Fluorinated Precursor Compounds in Sediments as a Source of Perfluorinated Alkyl Acids (PFAA) to Biota

The environmental behavior of perfluorinated alkyl acids (PFAA) and their precursors was investigated in lake Tyrifjorden, downstream a factory producing paper products coated with per- and polyfluorinated alkyl substances (PFAS). Low water concentrations (max 0.18 ng L–1 linear perfluorooctanesulfonic acid, L-PFOS) compared to biota (mean 149 μg kg–1 L-PFOS in perch livers) resulted in high bioaccumulation factors (L-PFOS BAFPerch liver: 8.05 × 105–5.14 × 106). Sediment concentrations were high, particularly for the PFOS precursor SAmPAP diester (max 1 872 μg kg–1). Biota-sediment accumulation factors (L-PFOS BSAFPerch liver: 22–559) were comparable to elsewhere, and concentrations of PFAA precursors and long chained PFAA in biota were positively correlated to the ratio of carbon isotopes (13C/12C), indicating positive correlations to dietary intake of benthic organisms. The sum fluorine from targeted analyses accounted for 54% of the extractable organic fluorine in sediment, and 9–108% in biota. This, and high trophic magnification factors (TMF, 3.7–9.3 for L-PFOS), suggests that hydrophobic precursors in sediments undergo transformation and are a main source of PFAA accumulation in top predator fish. Due to the combination of water exchange and dilution, transformation of larger hydrophobic precursors in sediments can be a source to PFAA, some of which are normally associated with uptake from water.publishedVersio

Desmoteplase 3 to 9 Hours After Major Artery Occlusion Stroke: The DIAS-4 Trial (Efficacy and Safety Study of Desmoteplase to Treat Acute Ischemic Stroke)

The DIAS-3 trial (Efficacy and Safety Study of Desmoteplase to Treat Acute Ischemic Stroke [phase 3]) did not demonstrate a significant clinical benefit of desmoteplase administered 3 to 9 hours after stroke in patients with major artery occlusion. We present the results of the prematurely terminated DIAS-4 trial together with a post hoc pooled analysis of the concomitant DIAS-3, DIAS-4, and DIAS-J (Japan) trials to better understand the potential risks and benefits of intravenous desmoteplase for the treatment of ischemic stroke in an extended time window

Clues for early detection of autoimmune Addison's disease - myths and realities

BACKGROUND: Early detection of autoimmune Addison's disease (AAD) is important as delay in diagnosis may result in a life-threatening adrenal crisis and death. The classical clinical picture of untreated AAD is well-described, but methodical investigations are scarce. OBJECTIVE: Perform a retrospective audit of patient records with the aim of identifying biochemical markers for early diagnosis of AAD. MATERIAL AND METHODS: A multicentre retrospective study including 272 patients diagnosed with AAD at hospitals in Norway and Sweden during 1978-2016. Scrutiny of medical records provided patient data and laboratory values. RESULTS: Low sodium occurred in 207 of 247 (84%), but only one-third had elevated potassium. Other common nonendocrine tests were largely normal. TSH was elevated in 79 of 153 patients, and hypoglycaemia was found in 10%. Thirty-three per cent were diagnosed subsequent to adrenal crisis, in whom electrolyte disturbances were significantly more pronounced (P < 0.001). Serum cortisol was consistently decreased (median 62 nmol L(-1) [1-668]) and significantly lower in individuals with adrenal crisis (38 nmol L(-1) [2-442]) than in those without (81 nmol L(-1) [1-668], P < 0.001). CONCLUSION: The most consistent biochemical finding of untreated AAD was low sodium independent of the degree of glucocorticoid deficiency. Half of the patients had elevated TSH levels. Only a minority presented with marked hyperkalaemia or other nonhormonal abnormalities. Thus, unexplained low sodium and/or elevated TSH should prompt consideration of an undiagnosed AAD, and on clinical suspicion bring about assay of cortisol and ACTH. Presence of 21-hydroxylase autoantibodies confirms autoimmune aetiology. Anticipating additional abnormalities in routine blood tests may delay diagnosis