Information about prenatal screening for Down syndrome: Ethnic differences in knowledge

Objective

To evaluate the provision of information about prenatal screening for Down syndrome to women of Dutch, Turkish and Surinamese origins, and to examine the effects of this provision on ethnic differences in knowledge about Down syndrome and prenatal screening.

Methods

The study population consisted of 105 Dutch, 100 Turkish and 65 Surinamese pregnant women attending midwifery or obstetrical practices in The Netherlands. Each woman was personally interviewed for 3 weeks (mean) after booking for prenatal care.

Results

Most women reported to have received oral and/or written information about prenatal screening by their midwife or obstetrician at booking for prenatal care. Turkish and Surinamese women less often read the information than Dutch women, more often reported difficulties in understanding the information, and had less knowledge about Down syndrome, prenatal screening and amniocentesis. Language skills and educational level contributed most to the explanation of these ethnic variations.

Conclusion

Although most Dutch, Turkish and Surinamese women reported to have received information from their midwife or obstetrician, ethnic differences in knowledge about Down syndrome and prenatal screening are substantial.

Practice implications

Interventions to improve the provision of information to women from ethnic minority groups should especially be aimed at overcoming language barriers, and targeting information to the women's abilities to comprehend the information about prenatal screening for Down syndrome.     

Sensitization by intratracheally injected dendritic cells is independent of antigen presentation by host antigen-presenting cells

Adoptive transfer of antigen-pulsed dendritic cells (DC) in the airways of mice has been used as a model system for eosinophilic airway inflammation, which allows studying the DC-specific contribution of genes of interest or reagents to induced inflammation by genetically modifying DC or exposure of DC to compounds prior to injection in the airways. Antigen transfer and CD4+ T cell priming by endogenous antigen-presenting cells (APCs) may interfere with the correct interpretation of the data obtained in this model, however. We therefore examined antigen transfer and indirect CD4+ T cell priming by host APCs in this model system. Transfer of antigen between injected DC and host cells appeared to be minimal but could not be totally excluded. However, only direct antigen presentation by injected DC resulted in robust CD4+ T cell priming and eosinophilic airway inflammation. Thus, this adoptive transfer model is well suited to study the role of DC in eosinophilic airway inflammation.     

