Objective:To investigate how urothelial carcinoma-associated 1 (UCA1) and miR-18a modulates acquired tamoxifen resistance and the relevant mechanisms in estrogen receptor (ER) positive cancer cells.Methods: qRT-PCR was performed to detect UCA1 and miR-18a expression in breast cancer cells.Dual luciferase assay was performed to detect the binding between miR-18a and UCA1 3′UTR.Tamoxifen sensitive MCF-7 cells were transfected with UCA1 expression vector or miR-18a inhi-bitors.Tamoxifen resistant LCC9 and BT474 cells were transfected with UCA1 siRNA or miR-18a mi-mics.CCK-8 assay was performed to detect cell viability.Soft agar assay was performed to assess cell colony formation.Flow cytometric analysis was performed to check cell cycle distribution.Results: UCA1 was significantly upregulated in tamoxifen resistant LCC2,LCC9,and BT474 cells than in tamoxifen sensitive MCF-7 cells.UCA1 expression was significantly upregulated in MCF-7 cells after treatment with 0.1 μmol/L tamoxifen.UCA1 overexpression enhanced cell viability of MCF-7 cells after tamoxifen treatment,while UCA1 siRNA significantly suppressed viability of LCC9 and BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with vector control+tamoxifen group,the average cell colony number and colony size of the UCA1+tamoxifen group was 19.0％ more and 29.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 7.3％ lower and 6.7％ higher respectively.In BT474 cells,compared with siRNA control+tamoxifen group,the average cell colony number and colony size of the si-UCA1+tamoxifen group were 54.0％ less and 42.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 9.0％ higher and 6.2％ lower respectively.UCA1 directly interacted with miR-18a and reduced its expression in ER positive breast cancer cells.Knockdown of miR-18a increased viability of MCF-7 cells after tamoxifen treatment,while miR-18a overexpression significantly reduced viability of BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with miRNA inhibitor control+tamoxifen group,the average cell colony number and colony size of the miR-18a inhibitor+tamoxifen group were 15.0％ more and 33.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 8.8％ lower and 5.3％ higher respectively.In BT474 cells,compared with miRNA control+tamoxifen group,the average cell colony number and colony size of the miR-18a mimics+tamoxifen group were 47.0％ less and 25.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 13.3％ higher and 7.9％ lower respectively.Conclusion: UCA1 can increase tamoxifen resistance of ER positive breast cancer cells via competitively inhibiting of miR-18a.

Objective To investigate the kinesin family member 17 (KIF17) expression and cellular localization in the hippocampus and temporal lobe cortex in the rat lithium-pilocarpine model of epilepsy,and discuss its function in the epilepsy pathogenesis.Methods The animal model was established by lithiumpilocarpine induction in rats.Totally 49 adult healthy male Wistar rats were randomly divided into control group (n =7) and experimental group (n =42).The experimental group included 6 subgroups (n =7)according to sacrifice time (24 h,72 h,7 d,14 d,1 month and 2 months).The expression and localization of KIF17 were examined by western blot and double-label immunofluorescence,respectively.Results In rat hippocampus,the expression of KIF17 protein increased after the onset of seizure (the ration of KIF17/β-actin were:24 h 0.516 ± 0.196,72 h 0.742 ± 0.313),reached its peak in 7 days (0.888 +0.319)and then slowed down (14 d 0.770 ± 0.271,1 month 0.742 ± 0.261,2 months 0.714 ± 0.271),all of which were significantly higher than that in the control group (0.495 ± 0.203).And all the differences had statistical significance (t =7.051,4.974,7.419,8.795,8.264,6.676,all P ＜ 0.05).In rat cortex of temporal lobe,the expression of KIF17 protein increased after the onset of seizure and reached its peak in 30 d.The optical density ration in the experimental groups were higher than that in the control group.Doublelabel immunofluorescence disclosed that the KIF17 localized in the neurons,including excitable neurons and inhibitory neurons,but not in the astrocytes which were performed with anti-microtubule-associated protein 2,anti-brain-specific Na-dependent inorganic phosphate cotransporter,anti-glutamate decarboxylase 1 and anti-glial fibrillary acidic protein,respectively.Conclusion KIF17 may play a potential role in the pathogenetic mechanisms of the rat lithium-pilocarpine model of epilepsy.

Objective:To explore the efficacy of the oncoplastic round block technique in surgical management of idiopathic granulomatous mastitis (IGM).Methods:From January 2014 to December 2019, a total of 18 patients (24 to 38 years old, 32.2 years in average) with IGM underwent excision of the inflammatory breast mass with oncoplastic round block technique, the postoperative clinical efficacy was summarized and analyzed.Results:All 18 patients with IGM underwent excision of the inflammatory breast mass with oncoplastic round block technique, among them 2 patients underwent round-block reduction surgery of contralateral breast at the same time. The median follow-up duration was 16.1 months (from 6 to 36 months). Incision poor healing occurred in two cases which was cured after dressing change. Recurrence occurred in one case at 6 months after operation, and then cured with conservative measures. No other severe complications occurred. All patients were satisfacted with the results.Conclusions:Application of oncoplastic round block technique in surgical management of IGM may remove more tissue in order to reduce the recurrent rate, and get a better cosmetic results.