Retraction Note: Quantification of ocean heat uptake from changes in atmospheric O2 and CO2 composition.

This Article has been retracted; see accompanying Retraction Note.

Quantification of ocean heat uptake from changes in atmospheric O2 and CO2 composition.

The ocean is the main source of thermal inertia in the climate system1. During recent decades, ocean heat uptake has been quantified by using hydrographic temperature measurements and data from the Argo float program, which expanded its coverage after 20072,3. However, these estimates all use the same imperfect ocean dataset and share additional uncertainties resulting from sparse coverage, especially before 20074,5. Here we provide an independent estimate by using measurements of atmospheric oxygen (O2) and carbon dioxide (CO2)-levels of which increase as the ocean warms and releases gases-as a whole-ocean thermometer. We show that the ocean gained 1.33 ± 0.20  × 1022 joules of heat per year between 1991 and 2016, equivalent to a planetary energy imbalance of 0.83 ± 0.11 watts per square metre of Earth's surface. We also find that the ocean-warming effect that led to the outgassing of O2 and CO2 can be isolated from the direct effects of anthropogenic emissions and CO2 sinks. Our result-which relies on high-precision O2 measurements dating back to 19916-suggests that ocean warming is at the high end of previous estimates, with implications for policy-relevant measurements of the Earth response to climate change, such as climate sensitivity to greenhouse gases7 and the thermal component of sea-level rise8.

Climate-driven variability of the Southern Ocean CO2 sink.

The Southern Ocean is a major sink of atmospheric CO2, but the nature and magnitude of its variability remains uncertain and debated. Estimates based on observations suggest substantial variability that is not reproduced by process-based ocean models, with increasingly divergent estimates over the past decade. We examine potential constraints on the nature and magnitude of climate-driven variability of the Southern Ocean CO2 sink from observation-based air-sea O2 fluxes. On interannual time scales, the variability in the air-sea fluxes of CO2 and O2 estimated from observations is consistent across the two species and positively correlated with the variability simulated by ocean models. Our analysis suggests that variations in ocean ventilation related to the Southern Annular Mode are responsible for this interannual variability. On decadal time scales, the existence of significant variability in the air-sea CO2 flux estimated from observations also tends to be supported by observation-based estimates of O2 flux variability. However, the large decadal variability in air-sea CO2 flux is absent from ocean models. Our analysis suggests that issues in representing the balance between the thermal and non-thermal components of the CO2 sink and/or insufficient variability in mode water formation might contribute to the lack of decadal variability in the current generation of ocean models. This article is part of a discussion meeting issue 'Heat and carbon uptake in the Southern Ocean: the state of the art and future priorities'.

Large historical growth in global terrestrial gross primary production.

Growth in terrestrial gross primary production (GPP)-the amount of carbon dioxide that is 'fixed' into organic material through the photosynthesis of land plants-may provide a negative feedback for climate change. It remains uncertain, however, to what extent biogeochemical processes can suppress global GPP growth. As a consequence, modelling estimates of terrestrial carbon storage, and of feedbacks between the carbon cycle and climate, remain poorly constrained. Here we present a global, measurement-based estimate of GPP growth during the twentieth century that is based on long-term atmospheric carbonyl sulfide (COS) records, derived from ice-core, firn and ambient air samples. We interpret these records using a model that simulates changes in COS concentration according to changes in its sources and sinks-including a large sink that is related to GPP. We find that the observation-based COS record is most consistent with simulations of climate and the carbon cycle that assume large GPP growth during the twentieth century (31% ± 5% growth; mean ± 95% confidence interval). Although this COS analysis does not directly constrain models of future GPP growth, it does provide a global-scale benchmark for historical carbon-cycle simulations.

Evaluation of Data-Based Estimates of Anthropogenic Carbon in the Arctic Ocean.

