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Patients undergoing gynecological surgery commonly receive indwelling transurethral Foley catheters, however duration of catheterization is associated with risk of urinary tract infections and other adverse effects. Early removal of catheters is encouraged, however optimal timing postsurgery remains unclear. This quasi-experimental study compared outcomes for women after removal of a Foley catheter at two different times following benign gynecological surgery. Participants received either early catheter removal, within 6 hours of surgery ( n = 38) or standard catheter removal, within 12 to 24 hours of surgery ( n = 45). There were no significant differences in outcomes for discomfort scores or re-catheterization rates between groups. However, the early removal group had a significantly shorter time to first ambulation and shorter hospital stays. Early removal of Foley catheters in patients who underwent gynecological surgery did not increase adverse events. Early removal of catheters after gynecological surgery may decrease re-catheterization rates and increase patient satisfaction.

Ovarian cancer is the most lethal cancer of the female reproductive system. In that regard, several epidemiological studies suggest that long‐term exposure to estrogen could increase ovarian cancer risk, although its precise role remains controversial. To decipher a mechanism for this, we previously generated a mathematical model of how estrogen‐mediated upregulation of the transcription factor, E2F6, upregulates the ovarian cancer stem/initiating cell marker, c‐Kit, by epigenetic silencing the tumor suppressor miR‐193a, and a competing endogenous (ceRNA) mechanism. In this study, we tested that previous mathematical model, showing that estrogen treatment of immortalized ovarian surface epithelial cells upregulated both E2F6 and c‐KIT, but downregulated miR‐193a. Luciferase assays further confirmed that microRNA‐193a targets both E2F6 and c‐Kit. Interestingly, ChIP‐PCR and bisulphite pyrosequencing showed that E2F6 also epigenetically suppresses miR‐193a, through recruitment of EZH2, and by a complex ceRNA mechanism in ovarian cancer cell lines. Importantly, cell line and animal experiments both confirmed that E2F6 promotes ovarian cancer stemness, whereas E2F6 or EZH2 depletion derepressed miR‐193a, which opposes cancer stemness, by alleviating DNA methylation and repressive chromatin. Finally, 118 ovarian cancer patients with miR‐193a promoter hypermethylation had poorer survival than those without hypermethylation. These results suggest that an estrogen‐mediated E2F6 ceRNA network epigenetically and competitively inhibits microRNA‐193a activity, promoting ovarian cancer stemness and tumorigenesis.

Hui Yang,* Lan Liu,* Gai Li, Yinchen Chen, Dong Jiang, Wei Wang, Tianyuan Wang, Jinshan Sun, Jianfang Che, Dongmei Gu, Meng Lu, Aiping Wang Department of Endocrinology, The Air Force Hospital from Eastern Theater of PLA, Nanjing 210029, People’s Republic of China*These authors contributed equally to this workCorrespondence: Aiping Wang; Meng LuDepartment of Endocrinology, The Air Force Hospital from Eastern Theater of PLA, 1 Malujie Road, Nanjing 210029, People’s Republic of ChinaTel +86-25-80865162Email wap454hospital@163.com; lumeng365@hotmail.comAim: To explore the growth-promoting effect of vacuum sealing drainage (VSD) during the healing processes of diabetic foot ulcers (DFUs).Methods: From November 2018 to December 2019, 38 patients with unilateral DFUs were enrolled in this retrospective study. All patients were divided into two groups according to the use of VSD or not: the VSD group (n=20) and the control group (n=18). The following parameters were used to evaluate the healing process: changes in the mean areas of the ulcers; healing rate (HR); epithelial hyperplasia and angiogenesis as determined by hematoxylin-eosin staining (HE staining); and expression of CD34, CD68 and VEGF as assessed through immunohistochemistry. Perioperative side effects and complications were also recorded.Results: All patients received follow-up and eventually healed. The mean area of wounds was reduced in the VSD group compared to the control group (1.75± 0.64 cm2 vs 0.88± 0.54 cm2, P=0.031). The mean HR of the ulcers in the VSD group was significantly higher than that in the control group (35.23± 2.87% vs 28.78± 1.09%, P=0.017). HE staining showed that the amount of epithelial hyperplasia and angiogenesis increased significantly after VSD, and the immunohistochemistry results showed that the expression of CD34, CD68 and VEGF increased significantly in the VSD group.Conclusion: VSD could significantly accelerate the wound healing process, probably by enhancing the inflammatory response and promoting granulation and angiogenesis in DFUs.Keywords: vacuum sealing drainage, diabetic foot ulcers, wound healing, CD34, CD68, VEGF

