Predicting the Distribution of Indicator Taxa of Vulnerable Marine Ecosystems in the Arctic and Sub-arctic Waters of the Nordic Seas

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Detecting changes in the Arctic Ecosystem – Long-Term Benthos Monitoring network for detecting changes in the Arctic benthic ecosystem (LTM-Benthos) 2017-2020

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First record of Halicardia flexuosa (Verrill & S. Smith, 1881) (Bivalvia: Verticordiidae) alive in Icelandic waters

Volume: 17Start Page: 55End Page: 5

Vulnerable marine ecosystems (VMEs) Coral and sponge VMEs in Arctic and sub-Arctic waters – Distribution and threats

This report presents results from the NovasArc project that has collated data on the distribution of vulnerable marine ecosystems (VMEs) in Arctic and sub-Arctic waters. Eleven VMEs were identified, based on management goals for coral and sponge communities. Many of the vulnerable marine ecosystems (VMEs) in the study area has a wide distribution. Soft and hard bottom sponge aggregations, hard bottom gorgonians, sublittoral sea pen communities, and cauliflower corals are predicted to cover > 20% of the study area shallower than 1000 meters. Of the anthropogenic activities in the study area bottom trawling represents the main threat to the VMEs. The compilation of trawling activity in the study area shows that fisheries mainly occurs shallower than 1000 meters and that 50 to 60% of the seafloor is not targeted. However, 30% of the seafloor has experienced intermediate to very high fishing effort. In general, the VMEs shows a larger overlap with fishing when the risk analysis is based on areas with an optimal habitat suitability. Using this conservative threshold to model the distribution of VMEs the results indicate that most VMEs have experienced an intermediate to high level of fishing in less than 40% of their distribution area in the whole study area

Lifelong Reduction in LDL (Low-Density Lipoprotein) Cholesterol due to a Gain-of-Function Mutation in LDLR

To access publisher's full text version of this article click on the hyperlink belowBackground: Loss-of-function mutations in the LDL (low-density lipoprotein) receptor gene (LDLR) cause elevated levels of LDL cholesterol and premature cardiovascular disease. To date, a gain-of-function mutation in LDLR with a large effect on LDL cholesterol levels has not been described. Here, we searched for sequence variants in LDLR that have a large effect on LDL cholesterol levels. Methods: We analyzed whole-genome sequencing data from 43 202 Icelanders. Single-nucleotide polymorphisms and structural variants including deletions, insertions, and duplications were genotyped using whole-genome sequencing-based data. LDL cholesterol associations were carried out in a sample of >100 000 Icelanders with genetic information (imputed or whole-genome sequencing). Molecular analyses were performed using RNA sequencing and protein expression assays in Epstein-Barr virus-transformed lymphocytes. Results: We discovered a 2.5-kb deletion (del2.5) overlapping the 3' untranslated region of LDLR in 7 heterozygous carriers from a single family. Mean level of LDL cholesterol was 74% lower in del2.5 carriers than in 101 851 noncarriers, a difference of 2.48 mmol/L (96 mg/dL; P=8.4×10-8). Del2.5 results in production of an alternative mRNA isoform with a truncated 3' untranslated region. The truncation leads to a loss of target sites for microRNAs known to repress translation of LDLR. In Epstein-Barr virus-transformed lymphocytes derived from del2.5 carriers, expression of alternative mRNA isoform was 1.84-fold higher than the wild-type isoform (P=0.0013), and there was 1.79-fold higher surface expression of the LDL receptor than in noncarriers (P=0.0086). We did not find a highly penetrant detrimental impact of lifelong very low levels of LDL cholesterol due to del2.5 on health of the carriers. Conclusions: Del2.5 is the first reported gain-of-function mutation in LDLR causing a large reduction in LDL cholesterol. These data point to a role for alternative polyadenylation of LDLR mRNA as a potent regulator of LDL receptor expression in humans. Keywords: cardiovascular disease; genetics; lipids; microRNA; polyadenylation.deCODE genetics/Amgen, In

Humoral Immune Response to SARS-CoV-2 in Iceland.

To access publisher's full text version of this article click on the hyperlink belowBackground: Little is known about the nature and durability of the humoral immune response to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Methods: We measured antibodies in serum samples from 30,576 persons in Iceland, using six assays (including two pan-immunoglobulin [pan-Ig] assays), and we determined that the appropriate measure of seropositivity was a positive result with both pan-Ig assays. We tested 2102 samples collected from 1237 persons up to 4 months after diagnosis by a quantitative polymerase-chain-reaction (qPCR) assay. We measured antibodies in 4222 quarantined persons who had been exposed to SARS-CoV-2 and in 23,452 persons not known to have been exposed. Results: Of the 1797 persons who had recovered from SARS-CoV-2 infection, 1107 of the 1215 who were tested (91.1%) were seropositive; antiviral antibody titers assayed by two pan-Ig assays increased during 2 months after diagnosis by qPCR and remained on a plateau for the remainder of the study. Of quarantined persons, 2.3% were seropositive; of those with unknown exposure, 0.3% were positive. We estimate that 0.9% of Icelanders were infected with SARS-CoV-2 and that the infection was fatal in 0.3%. We also estimate that 56% of all SARS-CoV-2 infections in Iceland had been diagnosed with qPCR, 14% had occurred in quarantined persons who had not been tested with qPCR (or who had not received a positive result, if tested), and 30% had occurred in persons outside quarantine and not tested with qPCR. Conclusions: Our results indicate that antiviral antibodies against SARS-CoV-2 did not decline within 4 months after diagnosis. We estimate that the risk of death from infection was 0.3% and that 44% of persons infected with SARS-CoV-2 in Iceland were not diagnosed by qPCR