The Arctic Ocean is particularly vulnerable to ocean acidification, a process that is mainly driven by the uptake of anthropogenic carbon (Cant) from the atmosphere. Although Cant concentrations cannot be measured directly in the ocean, they have been estimated using data-based methods such as the transient time distribution (TTD) approach, which characterizes the ventilation of water masses with inert transient tracers, such as CFC-12. Here, we evaluate the TTD approach in the Arctic Ocean using an eddying ocean model as a test bed. When the TTD approach is applied to simulated CFC-12 in that model, it underestimates the same model's directly simulated Cant concentrations by up to 12%, a bias that stems from its idealized assumption of gas equilibrium between atmosphere and surface water, both for CFC-12 and anthropogenic CO2. Unlike the idealized assumption, the simulated partial pressure of CFC-12 (pCFC-12) in Arctic surface waters is undersaturated relative to that in the atmosphere in regions and times of deep-water formation, while the simulated equivalent for Cant is supersaturated. After accounting for the TTD approach's negative bias, the total amount of Cant in the Arctic Ocean in 2005 increases by 8% to 3.3 ± 0.3 Pg C. By combining the adjusted TTD approach with scenarios of future atmospheric CO2, it is estimated that all Arctic waters, from surface to depth, would become corrosive to aragonite by the middle of the next century even if atmospheric CO2 could be stabilized at 540 ppm.

Quantification of ocean heat uptake from changes in atmospheric O2 and CO2 composition.

The ocean is the main source of thermal inertia in the climate system. Ocean heat uptake during recent decades has been quantified using ocean temperature measurements. However, these estimates all use the same imperfect ocean dataset and share additional uncertainty due to sparse coverage, especially before 2007. Here, we provide an independent estimate by using measurements of atmospheric oxygen (O2) and carbon dioxide (CO2) - levels of which increase as the ocean warms and releases gases - as a whole ocean thermometer. We show that the ocean gained 1.29 ± 0.79 × 1022 Joules of heat per year between 1991 and 2016, equivalent to a planetary energy imbalance of 0.80 ± 0.49 W watts per square metre of Earth's surface. We also find that the ocean-warming effect that led to the outgassing of O2 and CO2 can be isolated from the direct effects of anthropogenic emissions and CO2 sinks. Our result - which relies on high-precision O2 atmospheric measurements dating back to 1991 - leverages an integrative Earth system approach and provides much needed independent confirmation of heat uptake estimated from ocean data.

Ocean (de)oxygenation from the Last Glacial Maximum to the twenty-first century: insights from Earth System models.

All Earth System models project a consistent decrease in the oxygen content of oceans for the coming decades because of ocean warming, reduced ventilation and increased stratification. But large uncertainties for these future projections of ocean deoxygenation remain for the subsurface tropical oceans where the major oxygen minimum zones are located. Here, we combine global warming projections, model-based estimates of natural short-term variability, as well as data and model estimates of the Last Glacial Maximum (LGM) ocean oxygenation to gain some insights into the major mechanisms of oxygenation changes across these different time scales. We show that the primary uncertainty on future ocean deoxygenation in the subsurface tropical oceans is in fact controlled by a robust compensation between decreasing oxygen saturation (O2sat) due to warming and decreasing apparent oxygen utilization (AOU) due to increased ventilation of the corresponding water masses. Modelled short-term natural variability in subsurface oxygen levels also reveals a compensation between O2sat and AOU, controlled by the latter. Finally, using a model simulation of the LGM, reproducing data-based reconstructions of past ocean (de)oxygenation, we show that the deoxygenation trend of the subsurface ocean during deglaciation was controlled by a combination of warming-induced decreasing O2sat and increasing AOU driven by a reduced ventilation of tropical subsurface waters.This article is part of the themed issue 'Ocean ventilation and deoxygenation in a warming world'.

OCEANOGRAPHY. Contrasting futures for ocean and society from different anthropogenic CO2 emissions scenarios.

The ocean moderates anthropogenic climate change at the cost of profound alterations of its physics, chemistry, ecology, and services. Here, we evaluate and compare the risks of impacts on marine and coastal ecosystems­and the goods and services they provide­for growing cumulative carbon emissions under two contrasting emissions scenarios. The current emissions trajectory would rapidly and significantly alter many ecosystems and the associated services on which humans heavily depend. A reduced emissions scenario­consistent with the Copenhagen Accord's goal of a global temperature increase of less than 2°C­is much more favorable to the ocean but still substantially alters important marine ecosystems and associated goods and services. The management options to address ocean impacts narrow as the ocean warms and acidifies. Consequently, any new climate regime that fails to minimize ocean impacts would be incomplete and inadequate.