Gastric cancer is one of the leading causes of cancer death worldwide. Previous studies demonstrated that activation of STAT3 is crucial for the development and progression of gastric cancer. However, the role of STAT3 in neuronal related gene methylation in gastric cancer has never been explored. In this study, by using DNA methylation microarray, we identified a potential STAT3 target, C11orf87, showing promoter hypomethylation in gastric cancer patients with lower STAT3 activation and AGS gastric cancer cell lines depleted with STAT3 activation. Although C11orf87 methylation is independent of its expression, ectopic expression of a constitutive activated STAT3 mutant upregulated its expression in gastric cancer cell line. Further bisulfite pyrosequencing demonstrated a progressive increase in DNA methylation of this target in patient tissues from gastritis, intestinal metaplasia, to gastric cancer. Intriguingly, patients with higher C11orf87 methylation was associated with better survival. Furthermore, hypermethylation of C11orf87 was also frequently observed in other GI cancers, as compared to their adjacent normal tissues. These results suggested that C11orf87 methylation may serve as a biomarker for diagnosis and prognosis of GI cancers, including gastric cancer. We further postulated that constitutive activation of STAT3 might be able to epigenetically silence C11orf87 as a possible negative feedback mechanism to protect the cells from the overactivation of STAT3. Targeted inhibition of STAT3 may not be appropriate in gastric cancer patients with promoter hypermethylation of C11orf87.

The proportion of China’s 65-year-old population has increased year by year. As we enter old age, people’s average life expectancy increases year by year. The risk of disease in the elderly population increases. According to the statistics of the Ministry of Health and Welfare of Taiwan, most people over the age of 65 suffer from cancer and heart disease. Pneumonia, cerebrovascular disease, and diabetes. With medical advancement, more and more disease characteristics can be found in medical imaging. With the development of technology, the higher the resolution of the image, the more information that can be contained, and the doctor will spend more time marking and diagnosing. There is currently no open imaging training and recognition platform for users to use, so this study uses deep learning CNN technology to construct an image analysis and recognition platform with analysis and recognition interface. In the future, retraining and batch identification capabilities can be added to complete the integrity of the platform.

Aims The impaired angiogenesis is one of the main factors affecting the healing of diabetic foot ulcer (DFU) wounds. Maggot debridement therapy (MDT) promotes granulation tissue growth and angiogenesis during DFU wound healing. Non-coding microRNAs can also promote local angiogenesis in DFU wounds by regulating wound repairing related gene expression. The purpose of this study was to investigate the mechanism of microRNAs in MDT promoting DFU wound angiogenesis. Methods In this study, we applied MDT to treat DFU wound tissue and detect the expression of the miR-17–92 cluster. In vitro experiments, human umbilical vein endothelial cells (HUVECs) were treated with maggot excretions/secretions (ES), the miR-17–92 cluster and the predicted target gene expression were measured. Tube formation assay and cell scratch assay were performed when inhibition of miR-18a/19a or overexpression of thrombospondin-1 (TSP-1) were used in this study. Results miR-18a/19a transcription significantly up-regulated and TSP-1 expression down-regulated in patients wound tissue and in HUVECs. Inhibition of miR-18a/19a or overexpression of TSP-1 partially blocked the migration and tube formation ability stimulated by ES. Conclusion Targeted activation of miR-18a/19a transcription levels and subsequent regulation of TSP-1 expression may be a novel therapeutic strategy for DFU.