Essential Role of Osteopontin in Smoking-Related Interstitial Lung Diseases

Smoking-related interstitial lung diseases are characterized by the accumulation of macrophages and Langerhans cells, and fibrotic remodeling, which are linked to osteopontin (OPN) expression. Therefore, OPN levels were investigated in bronchoalveolar lavage (BAL) cells in 11 patients with pulmonary Langerhans cell histiocytosis (PLCH), 15 patients with desquamative interstitial pneumonitis (DIP), 10 patients with idiopathic pulmonary fibrosis, 5 patients with sarcoidosis, 13 otherwise healthy smokers, and 19 non-smoking controls. Furthermore, OPN overexpression was examined in rat lungs using adenoviral gene transfer. We found that BAL cells from patients with either PLCH or DIP spontaneously produced abundant amounts of OPN. BAL cells from healthy smokers produced 15-fold less OPN, and those cells from non-smoking healthy volunteers produced no OPN. BAL cells from patients with either idiopathic pulmonary fibrosis or sarcoidosis produced significantly less OPN, as compared with patients with PLCH. These data were confirmed by immunochemistry. Nicotine stimulation increased production of both OPN and granulocyte-macrophage colony stimulating factor by alveolar macrophages from smokers. Nicotinic acetylcholine receptor expression resembled the pattern of spontaneous OPN production and was dramatically increased in both PLCH and DIP. OPN overexpression in rat lungs induced lesions similar to PLCH with marked alveolar and interstitial accumulation of Langerhans cells. Our findings suggest a pathogenetic role of increased OPN production in both PLCH and DIP by promoting the accumulation of macrophages and Langerhans cells.Cigarette smoke is linked to a variety of lung diseases including chronic obstructive pulmonary disease, lung cancer, and interstitial lung diseases. Respiratory bronchiolar interstitial lung disease, desquamative interstitial pneumonitis (DIP), and pulmonary Langerhans cell histiocytosis (PLCH) belong to the group of smoking-related interstitial lung diseases.^1,2,3 Cigarette smoke is a complex mixture of more than 4000 compounds and is known to cause systemic and pulmonary effects.⁴ However, the underlying mechanisms as to how cigarette smoking leads to the changes observed in smoking-related interstitial lung diseases are largely unknown.^1,2,3Cigarette smoke induces inflammation, oxidative stress, and tissue injury, and has an important effect on the number, distribution, and activation state of macrophages and Langerhans cells.^5,6 There is a strong epidemiological link between PLCH and smoking. PLCH is characterized by the accumulation of activated Langerhans cells originating from the distal bronchiole walls.^1,2,3,7 The accumulations of Langerhans cells are poorly demarcated and extend to the adjacent alveoli, which often contain an abundance of pigmented macrophages. These areas show morphological changes similar to DIP.^7,8 In DIP, the predominant feature is the accumulation of alveolar macrophages, densely filling the alveolar lumen, combined with moderate fibrotic interstitial remodeling.^1,2As measured by bronchoalveolar lavage (BAL) in healthy individuals, cigarette smoking induces a 5- to 10-fold increase in alveolar macrophages in a dose-response curve.^9,10,11 It was shown that concentrations of granulocyte-macrophage colony stimulating factor (GMCSF) in patients with PLCH are increased,¹² but the mechanisms that lead to the expansion of the pulmonary macrophage pool and fibrosis in smokers are poorly understood.^1,2,3 Based on the findings of a microarray study, Woodruff et al¹³ have recently proposed that alveolar macrophages from smokers exhibit a distinctive macrophage activation state that is accompanied by increased OPN expression. Osteopontin is a glycoprotein found in the extracellular matrix of bone.¹⁴ However, multiple studies have reported cytokine properties of OPN in cell-mediated immunity.¹⁴ Further, OPN exhibits a strong chemotactic activity for macrophages, monocytes, Langerhans cells, and dendritic cells.^15,16,17In the context of these findings we speculated that OPN might be involved in the pathogenesis of smoking-related lung interstitial diseases. We found abundant OPN production by alveolar macrophages from patients with PLCH and DIP. Alveolar macrophages from both healthy smokers and patients with DIP and PLCH show up-regulated nicotine receptor expression as a sign of chronic nicotine stimulation. Further, nicotine directly induced OPN and GMCSF in alveolar macrophages. Our data provides evidence for a role of osteopontin in the pathogenesis of smoking- related interstitial lung diseases.     

Predictors of general quality of life and the mediating role of health related quality of life in patients with schizophrenia

Introduction  The concept ‘quality of life’ (QoL) has become increasingly important as an outcome measure in the evaluation of services and in clinical trials of people with schizophrenia. This study examines the mediating role of health related quality of life (HRQoL) in the prediction of general quality of life (GQoL). Method  QoL and other patient- and illness characteristics (psychopathology, overall functioning, illness history, self-esteem and social integration) were measured in a group of 143 outpatients with schizophrenia. GQoL was measured by the Lancashire Quality of Life Profile and HRQoL was measured by the MOS SF-36. To test the temporal stability of our findings, assessments were performed twice with an 18-month interval. Results  We found that patient’s GQoL is predicted mainly by anxiety and depression and self-esteem and to a lesser extent by global functioning and social integration. At both time intervals HRQoL appeared to be a significant mediator of the relationship between anxiety and depression and self esteem versus patient’s GQoL. Conclusions  The results of this study are important for mental health professionals, as these provide more insight in the mechanisms by which they could improve the GQoL of their patients with schizophrenia. The results confirm that diagnosis and treatment of anxiety and depression in outpatients with schizophrenia deserves careful attention of clinicians. Also strategies and specific interventions to improve self-esteem of patients with schizophrenia are very important to maximise patient’s QoL.     

Early relapse in ALL is identified by time to leukemia in NOD/SCID mice and is characterized by a gene signature involving survival pathways

We investigated the engraftment properties and impact on patient outcome of 50 pediatric acute lymphoblastic leukemia (ALL) samples transplanted into NOD/SCID mice. Time to leukemia (TTL) was determined for each patient sample engrafted as weeks from transplant to overt leukemia. Short TTL was strongly associated with high risk for early relapse, identifying an independent prognostic factor. This high-risk phenotype is reflected by a gene signature that upon validation in an independent patient cohort (n?= 197) identified a high-risk cluster of patients with early relapse. Furthermore, the signature points to independent pathways, including mTOR, involved in cell growth and apoptosis. The pathways identified can directly be targeted, thereby offering additional treatment approaches for these high-risk patients.     