Vancomycin-resistant enterococci in stool specimens submitted for Clostridium difficile cytotoxin assay.

The prevalence of, and clinical risk factors associated with, vancomycin-resistant enterococcal colonization were investigated in patients suspected of having Clostridium difficile infection. Stools submitted for C difficile cytotoxin testing were screened for vancomycin-resistant enterococci (VRE). Isolates were speciated and characterized further by antibiotic susceptibility testing, DNA fingerprinting, and DNA:DNA hybridization for detection of specific vancomycin resistance genes. Of the 79 evaluable patients identified during a 3-month period, 16.5% were VRE-positive. The VRE isolates were genetically heterogeneous, although all carried the vanA gene. DNA fingerprinting data suggest that patient-to-patient transmission occurred, implicating colonized patients as potential reservoirs for VRE transmission. A positive C difficile cytotoxin assay and diabetes mellitus were the only identifiable risk factors associated with VRE colonization. Patients at risk for C difficile infection therefore may serve as reservoirs for VRE.

Molecular epidemiology of vancomycin-resistant enterococci from 6 hospitals in New York State.

BACKGROUND: Vancomycin resistance among enterococci is an emerging nosocomial problem. Consequently, it is important to understand the distribution of vancomycin-resistant enterococci (VRE) within and between hospitals to implement appropriate infection control measures. METHODS: In this study, 116 VRE isolates obtained from patients in 6 New York State hospitals were analyzed by antibiotic susceptibility testing, pulsed-field gel electrophoresis (PFGE) fingerprinting, plasmid profile analysis, vanA and vanB polymerase chain reaction, and DNA:DNA hybridization with vanA and vanB probes. RESULTS: PFGE and plasmid typing generally agreed, but plasmid profiles were more variable. These analyses revealed that genetic heterogeneity among isolates from within each of the 6 hospitals varied considerably. Among 23 Enterococcus faecium isolates from one hospital, there were only 3 PFGE types, and 20 isolates had the same type. However, in another hospital, each isolate was genetically distinct. Closely related strains were not found in separate hospitals. VRE strains with vanA genes and strains with vanB genes were found in 3 hospitals. Both plasmid and chromosomal carriage of these genes was detected. CONCLUSIONS: PFGE typing showed that nosocomial VRE transmission had occurred in some hospitals. However, there was no evidence for it in others. Neither was there evidence for intrahospital transmission or for emergence of an endemic strain. These observations demonstrate that it is important to evaluate genetic heterogeneity among VRE before implementation of infection control measures. PFGE is the method of choice for epidemiologic typing, but polymerase chain reaction, plasmid, and hybridization studies can provide important information concerning the presence and potential for transfer of vancomycin resistance genes.

Microbicidal activity of MDI-P against Candida albicans, Staphylococcus aureus, Pseudomonas aeruginosa, and Legionella pneumophila.

BACKGROUND: MDI-P (Medical Discoveries, Inc-Pharmaceutical, Layton, Utah) is a clear, colorless liquid generated by electrolysis of preservative-free and endotoxin-free, nonpyrogenic, sterile, injection saline (0.9% NaCl, wt/vol). It contains numerous highly reactive chlorine and oxygen species, including HOCl(-1,) OCl-(1), Cl(-1), Cl(2), O(2-)(1), and O(3). This report presents data on the in vitro microbicidal activity of MDI-P against 4 clinically relevant microbial pathogens that are often difficult to eradicate. METHODS: MDI-P was generated from injection saline by using a patented electrolysis instrument. It was then tested for microbicidal activity at concentrations ranging from 0.01% to 50% against Staphylococcus aureus, Pseudomonas aeruginosa, Legionella pneumophila, and Candida albicans (10(5) to 10(9) colony-forming units/mL). The effect of serum (50% and 90%) and pH on MDI-P activity were also tested. The morphologic effects of MDI-P on microbial cells were studied by light microscopy of cells stained by Gram's method and by transmission electron microscopy. Morbidity, mortality, and the effect of MDI-P on tissues were studied by using a mouse model. RESULTS: The microbicidal activity of MDI-P occurred within the first minute of exposure for all the organisms tested. When 50% MDI-P was tested against cell titers of 10(5) or 10(7) colony-forming units/mL, all test organisms were killed within 1 minute; at lower MDI-P concentrations, C albicans was the most sensitive organism, and L pneumophila was the most resistant. Even with beginning cell titers of 10(9) colony-forming units/mL, killing by 50% MDI-P was >99.9% for all test strains. Furthermore, at the same beginning cell titer, killing of C albicans by MDI-P diluted to 50% with normal human serum rather than injection saline was only slightly reduced. No acute morbidity, mortality, or tissue damage was detected in mice that were intravenously given 17 mL/kg of undiluted MDI-P. CONCLUSIONS: MDI-P is a very fast-acting, broad-spectrum microbicidal material. The lack of evidence for acute morbidity, mortality, or tissue injury, ease of preparation, and low cost suggest that it may be useful for various sterilization and disinfection applications.

