin-binding sequences in FnIII(13-14) inhibited VEGF binding to Fn. Fn fragments containing both the alpha5beta1 integrin-binding domain (III 9 to 10) and the VEGF-binding domain (III 13 to 14) significantly enhanced VEGF-induced EC migration and proliferation and induced strong phosphorylation of the VEGF receptor and Erk. Neither the cell-binding or VEGF-binding fragment of Fn alone had comparable VEGF-promoting effects. These results suggest that the mechanism of VEGF/Fn synergism is mediated extracellularly by the formation of a novel VEGF/Fn complex requiring both the cell-binding and VEGF-binding domains linked in a single molecular unit. These data also highlight a new function for the Fn C-terminal heparin-binding domain that may have important implications for angiogenesis and tumor growth.

Neurite outgrowth-stimulating peptide derived from bovine kappa-casein.

We found a novel peptide that stimulates neurite outgrowth in Neuro-2a mouse neuroblastoma cells, from the pepsin-pancreatin digest of bovine kappa-casein. The amino acid sequence of this peptide is Phe-Leu-Pro-Tyr-Pro-Tyr (FLPYPY), corresponding to peptidic sequence 76-81 of bovine kappa-casein. The neurite outgrowth-stimulating activity of FLPYPY was seen over 10(-9) M. On the other hand, FLPYP and FLPYPYY, which corresponded to sequences 76-80 and 76-82 of bovine kappa-casein respectively, were ineffective.

Real-time analysis of ligand-induced cell surface and intracellular reactions of living mast cells using a surface plasmon resonance-based biosensor.

Surface plasmon resonance (SPR)-based sensors have been used to detect the binding between interactive molecules. We applied the SPR technology to the analysis of interactions between living cells and molecules reactive to the cells, using mast cells and mast cell-reactive antigens. The exposure of dinitrophenol-human serum albumin (DNP-HSA), an antigen that stimulates mast cells, to IgE-sensitized mast cells induced a robust and long-lasting SPR signal in a dose-dependent manner. The maximal increase in SPR signal induced by 100 ng/ml DNP-HSA was 0.200 +/- 0.120 angle (mean +/- SD, n = 37), about 1000 times larger than the theoretically expected increase for the simple binding of DNP-HSA to Fc(epsilon)RI, the high-affinity IgE receptor. A small, but similarly prolonged signal was observed when the cells were stimulated by an agonist of the adenosine A3 receptor. The signal induced by DNP-HSA was abolished by genistein, and partially inhibited by phorbol 12-myristate 13-acetate and wortmannin. Interestingly, the signal induced by DNP-HSA was only weakly inhibited by DNP-lysine, suggesting that DNP-lysine manifests its action not by inhibiting, but by modulating the crosslinking of Fc(epsilon)RI. We concluded that SPR sensors can detect biologically significant signals in a real-time manner from the interactions between cells and molecules reactive to the cells.