Self-assembling mixed polymeric micelles (saMPMs) were developed for overcoming major obstacles of poor bioavailability (BA) associated with curcumin delivery. Lecithin added was functioned to enlarge the hydrophobic core of MPMs providing greater solubilization capacity. Amphiphilic polymers (sodium deoxycholate [NaDOC], TPGS, CREMOPHOR, or a PLURONIC series) were examined for potentially self-assembling to form MPMs (saMPMs) with the addition of lecithin. Particle size, size distribution, encapsulation efficacy (E.E.), and drug loading (D.L.) of the mixed micelles were optimally studied for their influences on the physical stability and release of encapsulated drugs. Overall, curcumin:lecithin:NaDOC and curcumin:lecithin:PLURONIC P123 in ratios of 2:1:5 and 5:2:20, respectively, were optimally obtained with a particle size of 80%, and a D.L. of >10%. The formulated system efficiently stabilized curcumin in phosphate-buffered saline (PBS) at room temperature or 4 °C and in fetal bovine serum or PBS at 37 °C and delayed the in vitro curcumin release. In vivo results further demonstrated that the slow release of curcumin from micelles and prolonged duration increased the curcumin BA followed oral and intravenous administrations in rats. Thus, lecithin-based saMPMs represent an effective curcumin delivery system, and enhancing BA of curcumin can enable its wide applications for treating human disorders.

Ovarian cancer is one of the most lethal cancers in the female reproductive system. Previous study suggested that long term treatment of estrogen such as hormonal replacement therapy (HRT) may increase the risk of ovarian cancer, however the role of estrogen in ovarian carcinogenesis is still controversial. To decipher this complicated process, we generated a mathematical model and found that estrogen-mediated up-regulation of E2F6 could upregulate the ovarian cancer stem/initiating marker, c-kit by two means one through epigenetic silencing of their co-targeted miR193a by binding of E2F6 which subsequently recruit EZH2 to miR-193a promoter; and second, by competing endogenous (ceRNA) mechanism. To confirm this model, treatment of E2 or environmental hormone, BPA resulted in upregulation of both E2F6 and c-kit but down-regulation of miR-193a in immortalized ovarian surface epithelial cells. Further bisulfite pyrosequencing, ChIP-qPCR and epigenetic treatment found that miR193a was epigenetically silenced by DNA methylation and H3K27me3 in CP70 but not HeyC2 ovarian cancer cells. Overexpression of miR193a inhibited tumor growth in vitro and in vivo. Depletion of EZH2 or E2F6 in CP70 restored miR-193a expression and decreased the number of “ovo” spheroid by reversing the repressive chromatin status of miR-193a promoter. To further explore the biological significance of this E2F6 ceRNA network, integrative RNA-Seq and computational analysis found that PBX1, a miR-193a target and transcriptional activator of the immunosuppressive cytokine IL-10, was down-regulated in E2F6 and EZH2 knockdown CP70 cells. Overexpression of E2F6 3'UTR containing miR-193a MRE but not MRE mutant increased the expression of PBX1 and IL10 in ovarian cancer cells. Importantly, co-culture of conditional media from E2F6 3'UTR overexpressing CP70 cells inhibited the differentiation of THP-1 monocytes into dendritic cell and the T-cell activating function of this THP-1 derived DC. This phenomenon can be rescued by incubation of anti-IL-10 antibody or pretreatment of CP70 cells with EZH2 inhibitor. Finally, clinical studies demonstrated that patients with higher promoter methylation of miR193a were associated with poor survival. Serum IL10 level was found to be higher in high staged ovarian cancer patients and patients with higher E2F6 mRNA level. Additional analysis from TCGA ovarian cancer expression microarray dataset demonstrated that ovarian cancer patients with low expression of EZH2, showed a positive correlation between E2F6, c-KIT and PBX1 resembling the ceRNA phenomenon between these mRNAs. Taken together, our results showed that estrogen-mediated E2F6 ceRNA network can regulate cancer stemness and anti-tumor immunity of DC through epigenetic silencing of miR-193a. Anti-estrogen therapy together with the EZH2 inhibitor may be a novel strategy against this deadly cancer. Citation Format: Frank Hsueh-Che Cheng, Hon-Yi Lin, Yin-Chen Chen, Tzy-Wei Hwang, Rui-Lan Huang, Chia-Bin Chang, Ru-Inn Lin, Ching-Wen Lin, Gary C.W. Chen, Jora M. J. Lin, Yu-Ming Chuang, Jian-Liang Chou, Chin Li, Alfred S.L. Cheng, Hung-Cheng Lai, Shu-Fen Wu, Je-Chiang Tsai, Michael W.Y. Chan. E2F6-mediated ceRNA and epigenetic silencing of miR193a lead to cancer stemness and anticancer immunity in ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 74.