Pseudomonas aeruginosa cytotoxin as a pathogenicity factor in a systemic infection of leukopenic mice.

The effect of Pseudomonas aeruginosa cytotoxin was assessed in leukopenic outbred Swiss male mice (20 g) using a high cytotoxin-producing strain (PA158) and its cytotoxin-deficient isogenic mutant (PA114F5) generated by Tn7::Tn5 transposon mutagenesis of PA158. Leukopenia was induced by intraperitoneal (i.p.) administration of cyclophosphamide (150 micrograms/g). Anesthetized mice were infected via a 4 mm incision on the shaved back with 300 CFU/mouse (9 LD50; expected death rate 85%). Precleared mouse cytotoxin-specific heat inactivated rabbit polyclonal antibody (RPA) was administered i.p. (0.2 ml) 24 hr before challenge. Controls received i.p. normal rabbit serum, RPA, cyclophosphamide alone, or a sham procedure. Challenge with the high cytotoxin-producing strain PA158 caused earlier and a significantly greater mortality than that observed with a cytotoxin-deficient strain PA114F5 (P < 0.01). Cytotoxin-specific polyclonal antibody was protective. Pretreatment with antibody decreased the mortality rate following challenge with PA158 from 88.9% to 27.8% (P < 0.01). Pretreatment with antibody decreased the mortality rate following challenge with PA114F5 from 27.8% to 5.6% (P < 0.05). These results demonstrate that P. aeruginosa cytotoxin contributes to the pathogenicity of the organism and that cytotoxin antibody is protective in a systemic P. aeruginosa infection in leukopenic mice.

Impact of episodic vertical fluxes on sea surface pCO2.

Episodic events like hurricanes, storms and frontal- and eddy-driven upwelling can alter the partial pressure of CO(2) (pCO(2)) at the sea surface by entraining subsurface waters into the surface mixed layer (ML) of the ocean. Since pCO(2) is a function of total dissolved inorganic carbon (DIC), temperature (T), salinity and alkalinity, it responds to the combined impacts of physical, chemical and biological changes. Here, we present an analytical framework for assessing the relative magnitude and sign in the short-term perturbation of surface pCO(2) arising from vertical mixing events. Using global, monthly, climatological datasets, we assess the individual, as well as integrated, contribution of various properties to surface pCO(2) in response to episodic mixing. The response depends on the relative vertical gradients of properties beneath the ML. Many areas of the ocean exhibit very little sensitivity to mixing owing to the compensatory effects of DIC and T on pCO(2), whereas others, such as the eastern upwelling margins, have the potential to generate large positive/negative anomalies in surface pCO(2). The response varies seasonally and spatially and becomes more intense in subtropical and subpolar regions during summer. Regions showing a greater pCO(2) response to vertical mixing are likely to exhibit higher spatial variability in surface pCO(2) on time scales of days.

Chromate resistance plasmid in Pseudomonas fluorescens.

Chromate resistance of Pseudomonas fluorescens LB300, isolated from chromium-contaminated sediment in the upper Hudson River, was found to be plasmid specified. Loss of the plasmid (pLHB1) by spontaneous segregation or mitomycin C curing resulted in a simultaneous loss of chromate resistance. Subsequent transformation of such strains with purified pLHB1 plasmid DNA resulted in a simultaneous re-acquisition of the chromate resistance phenotype and the plasmid. When pLHB1 was transferred by conjugation to Escherichia coli, the plasmid still conferred chromate resistance.

