BackgroundMaternal report of events that occur during labour and delivery are used extensively in epidemiological research; however, the validity of these data are rarely confirmed. This study aimed to validate maternal self-report of events that occurred in labour and delivery with data found in electronic health records in a Canadian setting.MethodsData from the All Our Babies study, a prospective community-based cohort of women’s experiences during pregnancy, were linked to electronic health records to assess the validity of maternal recall at four months post-partum of events that occurred during labour and delivery. Sensitivity, specificity and kappa scores were calculated. Results were stratified by maternal age, gravidity and educational attainment.ResultsMaternal recall at four months post-partum was excellent for infant characteristics (gender, birth weight, gestational age, multiple births) and variables related to labour and delivery (mode of delivery, epidural, labour induction) (sensitivity and specificity >85%). Women who had completed a university degree had significantly better recall of labour induction and use of an epidural.ConclusionMaternal recall of infant characteristics and events that occurred during labour and delivery is excellent at four months post-partum and is a valid source of information for research purposes.
A proliferation-inducing ligand (APRIL), which induces survival and migration signals and tumor growth, is commonly observed in breast cancer tissues but is not often expressed in breast cancer cells themselves. Here, we examined whether breast cancer cells induce APRIL secretion from neutrophils, which are frequently recruited into the breast tumor microenvironment. We found that breast cancer cells do stimulate neutrophils to secrete APRIL through their glycosaminoglycans. Breast cancer cells depleted of heparan sulfate or chondroitin sulfate glycosaminoglycans lose their ability to induce APRIL secretion from neutrophils, and heparan sulfate and chondroitin sulfate can induce secretion that is comparable to that of breast cancer cell-induced secretion. While stimulation of the RNA-activated protein kinase (PKR) is sufficient to induce neutrophil APRIL secretion, both PKR and the toll-like receptor 4 (TLR4) are required for breast cancer cell glycosaminoglycan-induced secretion as separate and specific inhibition of TLR4 or PKR completely prevents the process, suggesting that breast cancer cell glycosaminoglycans target neutrophil TLR4 and PKR to trigger APRIL secretion. Thus, apart from the putative role of cell surface heparan sulfate in binding APRIL that leads to cell growth, we demonstrate that heparan sulfate, as well as chondroitin sulfate plays a novel role in promoting neutrophil secretion of APRIL that could lead to further cell growth. We propose that breast cancer cells take advantage of the neutrophil recruitment to the tumor microenvironment through the dual role of heparan sulfate as cell surface receptor or docking molecule for APRIL and as a ligand that induces neutrophil APRIL secretion to promote their own growth.
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