A basinwide warming (cooling) in the Indian Ocean is observed following the El Niño (La Niña) mature phase, with the amplitude of the warming being significantly larger than the cooling. A composite analysis reveals that the amplitude asymmetry (positive skewness) between the warm and cold Indian Ocean basinwide sea surface temperature anomaly pattern (IOB) appears only when ENSO is concurrent with the Indian Ocean dipole (IOD). The amplitude asymmetry becomes insignificant during the ENSO-only and the IOD-only events. The physical mechanism for the amplitude asymmetry is investigated by analyzing the mixed layer heat budget based on the Simple Ocean Data Assimilation (SODA) 2.0.2 data. It is found that the positive skewness in the IOD west pole (IODW) is mainly caused by the asymmetry of ocean temperature advection, whereas the positive skewness in the IOD east pole (IODE) is caused by the asymmetry of the surface heat flux anomaly (primarily shortwave radiation) in response to the ENSO remote forcing. The asymmetry of the mixed layer depth (MLD) between warm and cold events is another factor contributing to the IOB positive skewness. The MLD in IODE during the warm events (27 m) is shallower than that of the cold events (45 m), resulting a larger (smaller) temperature tendency during the warm (cold) events. In contrast, the MLD in IODW during the warm events (44 m) is deeper than that of the cold events (37 m). Because the positive skewness in IODW is caused by the ocean temperature advection and the surface heat flux plays a damping role, a larger (smaller) MLD leads to a weaker (stronger) thermodynamic damping. Thus the asymmetry of MLD in both IODE and IODW favors a greater basinwide warming than cooling.

Aim We aimed to evaluate the effectiveness of the application of activated autologous monocytes/macrophages (Mo/Mp) on wound healing in diabetic rats. Methods Sixty male SD rats were equally divided into the following: control group (normal, nondiabetic), PBS-treated diabetic group, and tumor necrotic factor alpha (TNF-α) plus interferon-γ (IFN-γ)-stimulated or unstimulated Mo/Mp-treated diabetic group. Full-thickness round wounds (1 cm × 1 cm) were created in the right hind foot of rats and the wounds were treated with PBS or Mo/Mp on day 1 after injury. In the following 14 days, the percentage of wound contraction was measured, histologic examination was performed with hematoxylin and eosin staining, and vascular endothelial growth factor (VEGF) in the wound was evaluated by Western blot analysis. Results Diabetic rats exhibited impaired wound healing with delayed angiogenesis and VEGF expression. The early application of TNF-α plus IFN-γ-stimulated autologous Mo/Mp to diabetic wounds significantly improved the delayed wound healing through the stimulation of angiogenesis and re-epithelization, as well as restoring the defect in VEGF expression. Conclusions Mo/Mp activated by TNF-α and IFN-γ promotes diabetic wound healing and normalizes the defect in VEGF regulation associated with diabetes-induced skin-repair disorders.

Nausea and vomiting is a common post-operative complication that exacerbates patient discomfort and puts tension on suture lines, which may cause hematomas beneath surgical flaps and place patient at risk of aspiration pneumonia. Nausea and vomiting decreases patient comfort and satisfaction and increases hospital stay length and costs. Postoperative nausea and vomiting are common occurrences. Nurses typically give medicine in accordance with doctors' orders without understanding patient symptoms. Such results in less than optimal holistic care management. This situation encouraged the author to collect references on current international trends related to postoperative nausea and vomiting treatment in the clinical setting. The author further worked to recommend a care management protocol based on findings. This paper describes risk factors of postoperative nausea and vomiting and the related drugs, prevention procedures, and treatment recommendations. Finally, the author developed a simple care flow chart suited for use in internal clinical situations that may provide a valuable reference for medical professionals.