Transposition of plasmid DNA segments specifying hydrocarbon degradation and their expression in various microorganisms.

The conjugative TOL plasmid (75 Mdal), specifying biodegradation of xylenes, toluene, and trimethylbenzene derivatives, undergoes dissociation in Pseudomonas aeruginosa PAO to a nonconjugative TOL(*) plasmid (28 Mdal) and a transfer plasmid termed TOLDelta (48 Mdal). The TOL(*) plasmid is rendered transmissible through introduction of a number of conjugative plasmids such as factor K, CAM, and TOLDelta but not by the FP2 derivative pR0271. Transfer of TOL(*) via factor K or TOLDelta is mediated by the formation of plasmid cointegrates; no recombination is observed with CAM. A recombinant RP4-TOL plasmid (76 Mdal), which has lost resistance to tetracycline, has been isolated. The TOL(*) segment can be transposed from this RP4-TOL recombinant plasmid to other antibiotic resistance plasmids such as R702. A segment of DNA, specifying salicylate degradation from SAL plasmid, was transposed onto pAC10, the TOL(*-) derivative of RP4-TOL recombinant plasmid, which has lost resistance to tetracycline but retains the transfer genes of RP4. Transposition of the salicylate degradative genes onto pAC10 results in the loss of kanamycin resistance. It has been possible to isolate SAL(+) segregants from pAC10[unk]SAL transposition derivatives that have lost the pAC10 plasmid. Such segregants harbor the salicylate degradative genes in the form of a nonconjugative plasmid (SAL(*)). Transfer of RP4[unk]TOL(*) or pAC10[unk]SAL(*) transposition derivatives to Escherichia coli, Salmonella typhimurium, Agrobacterium tumefaciens, or Azotobacter vinelandii results in the functional expression of the antibiotic resistance genes but not of the hydrocarbon degradative genes. Such genes, however, are fully expressed on being transferred back to Pseudomonas.

Cloning of a Thiobacillus ferrooxidans plasmid in Escherichia coli.

Three separate plasmids of 6, 7, 16, and greater than 23 kilobases were purified from a single clone of Thiobacillus ferrooxidans ATCC 33020 grown in the presence of uranium. The 6.7-kilobase plasmid (pTf1) was cloned separately into the HindIII or BamHI site of Escherichia coli plasmid pBR322. Restriction maps of the recombinant plasmids, termed pTf100 and pTf110, respectively, were constructed, creating potential cloning vehicles for exchanging genetic information between E. coli and T. ferrooxidans. Evidence from restriction enzyme analysis and Southern blot DNA-DNA hybridization indicates that the three native plasmids share little sequence homology.

Comparison of inhibitory and bactericidal activities and postantibiotic effects of LY333328 and ampicillin used singly and in combination against vancomycin-resistant Enterococcus faecium.

One hundred ninety-five individual vancomycin-resistant Enterococcus faecium (VRE) isolates from five upstate New York hospitals were studied for antimicrobial susceptibilities to LY333328, quinupristin-dalfopristin, teicoplanin, ampicillin, and gentamicin. LY333328 was the most active antibiotic against VRE. The effect of media and methods on the antibacterial activity of LY333328, its synergy with ampicillin, and the postantibiotic effects (PAE) of LY333328 and ampicillin were evaluated. In microdilution tests, the MIC of LY333328 at which 90% of the isolates were inhibited (MIC90) was 2 microg/ml in Mueller-Hinton II (MH II) broth and 1 microg/ml in brain heart infusion (BHI) broth. In contrast, on MH II agar the MIC90 was 4 microg/ml and on BHI agar it was >16 microg/ml. Bactericidal activity was observed for most strains at concentrations from 8 to >/=133 times the MIC of the tube macrodilution in MH II broth. A bactericidal effect of LY333328 plus ampicillin was demonstrated in time-kill studies, but there was great strain-to-strain variability. By the MH II agar dilution method, bacteristatic synergy (defined as a fractional inhibitory concentration of <0.5) with LY333328 and ampicillin was demonstrated for 61% of the strains tested. Under similar conditions, there was synergy with LY333328 and quinupristin-dalfopristin or gentamicin for 27 and 15% of the strains tested, respectively. The PAE of LY333328 was prolonged (23.0 h at 10 times the MIC). However, 50% normal pooled human serum decreased the PAE to 12.2 h at 10 times the MIC. Test conditions and media had a considerable effect on VRE susceptibilities to LY333328. The prolonged PAE of LY333328, a potent new bactericidal glycopeptide, and its synergy with ampicillin in a large proportion of strains suggest that further evaluation of this drug in pharmacokinetic studies and experimental infections, including those with VRE, is warranted.

