Prediction of stillbirth from maternal factors, fetal biometry and uterine artery Doppler at 19-24 weeks

Objectives: To evaluate the performance of screening for all stillbirths and those due to impaired placentation and unexplained or other causes by a combination of maternal factors, fetal biometry and uterine artery pulsatility index (UT-PI) at 19-24 weeks’ gestation and compare this performance to that of screening by UT-PI alone. Methods: This was a prospective screening study of 70,003 singleton pregnancies including 69,735 live births and 268 (0.38%) antepartum stillbirths; 159 (59%) were secondary to impaired placentation and 109 (41%) were due to other or unexplained causes. Multivariate logistic regression analysis was used to develop a model for prediction of stillbirth based on a combination of maternal factors, fetal biometry and UT-PI. Results: Combined screening predicted 55% of all stillbirths, including 75% of those due to impaired placentation and 23% of those that were due to other causes or unexplained, at false positive rate of 10%; within the impaired placentation group the detection rate of stillbirth at 37 weeks (88% vs 46%; p<0.001). The performance of screening by the combined test was superior to that of selecting the high-risk group on the basis of UT-PI being above the 90th percentile for gestational age, which predicted 48% of all stillbirths, 70% of those due to impaired placentation and 15% of those that were due to other causes or unexplained. Conclusions: Second-trimester screening by a combination of UT-PI with maternal factors and fetal biometry can predict a high proportion of stillbirths and in particular those due to impaired placentation

Candida soluble cell wall β-glucan facilitates ovalbumin-induced allergic airway inflammation in mice: Possible role of antigen-presenting cells

<p>Abstract</p> <p>Background</p> <p>Although fungi have been implicated as initiating/deteriorating factors for allergic asthma, their contributing components have not been fully elucidated. We previously isolated soluble β-glucan from <it>Candida albicans </it>(CSBG) (Ohno et al., 2007). In the present study, the effects of CSBG exposure on airway immunopathology in the presence or absence of other immunogenic allergen was investigated <it>in vivo</it>, and their cellular mechanisms were analyzed both <it>in vivo </it>and <it>in vitro</it>.</p> <p>Methods</p> <p><it>In vivo</it>, ICR mice were divided into 4 experimental groups: vehicle, CSBG (25 μg/animal), ovalbumin (OVA: 2 μg/animal), and CSBG + OVA were repeatedly administered intratracheally. The bronchoalveolar lavage cellular profile, lung histology, levels of cytokines and chemokines in the lung homogenates, the expression pattern of antigen-presenting cell (APC)-related molecules in the lung digests, and serum immunoglobulin values were studied. <it>In vitro</it>, the impacts of CSBG (0–12.5 μg/ml) on the phenotype and function of immune cells such as splenocytes and bone marrow-derived dendritic cells (BMDCs) were evaluated in terms of cell proliferation, the surface expression of APC-related molecules, and OVA-mediated T-cell proliferating activity.</p> <p>Results</p> <p><it>In vivo</it>, repeated pulmonary exposure to CSBG induced neutrophilic airway inflammation in the absence of OVA, and markedly exacerbated OVA-related eosinophilic airway inflammation with mucus metaplasia in mice, which was concomitant with the amplified lung expression of Th2 cytokines and IL-17A and chemokines related to allergic response. Exposure to CSBG plus OVA increased the number of cells bearing MHC class II with or without CD80 in the lung compared to that of others. <it>In vitro</it>, CSBG significantly augmented splenocyte proliferation in the presence or absence of OVA. Further, CSBG increased the expression of APC-related molecules such as CD80, CD86, and DEC205 on BMDCs and amplified OVA-mediated T-cell proliferation through BMDCs.</p> <p>Conclusion</p> <p>CSBG potentiates allergic airway inflammation with maladaptive Th immunity, and this potentiation was associated with the enhanced activation of APCs including DC.</p