Global reconstruction reduces the uncertainty of oceanic nitrous oxide emissions and reveals a vigorous seasonal cycle.

Assessment of the global budget of the greenhouse gas nitrous oxide ([Formula: see text]O) is limited by poor knowledge of the oceanic [Formula: see text]O flux to the atmosphere, of which the magnitude, spatial distribution, and temporal variability remain highly uncertain. Here, we reconstruct climatological [Formula: see text]O emissions from the ocean by training a supervised learning algorithm with over 158,000 [Formula: see text]O measurements from the surface ocean-the largest synthesis to date. The reconstruction captures observed latitudinal gradients and coastal hot spots of [Formula: see text]O flux and reveals a vigorous global seasonal cycle. We estimate an annual mean [Formula: see text]O flux of 4.2 ± 1.0 Tg N[Formula: see text], 64% of which occurs in the tropics, and 20% in coastal upwelling systems that occupy less than 3% of the ocean area. This [Formula: see text]O flux ranges from a low of 3.3 ± 1.3 Tg N[Formula: see text] in the boreal spring to a high of 5.5 ± 2.0 Tg N[Formula: see text] in the boreal summer. Much of the seasonal variations in global [Formula: see text]O emissions can be traced to seasonal upwelling in the tropical ocean and winter mixing in the Southern Ocean. The dominant contribution to seasonality by productive, low-oxygen tropical upwelling systems (>75%) suggests a sensitivity of the global [Formula: see text]O flux to El Niño-Southern Oscillation and anthropogenic stratification of the low latitude ocean. This ocean flux estimate is consistent with the range adopted by the Intergovernmental Panel on Climate Change, but reduces its uncertainty by more than fivefold, enabling more precise determination of other terms in the atmospheric [Formula: see text]O budget.

Single cell genomic and transcriptomic evidence for the use of alternative nitrogen substrates by anammox bacteria.

Anaerobic ammonium oxidation (anammox) contributes substantially to ocean nitrogen loss, particularly in anoxic marine zones (AMZs). Ammonium is scarce in AMZs, raising the hypothesis that organic nitrogen compounds may be ammonium sources for anammox. Biochemical measurements suggest that the organic compounds urea and cyanate can support anammox in AMZs. However, it is unclear if anammox bacteria degrade these compounds to ammonium themselves, or rely on other organisms for this process. Genes for urea degradation have not been found in anammox bacteria, and genomic evidence for cyanate use for anammox is limited to a cyanase gene recovered from the sediment bacterium Candidatus Scalindua profunda. Here, analysis of Ca. Scalindua single amplified genomes from the Eastern Tropical North Pacific AMZ revealed genes for urea degradation and transport, as well as for cyanate degradation. Urease and cyanase genes were transcribed, along with anammox genes, in the AMZ core where anammox rates peaked. Homologs of these genes were also detected in meta-omic datasets from major AMZs in the Eastern Tropical South Pacific and Arabian Sea. These results suggest that anammox bacteria from different ocean regions can directly access organic nitrogen substrates. Future studies should assess if and under what environmental conditions these substrates contribute to the ammonium budget for anammox.

NC10 bacteria in marine oxygen minimum zones.

Bacteria of the NC10 phylum link anaerobic methane oxidation to nitrite denitrification through a unique O2-producing intra-aerobic methanotrophy pathway. A niche for NC10 in the pelagic ocean has not been confirmed. We show that NC10 bacteria are present and transcriptionally active in oceanic oxygen minimum zones (OMZs) off northern Mexico and Costa Rica. NC10 16S rRNA genes were detected at all sites, peaking in abundance in the anoxic zone with elevated nitrite and methane concentrations. Phylogenetic analysis of particulate methane monooxygenase genes further confirmed the presence of NC10. rRNA and mRNA transcripts assignable to NC10 peaked within the OMZ and included genes of the putative nitrite-dependent intra-aerobic pathway, with high representation of transcripts containing the unique motif structure of the nitric oxide (NO) reductase of NC10 bacteria, hypothesized to participate in O2-producing NO dismutation. These findings confirm pelagic OMZs as a niche for NC10, suggesting a role for this group in OMZ nitrogen, methane and oxygen cycling.

Plasma nonesterified Fatty Acid intolerance and hyperglycemia are associated with intravenous lipid-induced impairment of insulin sensitivity and disposition index.

