Since December 2019, the medical staff fighting against COVID-19 frequently reported the device-related pressure injury (DRPI) caused by personal protective equipment (PPE). We conducted a cross-sectional survey online to investigate the prevalence and characteristics of DRPI among medical staff.Univariate and multivariate logistic regression analyses were employed to explore the risk factors associated with DRPI. A total of 4308 participants were collected and 4306 participants were valid from 161 hospitals in China. The overall prevalence of DRPI caused by PPE among medical staff was 30.03% Int Wound J. 2020;1-10.wileyonlinelibrary.com/journal/iwj (95% CI 28.69%-31.41%). The prevalence of male was more than that of female (42.25%, 95% CI 37.99-46.51% vs 26.36%, 95% CI 26.93-29.80%, P < .001).The categories were mainly stages 1 and 2, and the common anatomical locations were nose bridge, cheeks, ears, and forehead. Logistic regression analysis revealed that the risk factors were sweating (OR = 43.99, 95% CI 34.46-56.17), male (OR = 1.50, 95% CI 1.12-1.99), level 3 PPE (OR = 1.44, 95% CI 1.14-1.83), and longer wearing time (OR = 1.28, 95% CI 0.97-1.68). The prevalence of DRPI was high among medical staff wearing PPE against COVID-19, and the risk factors were sweating, male, wearing level 3 PPE, and longer wearing time.Comprehensive preventive interventions should be taken.

BACKGROUND. Endometrial cancer is a common gynecologic malignancy among women. The molecular mechanisms involved in the progression of endometrial cancer are unclear, which has hampered the development of an effective treatment. Survivin, a newly identified member of the inhibitor of apoptosis (IAP) family, regulates 2 critical processes in neoplastic transformation: cell proliferation and apoptosis. METHODS. Survivin mRNA and protein expression levels were analyzed in human normal cycling endometrium, atypical endometrium, and endometrial adenocarcinoma by immunohistochemical, reverse-transcriptase polymerase chain reaction (RT-PCR), and Western blot analyses. To study the biological function of survivin in endometrial cancer, RNA interference was applied to knock down survivin expression in the Ishikawa endometrial cancer cell line by recombinant plasmids producing survivin small hairpin RNA. Furthermore, the signal pathway that regulates survivin expression was investigated. RESULTS. Higher levels of survivin mRNA and protein expression were observed in endometrial adenocarcinomas than in atypical or normal endometrium. Immunohistochemical staining revealed that 83.3% (50 of 60) of endometrial adenocarcinoma samples, 55.0% (11 of 20) of atypical endometrium samples, and 25.0% (5 of 20) of normal endometrium samples were positive for survivin protein. Inhibition of survivin by RNA interference reduced cell proliferation and induced apoptosis in Ishikawa cells by down-regulating cyclin D1 and phosphorylated RB and activating caspase-3 and caspase-8. The authors also found that the MAPK pathway was a signal transduction pathway upstream of survivin. Epidermal growth factor (EGF) and transforming growth factor-a (TGF-a) upregulated survivin protein expression by activating the MAPK pathway in endometrial cancer cells. CONCLUSIONS.Survivin is an attractive target for endometrial cancer treatment.Growth factors could regulate survivin expression by activating the MAPK pathway.

Propagation and differentiation of stem cell populations are tightly regulated to provide sufficient cell numbers for tissue formation while maintaining the stem cell pool. Embryonic parts of the mammalian placenta are generated from differentiating trophoblast stem cells (TSCs) invading the maternal decidua. Here we demonstrate that lysine-specific demethylase 1 (Lsd1) regulates differentiation onset of TSCs. Deletion of Lsd1 in mice results in the reduction of TSC number, diminished formation of trophectoderm tissues and early embryonic lethality. Lsd1-deficient TSCs display features of differentiation initiation, including alterations of cell morphology, and increased migration and invasion. We show that increased TSC motility is mediated by the premature expression of the transcription factor Ovol2 that is directly repressed by Lsd1 in undifferentiated cells. In summary, our data demonstrate that the epigenetic modifier Lsd1 functions as a gatekeeper for the differentiation onset of TSCs, whereby differentiation-associated cell migration is controlled by the transcription factor Ovol2.

Gastric carcinoma (GC) is the second leading cause of cancer-related mortality worldwide. The efficacy of standard chemotherapy for GC, such as cisplatin (CDDP), is dissatisfactory partly due to the toxic/side-effects. Sulforaphane (SFN), which exhibits effective anti-cancer functions, is a phytochemical converted from cruciferous plants. Our present study aimed to identify whether SFN could enhance the anti-cancer effects of low-dose CDDP and to determine the underlying mechanisms. Herein, co-exposure of SFN and CDDP significantly inhibited the viabilities of gastric cancer cells. For the molecular mechanisms, CDDP alone increased the cancer stem cell (CSC)-like properties in gastric cancer cells via activating the interleukin-6 (IL-6)/IL-6 receptor (IL-6R)/signal transducer and activator of transcription 3 (STAT3) signaling. However, SFN could activate the microRNA-124 (miR-124), which directly targets the 3′-untranslated regions (UTR) of the IL-6R and STAT3. Moreover, knockdown of miR-124 eliminated the effects of SFN on CSC-like properties in GC cells, and in turn enhanced the anti-cancer effects of low-dose CDDP. These findings not only suggested a mechanism whereby SFN enhanced the anti-cancer functions of CDDP, but also helped to regard SFN as a potential chemotherapeutic factor in gastric cancer.