Description: Pelagic processes and their relation to vertical flux have been studied in the Norwegian and Greenland Seas since 1986. Results of long-term sediment trap deployments and adjoining process studies are presented, and the underlying methodological and conceptional background is discussed. Recent extension of these investigations at the Barents Sea continental slope are also presented. With similar conditions of input irradiation and nutrient conditions, the Norwegian and Greenland Seas exhibit comparable mean annual rates of new and total production. Major differences can be found between these regions, however, in the hydrographic conditions constraining primary production and in the composition and seasonal development of the plankton. This is reflected in differences in the temporal patterns of vertical particle flux in relation to new production in the euphotic zone, the composition of particles exported and in different processes leading to their modification in the mid-water layers. In the Norwegian Sea heavy grazing pressure during early spring retards the accumulation of phytoplankton stocks and thus a mass sedimentation of diatoms that is often associated with spring blooms. This, in conjunction with the further seasonal development of zooplankton populations, serves to delay the annual peak in sedimentation to summer or autumn. Carbonate sedimentation in the Norwegian Sea, however, is significantly higher than in the Greenland Sea, where physical factors exert a greater control on phytoplankton development and the sedimentation of opal is of greater importance. In addition to these comparative long-term studies a case study has been carried out at the continental slope of the Barents Sea, where an emphasis was laid on the influence of resuspension and across-slope lateral transport with an analysis of suspended and sedimented material.

Description: Fragile X Syndrome is the most common inherited cause of autism. Fragile X mental retardation protein (FMRP), which is absent in fragile X, is an mRNA binding protein that regulates the translation of hundreds of different mRNA transcripts. In the adult brain, FMRP is expressed primarily in the neurons; however, it is also expressed in developing glial cells, where its function is not well understood. Here, we show that fragile X (Fmr1) knockout mice display abnormalities in the myelination of cerebellar axons as early as the first postnatal week, corresponding roughly to the equivalent time in human brain development when symptoms of the syndrome first become apparent (1–3 years of age). At postnatal day (PND) 7, diffusion tensor magnetic resonance imaging showed reduced volume of the Fmr1 cerebellum compared with wild-type mice, concomitant with an 80–85% reduction in the expression of myelin basic protein, fewer myelinated axons and reduced thickness of myelin sheaths, as measured by electron microscopy. Both the expression of the proteoglycan NG2 and the number of PDGFRα+/NG2+ oligodendrocyte precursor cells were reduced in the Fmr1 cerebellum at PND 7. Although myelin proteins were still depressed at PND 15, they regained wild-type levels by PND 30. These findings suggest that impaired maturation or function of oligodendrocyte precursor cells induces delayed myelination in the Fmr1 mouse brain. Our results bolster an emerging recognition that white matter abnormalities in early postnatal brain development represent an underlying neurological deficit in Fragile X syndrome.

Description: Perfluorooctane sulfonate and perfluorooctanoic acid are perfluorinated compounds (PFCs) widely distributed in the environment. Previous studies of PFCs and birth weight are equivocal. The authors examined this association in the Norwegian Mother and Child Cohort Study (MoBa), using data from 901 women enrolled from 2003 to 2004 and selected for a prior case-based study of PFCs and subfecundity. Maternal plasma samples were obtained around 17 weeks of gestation. Outcomes included birth weight z scores, preterm birth, small for gestational age, and large for gestational age. The adjusted birth weight z scores were slightly lower among infants born to mothers in the highest quartiles of PFCs compared with infants born to mothers in the lowest quartiles: for perfluorooctane sulfonate, β = –0.18 (95% confidence interval: –0.41, 0.05) and, for perfluorooctanoic acid, β = –0.21 (95% confidence interval: –0.45, 0.04). No clear evidence of an association with small for gestational age or large for gestational age was observed. Perfluorooctane sulfonate and perfluorooctanoic acid were each associated with decreased adjusted odds of preterm birth, although the cell counts were small. Whether some of the associations suggested by these findings may be due to a noncausal pharmacokinetic mechanism remains unclear.

Description: To clarify the potential role of coronary computed tomographic angiography (CCTA) in characterizing and prognosticating high-risk coronary plaques. A systematic review and meta-analysis were conducted to compare high-risk vs. low-risk plaques and culprit vs. non-culprit lesions in patients with acute coronary syndrome (ACS) vs. stable angina (SA). High-risk plaques were defined by at least one of the following features: non-calcified plaque (NCP), the presence of spotty calcified plaque (SCP), or increased remodelling index (RI). Results of included studies were pooled as odds ratios (OR) or weighted mean differences (WMD) with 95% confidence interval (CI). Eighteen eligible studies provided data to compare plaque types, plaque volume, and RI. Six studies provided data on ACS events in vulnerable high-risk vs. low-risk calcified plaques after 35 ± 2 months of follow-up. ACS patients had significantly higher number of NCP and SCP compared with SA patients with OR = 1.96 (1.47–2.60; 95% CI) P = 0.0001 and OR = 4.5 (2.98–6.83; 95% CI) P = 0.0001, respectively. Total plaque volume in ACS was not larger than SA: WMD = 22.9 (–22.1 to 67; 95% CI) mm 3 , P = 0.32, but NCP volume was significantly larger: WMD = 28.8 (10.9–46.7; 95% CI) mm 3 , P = 0.002. RI was higher in culprit lesions in ACS compared with SA and compared with non-culprit lesions in ACS patients: WMD = 0.48 (0.25–0.70; 95% CI) P = 0.0001 and 0.19 (0.07–0.30) P = 0.0001, respectively. The associated risk of future ACS was significantly higher in high-risk than in low-risk plaques: OR = 12.1 (5.24–28.1; 95% CI) P = 0.0001. CCTA can non-invasively characterize high-risk vulnerable coronary plaques and can predict future ACS events in patients with high-risk plaques.

Description: Perfluoroalkyl substances (PFAS) are persistent and ubiquitous environmental contaminants, and human exposure to these substances may be related to preeclampsia, a common pregnancy complication. Previous studies have found serum concentrations of PFAS to be positively associated with pregnancy-induced hypertension and preeclampsia in a population with high levels of exposure to perfluorooctanoate. Whether this association exists among pregnant women with background levels of PFAS exposure is unknown. Using data from the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health, we carried out a study of nulliparous pregnant women enrolled in 2003–2007 (466 cases, 510 noncases) to estimate associations between PFAS concentrations and an independently validated diagnosis of preeclampsia. We measured levels of 9 PFAS in maternal plasma extracted midpregnancy; statistical analyses were restricted to 7 PFAS that were quantifiable in more than 50% of samples. In proportional hazards models adjusted for maternal age, prepregnancy body mass index (weight (kg)/height (m) 2 ), educational level, and smoking status, we observed no strongly positive associations between PFAS levels and preeclampsia. We found an inverse association between preeclampsia and the highest quartile of perfluoroundecanoic acid concentration relative to the lowest quartile (hazard ratio = 0.55, 95% confidence interval: 0.38, 0.81). Overall, our findings do not support an increased risk of preeclampsia among nulliparous Norwegian women with background levels of PFAS exposure.