DNA probes for the identification of Haemophilus ducreyi.

Haemophilus ducreyi ATCC 33922, a virulent, well-characterized strain, was used to construct a genomic library in a bacteriophage expression vector. Three DNA fragments were selected for use as probes on the basis of their ability to encode H. ducreyi-specific proteins, as demonstrated by reactivity with rabbit polyclonal antiserum. With DNA-DNA hybridization, the three probes, labeled with 32P, reacted strongly with 16 strains of H. ducreyi obtained from a variety of sources. Thirty-seven other bacterial isolates, representing 33 different species and including organisms likely to be encountered in the urogenital tract, were also tested with the three probes. Twenty-eight of these isolates, including the genital pathogen Neisseria gonorrhoeae, showed no hybridization with the probes. In addition, herpes simplex virus-infected tissue culture cells and Treponema pallidum-infected rabbit testicular fluid were also completely nonreactive. Nine isolates, six belonging to other Haemophilus species and three belonging to Pasteurella species, reacted weakly with the probes when approximately 3.0 x 10(7) to 6.0 x 10(7) CFU was tested. When 10(5) to 10(6) CFU of these organisms was tested, the weak reactions could no longer be seen. Yet this number of H. ducreyi still reacted strongly. In fact, the three probes consistently detected 10(4) CFU of H. ducreyi in pure and mixed cultures and even produced a weak signal when only 10(3) CFU was present. It is clear from our results that use of these probes will greatly facilitate the laboratory diagnosis of this genital pathogen.

Inhibitory and bactericidal effects of telithromycin (HMR 3647, RU 56647) and five comparative antibiotics, used singly and in combination, against vancomycin-resistant and vancomycin-susceptible enterococci.

The inhibitory and bactericidal effects of telithromycin (HMR 3647, RU 66647) were compared with those of gentamicin, ampicillin, erythromycin, azithromycin and vancomycin against 74 strains of enterococci (34 Enterococcus faecalis and 40 Enterococcus faecium) by agar dilution, broth dilution, time kill assays and postantibiotic effect (PAE). The telithromycin MIC(90) for vancomycin-sensitive (VSE) E. faecalis strains tested using the agar dilution method was 8 microg/ml. For a different group of VSE E. faecalis strains tested using the broth dilution method it was 0.06 microg/ml The telithromycin MIC(90)s for vancomycin-resistant (VRE) and VSE E. faecium strains, determined using the agar dilution method, were 4 and 8 microg/ml, respectively, while for a different set of VRE and VSE E. faecium strains tested using the broth macrodilution method, they were 32 and 16 microg/ml, respectively. Telithromycin MBC(90)s for E. faecalis were 4-6 tubes higher and for E. faecium 3-5 tubes higher, respectively, than the MIC(90)s. In time kill assays, telithromycin had bactericidal activity against only 1 of 7 E. faecium strains; for all other E. faecium and E. faecalis strains, only inhibitory activity was demonstrated. Neither synergy nor drug interference was observed when telithromycin was used in combination with ampicillin, vancomycin or gentamicin. At 10 times the MIC, the PAE of telithromycin against E. faecalis was 2.8 h, while for E. faecium it was 1.6 h. Telithromycin should be evaluated for therapy of enterococcal infections, including those caused by VRE organisms. However, because of the strain-to-strain variability in susceptibility to telithromycin, MIC determinations are important, especially for erythromycin-resistant strains.