Clearance of influenza virus from the lung depends on migratory langerin+CD11b- but not plasmacytoid dendritic cells

Although dendritic cells (DCs) play an important role in mediating protection against influenza virus, the precise role of lung DC subsets, such as CD11b- and CD11b+ conventional DCs or plasmacytoid DCs (pDCs), in different lung compartments is currently unknown. Early after intranasal infection, tracheal CD11b-CD11chi DCs migrated to the mediastinal lymph nodes (MLNs), acquiring co-stimulatory molecules in the process. This emigration from the lung was followed by an accumulation of CD11b+CD11chi DCs in the trachea and lung interstitium. In the MLNs, the CD11b+ DCs contained abundant viral nucleoprotein (NP), but these cells failed to present antigen to CD4 or CD8 T cells, whereas resident CD11b-CD8+ DCs presented to CD8 cells, and migratory CD11b-CD8- DCs presented to CD4 and CD8 T cells. When lung CD11chi DCs and macrophages or langerin+CD11b-CD11chi DCs were depleted using either CD11c-diphtheria toxin receptor (DTR) or langerin-DTR mice, the development of virus-specific CD8+ T cells was severely delayed, which correlated with increased clinical severity and a delayed viral clearance. 120G8+ CD11cint pDCs also accumulated in the lung and LNs carrying viral NP, but in their absence, there was no effect on viral clearance or clinical severity. Rather, in pDC-depleted mice, there was a reduction in antiviral antibody production after lung clearance of the virus. This suggests that multiple DCs are endowed with different tasks in mediating protection against influenza virus.     

Islet inflammation in type 2 diabetes: from metabolic stress to therapy

Decreases in both mass and secretory function of insulin-producing beta-cells contribute to the pathophysiology of type 2 diabetes. The histology of islets from patients with type 2 diabetes displays an inflammatory process characterized by the presence of cytokines, apoptotic cells, immune cell infiltration, amyloid deposits, and eventually fibrosis. This inflammatory process is probably the combined consequence of dyslipidemia, hyperglycemia, and increased circulating adipokines. Therefore, modulation of intra-islet inflammatory mediators, in particular interleukin-1 beta, appears as a promising therapeutic approach.     

Formal definitions of measurement bias and explanation bias clarify measurement and conceptual perspectives on response shift

ObjectiveResponse shift is generally associated with a change in the meaning of test scores, impeding the comparison of repeated measurements. Still, different researchers have different views of response shift. From a measurement perspective, response shift can be considered as bias in the measurement of change, whereas from a more conceptual perspective, it can be considered as bias in the explanation of change. We propose definitions to accommodate both interpretations of response shift.Study Design and SettingFormal definitions of measurement bias and explanation bias serve to define response shift in measurement and conceptual perspectives. Examples from the field of health-related quality of life research illustrate the definitions.ResultsDefinitions of response shifts as special cases of either measurement bias or explanation bias clarify different interpretations of response shift and lead to different research methods. Different structural equation models are suggested to investigate biases and response shifts in each of the two perspectives.ConclusionIt is important to distinguish between measurement and conceptual perspectives as they involve different ideas about response shift. Definitions from both perspectives help to resolve conceptual and methodological confusion around response shift and to further its research.     

Ultrasound-guided near-nerve neurography for early evaluation of nerve regeneration

For early assessment of axonal outgrowth after trauma, the nerve is surgically exposed to enable compound nerve action potential (CNAP) recordings across the lesion site. Near-nerve neurography, with needle electrodes placed transcutaneously near the nerve, could be a minimally invasive alternative if the needle placement procedure and low reproducibility are improved. We developed ultrasound-guided near-nerve neurography, which facilitates needle placement, and assessed its potential for evaluating nerve regeneration. Measurements were performed at varying times after crush lesion of the peroneal nerve of 25 rabbits. To test if ultrasound-guided near-nerve signals could be measured prior to muscle reinnervation, they were compared with recordings of compound muscle action potentials. A comparison with conventional intra-operative CNAP recordings was made by measuring nerve signal amplitude with both techniques and by assessing reproducibility. In all cases where intra-operative signals could be measured, near-nerve signals were also detected. Compound nerve activity could be recorded after 5 weeks, whereas compound muscle activity appeared after approximately 8 weeks. Reproducibility was slightly better for near-nerve than for intra-operative recordings. We conclude that ultrasound-guided near-nerve neurography is able to assess nerve regeneration well before compound muscle activity can be detected. Its accuracy and reproducibility are similar to those of conventional intra-operative recordings.