Evaluation of choroid plexus with fetal magnetic resonance imaging: What happens in ventriculomegaly?

OBJECTIVES: Diagnosis of ventriculomegaly (VM) and identification of choroid plexus (CP) can be challenging with fetal magnetic resonance imaging (MRI). Our aim is to create an adjunct method for supporting the diagnosis of VM by investigating the CP-ventricular wall separation distance in fetuses with and without VM (nV) with fetal MRI. METHODS: T2-weighted fetal MRIs of 154 fetuses were retrospectively evaluated. The CP separation was defined as the distance between the medial wall of the dependent ventricle and distal tip of the CP glomus. The measurement was performed at the same plane with the dependent ventricle measurement by two blinded readers. RESULTS: 41 fetuses with VM (mean gestational age 27 (19-35 weeks), and 44 nV fetuses (mean gestational age 28 (20-39 weeks) were included. Interobserver reliability was excellent for ventricle diameters (R = 0.99, confidence interval (CI) 95%) and the separation of CP (R = 0.98, CI 95%). Mean distance of CP separation was 10.7 mm ±â€¯4.2 mm and 3.0 ±â€¯1.6 mm in VM and nV fetuses, respectively (p < 0.001). The distance of CP separation to differentiate VM cases was 6.5 mm (sensitivity: 0.98, specificity: 0.98). Separation of CP was correlated to ventricle diameter in cases with (R = 0.674) and without VM (R = 0.805). For the cut-off value >0.65 cm for the distance between the medial wall of the dependent ventricle and the medial border of choroid plexus sensitivity is 97.56, specificity 95.45, positive predictive value (PPV) 95.20, negative predictive value (NPV) 97.70, and likelihood ratio (LR) (+) is 21.46. CONCLUSION: Fetal CP can be efficiently evaluated with MRI, and the increase of CP-ventricular wall separation distance in correlation with the ventricle diameter is a reliable sign in the diagnosis of fetal VM.

Exposure to Perchlorate in Lactating Women and Its Associations With Newborn Thyroid Stimulating Hormone.

Background: Perchlorate, thiocyanate, and nitrate can block iodide transport at the sodium iodide symporter (NIS) and this can subsequently lead to decreased thyroid hormone production and hypothyroidism. NIS inhibitor exposure has been shown to reduce iodide uptake and thyroid hormone levels; therefore we hypothesized that maternal NIS inhibitor exposure will influence both maternal and newborn thyroid function. Methods: Spot urine samples were collected from 185 lactating mothers and evaluated for perchlorate, thiocyanate, and nitrate concentrations. Blood and colostrum samples were collected from the same participants in the first 48 h after delivery. Thyroid hormones and thyroid-related antibodies (TSH, fT3, fT4, anti-TPO, anti-Tg) were analyzed in maternal blood and perchlorate was analyzed in colostrum. Also, spot blood samples were collected from newborns (n = 185) between 48 and 72 postpartum hours for TSH measurement. Correlation analysis was performed to assess the effect of NIS inhibitors on thyroid hormone levels of lactating mothers and their newborns in their first 48 postpartum hours. Results: The medians of maternal urinary perchlorate (4.00 µg/g creatinine), maternal urinary thiocyanate (403 µg/g creatinine), and maternal urinary nitrate (49,117 µg/g creatinine) were determined. Higher concentrations of all three urinary NIS inhibitors (µg/g creatinine) at their 75th percentile levels were significantly correlated with newborn TSH (r = 0.21, p < 0.001). Median colostrum perchlorate level concentration of all 185 participants was 2.30 µg/L. Colostrum perchlorate was not significantly correlated with newborn TSH (p > 0.05); however, there was a significant correlation between colostrum perchlorate level and maternal TSH (r = 0.21, p < 0.01). Similarly, there was a significant positive association between colostrum perchlorate and maternal urinary creatinine adjusted perchlorate (r = 0.32, p < 0.001). Conclusion: NIS inhibitors are ubiquitous in lactating women in Turkey and are associated with increased TSH levels in newborns, thus signifying for the first time that co-exposure to maternal NIS inhibitors can have a negative effect on the newborn thyroid function.

Spleen-derived classical monocytes mediate lung ischemia-reperfusion injury through IL-1ß.

Ischemia-reperfusion injury, a form of sterile inflammation, is the leading risk factor for both short-term mortality following pulmonary transplantation and chronic lung allograft dysfunction. While it is well recognized that neutrophils are critical mediators of acute lung injury, processes that guide their entry into pulmonary tissue are not well understood. Here, we found that CCR2+ classical monocytes are necessary and sufficient for mediating extravasation of neutrophils into pulmonary tissue during ischemia-reperfusion injury following hilar clamping or lung transplantation. The classical monocytes were mobilized from the host spleen, and splenectomy attenuated the recruitment of classical monocytes as well as the entry of neutrophils into injured lung tissue, which was associated with improved graft function. Neutrophil extravasation was mediated by MyD88-dependent IL-1ß production by graft-infiltrating classical monocytes, which downregulated the expression of the tight junction-associated protein ZO-2 in pulmonary vascular endothelial cells. Thus, we have uncovered a crucial role for classical monocytes, mobilized from the spleen, in mediating neutrophil extravasation, with potential implications for targeting of recipient classical monocytes to ameliorate pulmonary ischemia-reperfusion injury in the clinic.