Previous studies have indicated that long non-coding RNA (lncRNA) down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) serves an oncogenic role in numerous cancer types. However, its role in endometrial cancer (EC) remains largely unknown. In the present study, DSCAM-AS1 expression levels in EC tissues and cells and their normal counterparts were analyzed using reverse transcription-quantitative. In vitro and in vivo experiments were conducted to validate the functions of DSCAM-AS1 in EC. It was revealed that DSCAM-AS1 was expressed at a high level in EC tissues and cells after analyzing patient data and data obtained from The Cancer Genome Atlas. Notably, it was also revealed that high DSCAM-AS1 expression was associated with a less favorable overall survival in patients with EC. Knockdown of DSCAM-AS1 was able to suppress EC cell proliferation by upregulating cell apoptosis in vitro. Furthermore, it was revealed that DSCAM-AS1 acted as a microRNA (miR)-136-5p sponge to exert its oncogenic roles in EC. Collectively and to the best of our knowledge, the current results provided first evidence that DSCAM-AS1 stimulated EC progression by regulating miR-136-5p, which may improve the understanding of the roles of ncRNAs in EC, and may help identify novel targets for anticancer treatment.

Background and objective Rivaroxaban – an oral, direct Factor Xa inhibitor – inhibits thrombus formation and growth in animal models. We have investigated the effects of rivaroxaban on thrombolysis because impaired fibrinolysis is a risk factor for venous thrombosis and it occurs more often in patients who had a myocardial infarction. As the propensity of a clot to be degraded depends on its structure, we tested the effects of rivaroxaban on clot structure and degradability by tissue plasminogen activator (t-PA). This was done in the absence and presence of thrombomodulin because the thrombin - thrombomodulin complex is the activator of TAFI (thrombin-activatable fibrinolysis inhibitor), a potent inhibitor of fibrinolysis. Methods Clots were formed in a microchamber in the presence or absence of rivaroxaban at pharmacological concentrations (0.15 and 0.25 μg/ml). Clot structure was analyzed by confocal microscopy, and permeability calculated by measuring flow rates. Degradation was evaluated by the amount of D-dimers in the eluate of clot perfused with t-PA, in the presence or absence of thrombomodulin. Results Microscopy showed that clots formed in the presence of rivaroxaban had thicker fibers and a looser fibrin structure with larger pores than controls, leading to increased permeation rate (Darcy constant 2.16-fold and 2.45-fold higher than controls with rivaroxaban at 0.15 μg/ml and 0.25 μg/ml, respectively). This clot structure modification renders the clots more susceptible to fibrinolytic enzymes. The degradation of clots containing 0.15 μg/ml of rivaroxaban was 3.6-fold higher than that of control clots, after 90 minutes perfusion with t-PA. In addition, when clots are formed in the presence of thrombomodulin, the degradability is decreased in control, while In the presence of rivaroxaban, fibrin degradation remains enhanced. Conclusion Rivaroxaban increased thrombolysis by t-PA. This was due to a decrease in thrombin generation. Two mechanisms are involved: modification of clot structure, which makes it more accessible to thrombolytic enzymes; and decrease in TAFI activation by the thrombomodulin–thrombin complex. This property of rivaroxaban may contribute to its antithrombotic effect.

Objective No guideline has been provided to assess the minimal number of lymph nodes (LNs) that should be dissected for accurate staging in patients with epithelial ovarian cancer (EOC). The aim of the study was to develop a nodal staging score (NSS) as an index to assess whether a pathologic (p)N0 EOC patient is indeed free of a nodal disease. Methods A total of 16,361 EOC patients staged I–III between 2004 and 2013 were identified from the Surveillance, Epidemiology and End Result database. With a β-binomial model, NSS was calculated to assess the probability of true-negative findings of LN status. Results With an increased number of LNs examined, the probability of missing a nodal disease decreased and varied among different pT stages. Given 1 LN examined, an NSS of 93.76% calculated could ensure a high adequacy of nodal-negative classification for pT1N0 EOC patients. For pT2N0 patients, 5 LNs examined could guarantee an NSS of 90% for adequate staging. Likewise, 11 and 29 LNs examined in pT3N0 patients could maintain NSS at the level of 80% and 90%, respectively. Our study suggested the optimal number of LNs that could be examined and stratified by the pT stages for EOC patients based on this statistical model derived from large pathologic data of clinical surgery patients. Conclusion NSS, as an auxiliary tool, not only could assist the International Federation of Gynecology and Obstetrics staging more precisely, but also would provide a statistical basis for postoperative evaluation for further clinical decision-making.

Purpose: To investigate the protective effect of icariin (ICA) on myocardial cells in spontaneously hypertensive rats (SHRs), and the mechanism involved. Methods: Twenty-four SPF-grade, 12-week-old SHRs were randomly assigned to model group and ICA group, with 12 rats/group. There were 12 Wistar-Kyoto (WKY) rats (aged 12 weeks) in the control group. Rats in ICA group were given ICA suspension (40 mg/kg) through gavage, daily for 3 months, while model rats were given equivalent volume of double distilled water (in place of ICA suspension) via gavage for 12 weeks. Blood pressure, cardiac function, left ventricular (LV) mass index, myocardial morphology and apoptosis-related protein levels were determined and compared among the four groups. Results: The myocardial cells were hypertrophic and disorderly arranged, with widened intercellular spaces. Besides, there were increases in protein expression levels of p53, caspase 3, Bok, Bax, GRP78, p-PERK, ATF-4, CHOP and DR5, while Bcl-2 protein was down-regulated. In contrast, the levels of these indicators in the ICA group were significantly better than those in the model group (p < 0.05). Conclusion: ICA reduces blood pressure in rats, but improves cardiac function and cardiomyocyte morphology by decreasing apoptosis in cardiomyocytes through down-regulation of mitochondrial and endoplasmic reticulum (ER) stress-related apoptosis pathways. Thus, icariin may be suitable for the treatment of hypertension; however, clinical trials need to be undertaken first.

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