Water mass transformation in the Greenland Sea during the 1990s

Time series of hydrographic and transient tracer measurements were used to study the variability of Greenland Sea water mass transformation between 1991 and 2000. Increases in tracer inventories indicate active renewal of Greenland Sea Intermediate Water (GSIW) at a rate of 0.1 to 0.2 Sv (1 Sv = 1 × 106 m3 s−1) (10-year average). A temperature maximum (Tmax) was established at the base of the upper layer (500 m) as a consequence of anomalously strong freshwater input into the near-surface layer at the beginning of the 1990s. Tmax rapidly descended to 1500 m by 1995 followed by a much slower rate of descent. GSIW became warmer and less saline compared to the 1980s. During the deepening phase of Tmax, atmospheric data revealed above-average wind stress curl and oceanic heat loss. In addition, high Arctic Ocean sea-ice export and lack of local sea-ice formation have been documented for that period. A combination of all these factors may have evoked the renewal of GSIW with anomalously freshwater from the upper layers. The Tmax layer established a stability maximum that inhibits vertical exchange between intermediate and deeper waters. Temperature and salinity of deep waters continued to increase at rates of 0.01°C yr−1 and 0.001 yr−1, respectively. However, since 1993, decrease in and homogenization of deep water transient tracer concentrations indicate that renewal occurred predominantly by addition of Arctic Ocean waters. In 2000 the water column (500 m to 3400 m) required an additional 60 W m−2 (110 W m−2) over the annual mean heat loss to restore its heat content to 1989 (1971) values

Diversity, functional classification and genotyping of SHV β-lactamases in Klebsiella pneumoniae

Interpreting the phenotypes of $\it{bla}_{SHV}$ alleles in $\it{Klebsiella\ pneumoniae}$ genomes is complex. Whilst all strains are expected to carry a chromosomal copy conferring resistance to ampicillin, they may also carry mutations in chromosomal $\it{bla}_{SHV}$ alleles or additional plasmid-borne $\it{bla}_{SHV}$ alleles that have extended-spectrum $\beta$-lactamase (ESBL) activity and/or $\beta$-lactamase inhibitor (BLI) resistance activity. In addition, the role of individual mutations/aa changes is not completely documented or understood. This has led to confusion in the literature and in antimicrobial resistance (AMR) gene databases [e.g. the National Center for Biotechnology Information (NCBI) Reference Gene Catalog and the $\beta$-lactamase database (BLDB)] over the specific functionality of individual sulfhydryl variable (SHV) protein variants. Therefore, the identification of ESBL-producing strains from $\it{K.\ pneumoniae}$ genome data is complicated. Here, we reviewed the experimental evidence for the expansion of SHV enzyme function associated with specific aa substitutions. We then systematically assigned SHV alleles to functional classes (WT, ESBL and BLI resistant) based on the presence of these mutations. This resulted in the re-classification of 37 SHV alleles compared with the current assignments in the NCBI''s Reference Gene Catalog and/or BLDB (21 to WT, 12 to ESBL and 4 to BLI resistant). Phylogenetic and comparative genomic analyses support that (i) SHV-1 (encoded by $\it{bla}_{SHV-1}$) is the ancestral chromosomal variant, (ii) ESBL- and BLI-resistant variants have evolved multiple times through parallel substitution mutations, (iii) ESBL variants are mostly mobilized to plasmids and (iv) BLI-resistant variants mostly result from mutations in chromosomal $\it{bla}_{SHV}$. We used matched genome-phenotype data from the KlebNET-GSP AMR Genotype-Phenotype Group to identify 3999 $\it{K. pneumoniae}$ isolates carrying one or more $\it{bla}_{SHV}$ alleles but no other acquired $\beta$-lactamases to assess genotype-phenotype relationships for $\it{bla}_{SHV}$. This collection includes human, animal and environmental isolates collected between 2001 and 2021 from 24 countries. Our analysis supports that mutations at Ambler sites 238 and 179 confer ESBL activity, whilst most omega-loop substitutions do not. Our data also provide support for the WT assignment of 67 protein variants, including 8 that were noted in public databases as ESBL. These eight variants were reclassified as WT because they lack ESBL-associated mutations, and our phenotype data support susceptibility to third-generation cephalosporins (SHV-27, SHV-38, SHV-40, SHV-41, SHV-42, SHV-65, SHV-164 and SHV-187). The approach and results outlined here have been implemented in Kleborate v2.4.1 (a software tool for genotyping $\it{K. pneumoniae}$), whereby known and novel $\it{bla}_{SHV}$ alleles are classified based on causative mutations. Kleborate v2.4.1 was updated to include ten novel protein variants from the KlebNET-GSP dataset and all alleles in public databases as of November 2023. This study demonstrates the power of sharing AMR phenotypes alongside genome data to improve the understanding of resistance mechanisms.

