ABSTRACT
BACKGROUND: The prevalence of anaemia in pregnancy in Europe is 25% and that resulting from iron deficiency is estimated at 40%. The maternal and fetal morbidity of non-anaemic iron deficiency (NAID) in pregnancy is likely to be significant. OBJECTIVES: To determine the views and opinions of health service users and clinicians concerning NAID in pregnancy in order to inform future research. METHODS: Two semi-structured focus groups were carried out to determine health service users' views on anaemia and NAID in pregnancy. A questionnaire was administered to obstetricians, haematologists, midwives and anaesthetists to elucidate their views on NAID in pregnancy. RESULTS: The study indicated that health service users and clinicians were interested in implementing testing for NAID in pregnancy with serum ferritin, if proven to be effective at reducing the effects of anaemia and improving maternal and neonatal outcomes. Clinicians had reservations in the use of intravenous iron supplementation for NAID in pregnancy. CONCLUSION: NAID is now accepted as a target condition for research by health service users and clinicians. The focus of future research should be on screening for NAID and its treatment.
Subject(s)
Ferritins/blood , Iron Deficiencies , Physicians , Pregnancy Complications, Hematologic/epidemiology , Pregnancy Complications, Hematologic/therapy , Surveys and Questionnaires , Adult , Delivery of Health Care , Female , Humans , Iron/blood , Pregnancy , Pregnancy Complications, Hematologic/bloodABSTRACT
Elevated expression of the integrin-linked kinase (ILK) has been observed in a variety of cancers and has been further correlated with poor clinical outcome. Here, we show that mammary epithelial disruption of ILK results in a profound block in mammary tumor induction. Consistent with these observations, inhibition of ILK function in ErbB2-expressing cells with small molecule inhibitor or RNA interference resulted in profound block in their in vitro invasive properties due to the induction of apoptotic cell death. The rare ILK-deficient tumors that eventually arose overcame this block in tumor induction by an upregulation of ErB3 phosphorylation. These observations provide direct evidence that ILK has a critical role in the initiation phase of ErbB2 tumor induction.
