Background Besides reducing the quality of obstetric care, the direct impact of COVID‐19 on pregnancy and postpartum is uncertain. Objective To evaluate the characteristics of pregnant women who died due to COVID‐19. Search strategy Cochrane Library, Embase, MEDLINE, Scopus, and Google Scholar were searched from inception to February 2021. Selection criteria Studies that compared deceased and survived pregnant women with COVID‐19. Data collection and analysis Relevant data were extracted and tabulated. The primary outcome was maternal co‐morbidity. Main results Thirteen studies with 154 deceased patients were included. Obesity doubled the risk of death (relative risk [RR] 2.48, 95% confidence interval [CI] 1.41–4.36, I2 = 0%). No differences were found for gestational diabetes (RR 5.71; 95% CI 0.77–42.44, I2 = 94%) or asthma (RR 2.05, 95% CI 0.81–5.15, I2 = 0%). Overall, at least one severe co‐morbidity showed a twofold increased risk of death (RR 2.26, 95% CI 1.77–2.89, I2 = 76%). Admission to intensive care was related to a fivefold increased risk of death (RR 5.09, 95% CI 2.00–12.98, I2 = 56%), with no difference in need for respiratory support (RR 0.53, 95% CI 0.23–1.48, I2 = 95%) or mechanical ventilation (RR 4.34, 95% CI 0.96–19.60, I2 = 58%). Conclusion COVID‐19 with at least one co‐morbidity increases risk of intensive care and mortality.

Background: Ion channels play a crucial role in many physiological processes. Several subtypes are expressed in the endometrium. Endometriosis is strictly correlated to estrogens and it is evident that expression and functionality of different ion channels are estrogen-dependent, fluctuating between the menstrual phases. However, their relationship with endometriosis is still unclear. Objective: To summarize the available literature data about the role of ion channels in the etiopathogenesis of endometriosis. Methods: A search on PubMed and Medline databases was performed from inception to November 2019. Results: Cystic fibrosis transmembrane conductance regulator (CFTR), transient receptor potentials (TRPs), aquaporins (AQPs), and chloride channel (ClC)-3 expression and activity were analyzed. CFTR expression changed during the menstrual phases and was enhanced in endometriosis samples; its overexpression promoted endometrial cell proliferation, migration, and invasion throughout nuclear factor kappa-light-chain-enhancer of activated B cells-urokinase plasminogen activator receptor (NFκB-uPAR) signaling pathway. No connection between TRPs and the pathogenesis of endometriosis was found. AQP5 activity was estrogen-increased and, through phosphatidylinositol-3-kinase and protein kinase B (PI3K/AKT), helped in vivo implantation of ectopic endometrium. In vitro, AQP9 participated in extracellular signal-regulated kinases/p38 mitogen-activated protein kinase (ERK/p38 MAPK) pathway and helped migration and invasion stimulating matrix metalloproteinase (MMP)2 and MMP9. ClC-3 was also overexpressed in ectopic endometrium and upregulated MMP9. Conclusion: Available evidence suggests a pivotal role of CFTR, AQPs, and ClC-3 in endometriosis etiopathogenesis. However, data obtained are not sufficient to establish a direct role of ion channels in the etiology of the disease. Further studies are needed to clarify this relationship.

Fully synthetic tumor-associated carbohydrate antigen (TACA)-based vaccines are a promising strategy to treat cancer. To overcome the intrinsic low immunogenicity of TACAs, the choice of the antigens’ analogues and multivalent presentation have been proved to be successful. Here, we present the preparation, characterization, and in vitro screening of niosomes displaying multiple copies of the mucin antigen TnThr (niosomes-7) or of TnThr mimetic 1 (niosomes-2). Unprecedentedly, structural differences, likely related to the carbohydrate portions, were observed for the two colloidal systems. Both niosomal systems are stable, nontoxic and endowed with promising immunogenic properties.