Diversity, functional classification and genotyping of SHV β-lactamases in Klebsiella pneumoniae.

Interpreting the phenotypes of bla SHV alleles in Klebsiella pneumoniae genomes is complex. Whilst all strains are expected to carry a chromosomal copy conferring resistance to ampicillin, they may also carry mutations in chromosomal bla SHV alleles or additional plasmid-borne bla SHV alleles that have extended-spectrum β-lactamase (ESBL) activity and/or β-lactamase inhibitor (BLI) resistance activity. In addition, the role of individual mutations/a changes is not completely documented or understood. This has led to confusion in the literature and in antimicrobial resistance (AMR) gene databases [e.g. the National Center for Biotechnology Information (NCBI) Reference Gene Catalog and the β-lactamase database (BLDB)] over the specific functionality of individual sulfhydryl variable (SHV) protein variants. Therefore, the identification of ESBL-producing strains from K. pneumoniae genome data is complicated. Here, we reviewed the experimental evidence for the expansion of SHV enzyme function associated with specific aa substitutions. We then systematically assigned SHV alleles to functional classes (WT, ESBL and BLI resistant) based on the presence of these mutations. This resulted in the re-classification of 37 SHV alleles compared with the current assignments in the NCBI's Reference Gene Catalog and/or BLDB (21 to WT, 12 to ESBL and 4 to BLI resistant). Phylogenetic and comparative genomic analyses support that (i) SHV-1 (encoded by bla SHV-1) is the ancestral chromosomal variant, (ii) ESBL- and BLI-resistant variants have evolved multiple times through parallel substitution mutations, (iii) ESBL variants are mostly mobilized to plasmids and (iv) BLI-resistant variants mostly result from mutations in chromosomal bla SHV. We used matched genome-phenotype data from the KlebNET-GSP AMR Genotype-Phenotype Group to identify 3999 K. pneumoniae isolates carrying one or more bla SHV alleles but no other acquired β-lactamases to assess genotype-phenotype relationships for bla SHV. This collection includes human, animal and environmental isolates collected between 2001 and 2021 from 24 countries. Our analysis supports that mutations at Ambler sites 238 and 179 confer ESBL activity, whilst most omega-loop substitutions do not. Our data also provide support for the WT assignment of 67 protein variants, including 8 that were noted in public databases as ESBL. These eight variants were reclassified as WT because they lack ESBL-associated mutations, and our phenotype data support susceptibility to third-generation cephalosporins (SHV-27, SHV-38, SHV-40, SHV-41, SHV-42, SHV-65, SHV-164 and SHV-187). The approach and results outlined here have been implemented in Kleborate v2.4.1 (a software tool for genotyping K. pneumoniae), whereby known and novel bla SHV alleles are classified based on causative mutations. Kleborate v2.4.1 was updated to include ten novel protein variants from the KlebNET-GSP dataset and all alleles in public databases as of November 2023. This study demonstrates the power of sharing AMR phenotypes alongside genome data to improve the understanding of resistance mechanisms

The East Greenland Current and its impacts on the Nordic Seas: observed trends in the past decade

For the past 30 years, it has been known that dense waters are created in the Arctic Ocean. However, before the late 1980s, observations indicated that Arctic Ocean deep waters only modified the deep water in the Greenland Sea, which was still thought of as the major source of dense water. In the mid-1990s, this picture began to fade. The deep convection in the Greenland Sea weakened and only Arctic Intermediate Water was formed. A deep salinity maximum was reinforced and a temperature maximum emerged at middepth. The densities of the salinity and temperature maxima were those of the deep waters in the Arctic Ocean, and one possibility was that waters below the convection were ventilated by Arctic Ocean deep waters from the East Greenland Current. Between 1998 and 2010, the salinity and temperature of the deep water in the Greenland Sea increased, implying continuous input from the East Greenland Current. Water from the Greenland Sea advected to Fram Strait now has almost Arctic Ocean characteristics and cannot significantly change the outflowing Arctic Ocean waters by mixing in the East Greenland Current, leading to a more-rapid transformation of the deep Greenland Sea water column