Melanie L. Conrad

German translation, cultural adaptation, and validation of the Health Literacy Questionnaire (HLQ)

The Health Literacy Questionnaire (HLQ), developed in Australia in 2012 using a ‘validity-driven’ approach, has been rapidly adopted and is being applied in many countries and languages. It is a multidimensional measure comprising nine distinct domains that may be used for surveys, needs assessment, evaluation and outcomes assessment as well as for informing service improvement and the development of interventions. The aim of this paper is to describe the German translation of the HLQ and to present the results of the validation of the culturally adapted version. The HLQ comprises 44 items, which were translated and culturally adapted to the German context. This study uses data collected from a sample of 1,058 persons with chronic conditions. Statistical analyses include descriptive and confirmatory factor analyses. In one-factor congeneric models, all scales demonstrated good fit after few model adjustments. In a single, highly restrictive nine-factor model (no cross-loadings, no correlated errors) replication of the original English-language version was achieved with fit indices and psychometric properties similar to the original HLQ. Reliability for all scales was excellent, with a Cronbach’s Alpha of at least 0.77. High to very high correlations between some HLQ factors were observed, suggesting that higher order factors may be present. Our rigorous development and validation protocol, as well as strict adaptation processes, have generated a remarkable reproduction of the HLQ in German. The results of this validation provide evidence that the HLQ is robust and can be recommended for use in German-speaking populations. Trial Registration: German Clinical Trial Registration (DRKS): DRKS00000584. Registered 23 March 2011.

Galectins in angiogenesis: consequences for gestation

Members of the galectin family have been shown to exert several roles in the context of reproduction. They contribute to placentation, maternal immune regulation and facilitate angiogenesis encompassing decidualisation and placenta formation during pregnancy. In the context of neo-vascularisation, galectins have been shown to augment signalling pathways that lead to endothelial cell activation, cell proliferation, migration and tube formation in vitro in addition to angiogenesis in vivo. Angiogenesis during gestation ensures not only proper foetal growth and development, but also maternal health. Consequently, restriction of placental blood flow has major consequences for both foetus and mother, leading to pregnancy diseases. In this review we summarise both the established and the emerging roles of galectin in angiogenesis and discuss the possible implications during healthy and pathological gestation.

Getting too sweet: galectin-1 dysregulation in gestational diabetes mellitus

Galectin-1 (gal-1) is a prototype carbohydrate-binding protein, whose dysregulation is associated with adverse pregnancy outcomes such as spontaneous abortion and pre-eclampsia. Furthermore, it is known that faulty gal-1 protein production or gene regulation can be caused by single-nucleotide polymorphisms in the LGALS1 gene. Gestational diabetes mellitus (GDM) is also an adverse pregnancy outcome and the most common metabolic disorder during gestation. However, gal-1 expression patterns during GDM remain largely unknown. Our aims were to define local and peripheral gal-1 expression patterns during pregnancy, and to investigate LGALS1 gene polymorphisms in GDM patients. Circulating gal-1 levels were determined by ELISA in GDM patients and normal pregnant controls, and LGALS1 gene polymorphisms were assessed for association with GDM. Placental tissues were collected from control and GDM term pregnancies to evaluate local gal-1 expression by immunofluorescence. Our results show that GDM is associated with a failure to increase circulating gal-1 levels during the second and third trimester, as well as overexpression of gal-1 in placental tissue. Additionally, the LGALS1 polymorphism rs4820294 was associated with the development of GDM. In pregnancies complicated by GDM, we observed gal-1 dysregulation both locally in the placenta and peripherally in the circulation. Furthermore, the association between the LGALS1 polymorphism and GDM may indicate a genetic contribution to this adverse pregnancy outcome.

S100A12 is up-regulated in pulmonary tuberculosis and predicts the extent of alveolar infiltration on chest radiography: an observational study

Pulmonary tuberculosis (PTB) results in lung functional impairment and there are no surrogate markers to monitor the extent of lung involvement. We investigated the clinical significance of S100A12 and soluble receptor for advanced glycation end-products (sRAGE) for predicting the extent of lung involvement. We performed an observational study in India with 119 newly diagnosed, treatment naïve, sputum smear positive, HIV-negative PTB patients and 163 healthy controls. All patients were followed-up for six months. Sociodemographic variables and the serum levels of S100A12, sRAGE, esRAGE, HMGB-1, TNF-α, IFN-γ and CRP were measured. Lung involvement in PTB patients was assessed by chest radiography. Compared with healthy controls, PTB patients had increased serum concentrations of S100A12 while sRAGE was decreased. S100A12 was an independent predictor of disease occurrence (OR 1.873, 95%CI 1.212–2.891, p = 0.004). Under DOTS therapy, S100A12 decreased significantly after 4 months whereas CRP significantly decreased after 2 months (p < 0.0001). Importantly, although CRP was also an independent predictor of disease occurrence, only S100A12 was a significant predictor of lung alveolar infiltration (OR 2.60, 95%CI 1.35–5.00, p = 0.004). These results suggest that S100A12 has the potential to assess the extent of alveolar infiltration in PTB.

Differential Spatiotemporal Patterns of Galectin Expression are a Hallmark of Endotheliochorial Placentation

Galectins influence the progress of pregnancy by regulating key processes associated with embryo‐maternal cross talk, including angiogenesis and placentation. Galectin family members exert multiple roles in the context of hemochorial and epitheliochorial placentation; however, the galectin prolife in endotheliochorial placenta remains to be investigated.

NK cell-derived IL-10 is critical for DC-NK cell dialogue at the maternal-fetal interface

DC-NK cell interactions are thought to influence the development of maternal tolerance and de novo angiogenesis during early gestation. However, it is unclear which mechanism ensures the cooperative dialogue between DC and NK cells at the feto-maternal interface. In this article, we show that uterine NK cells are the key source of IL-10 that is required to regulate DC phenotype and pregnancy success. Upon in vivo expansion of DC during early gestation, NK cells expressed increased levels of IL-10. Exogenous administration of IL-10 was sufficient to overcome early pregnancy failure in dams treated to achieve simultaneous DC expansion and NK cell depletion. Remarkably, DC expansion in IL-10−/− dams provoked pregnancy loss, which could be abrogated by the adoptive transfer of IL-10+/+ NK cells and not by IL-10−/− NK cells. Furthermore, the IL-10 expressing NK cells markedly enhanced angiogenic responses and placental development in DC expanded IL-10−/− dams. Thus, the capacity of NK cells to secrete IL-10 plays a unique role facilitating the DC-NK cell dialogue during the establishment of a healthy gestation.

Elevated systemic galectin-1 levels characterize HELLP syndrome.

Galectin-1 (gal-1), a member of a family of conserved β-galactoside-binding proteins, has been shown to exert a key role during gestation. Though gal-1 is expressed at higher levels in the placenta from HELLP patients, it is still poorly understood whether systemic gal-1 levels also differ in HELLP patients. In the present study, we evaluated the systemic expression of gal-1, together with the angiogenic factors, placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) in conjunction with HELLP syndrome severity. Systemic levels of gal-1 and sFlt-1 were elevated in patients with both early- and late-onset HELLP syndrome as compared to healthy controls. In contrast, peripheral PlGF levels were decreased in early- and late-onset HELLP. A positive correlation between systemic gal-1 levels and sFlt-1/PlGF ratios was found in early onset HELLP patients. Our results show that HELLP syndrome is associated with increased circulating levels of gal-1; integrating systemic gal-1 measurements into the diagnostic analyses of pregnant women may provide more effective prediction of HELLP syndrome development.