CONTEXT: It is currently unclear why susceptibility to lipid-induced impairment of beta-cell function varies in different populations. OBJECTIVE: The aim of the study was to determine whether mild hyperglycemia may be associated with nonesterified fatty acid (NEFA) intolerance and increased iv lipid-induced lipotoxic effect on the beta-cell. DESIGN AND SETTING: The study consisted of an experimental design with control group conducted at an academic clinical research center. PARTICIPANTS: Twenty-six overweight or obese individuals (12 with normal glucose tolerance, nine with impaired glucose tolerance or type 2 diabetes, and five subjects who previously had impaired glucose tolerance or type 2 diabetes but at the time of study had normal glucose tolerance after biliopancreatic diversion). INTERVENTIONS: We assessed insulin sensitivity (S(I)) and beta-cell function [insulin disposition index (DI)] after an overnight iv infusion of heparin + Intralipid (HI) vs. normal saline for 16 h using a stepwise, incremental iv glucose infusion followed by a hyperglycemic clamp. MAIN OUTCOME MEASURES: We measured S(I), DI, HI-induced change in plasma NEFA, and its association with HI-induced change in S(I) and DI. RESULTS: HI resulted in significant reduction in S(I) and DI across the three groups of participants. HI-induced elevation of plasma NEFA was higher in hyperglycemic vs. normoglycemic groups. Both fasting glucose level and the magnitude of HI-induced NEFA elevation were associated with the reduction in S(I) (P = 0.007 and P = 0.01, respectively) and DI (P = 0.001 and P = 0.007, respectively). CONCLUSION: Mild hyperglycemia and NEFA intolerance to iv lipid are associated with susceptibility to lipid-induced reduction in S(I) and DI.

Comparison of foot-to-foot and hand-to-foot bioelectrical impedance methods in a population with a wide range of body mass indices.

BACKGROUND: Several techniques are currently used for measurement of body composition. Bioelectrical impedance assessment (BIA) is a simple, noninvasive method of assessing body composition. We aimed to compare multifrequency hand-to-foot (HF-BIA) and foot-to-foot (FF-BIA) bioelectrical impedance analysis techniques to assess fat-free mass (FFM) in a population with a wide range of body mass indices (BMI). METHODS: This was a cross-sectional study of 198 adult subjects. Anthropometric and BIA measures (HF-BIA with Hydra ICF/ECF, Xitron Technologies and FF-BIA with Tanita, model TBF-300A) were recorded after a 12-h fast. RESULTS: Participants had a mean age of 42 years and BMI of 33.50.7 (range, 17.7-65.6) kg/m2. Mean FFM with HF-BIA (FFM BIA/HF) and FF-BIA (FFM BIA/FF) were 61.31.3 kg and 58.10.9 kg, respectively (P < 0.001). In subjects with BMI <25 kg/m2, FFM BIA/FF was not significantly different compared to FFMBIA/HF (-0.2 kg; P=0.8). However, FFM BIA/FF was significantly lower in subjects with BMI 25-30 kg/m2 (-2.0 kg; P=0.009), 30-34 kg/m2 (-1.8 kg; P»0.04), 34-42 kg/m2 (-4.7 kg; P<0.001) and >42 kg/m2 (-8.0 kg; P=0.001). Pearson correlations between both methods were very high for FFM (r=0.92), fat mass (r=0.91), and % fat mass (r=0.85), all P<0.001. Correlation coefficients for FFM were high in each quintile of BMI. FFM BIA/FF was the only significant independent predictor of FFM BIA/HF (P<0.001) in linear regression analyses using clinical and FF-BIA variables, but introducing BMI in the model added precision. CONCLUSION: FFM BIA/FF correlates closely with FFM BIA/HF across all quintiles of BMI, but FF-BIA gives lower FFM in overweight and obese subjects.

Mechanism of insulin-stimulated clearance of plasma nonesterified fatty acids in humans.

Insulin increases plasma nonesterified fatty acid (NEFA) clearance in humans, but whether this is independent of change in plasma NEFA appearance is currently unknown. Nine nondiabetic men (age: 28+/-3 yr, body mass index: 27.2+/-1.7 kg/m2) underwent euglycemic clamps to maintain low (LINS) vs. high (HINS) physiological insulin levels for 6 h. An intravenous infusion of heparin+Intralipid (HI) was performed during 4 of the 6 h of the clamps (in the last 4 h at LINS and in the first 4 h at HINS), whereas saline infusion (SAL) was administered in the remaining 2 h to modulate plasma NEFA levels independently of plasma insulin levels. Four experimental conditions were obtained in each individual: LINS with saline (LINS/SAL) and with HI infusion (LINS/HI) and HINS with saline (HINS/SAL) and with HI infusion (HINS/HI). Plasma palmitate appearance during HINS/SAL was lower than during the three other experimental conditions (P<0.05). In contrast, plasma linoleate appearance, as expected, was increased by HI independently of insulin level (P<0.02). Plasma palmitate clearance during HINS/SAL was higher than LINS/SAL and LINS/HI (P<0.008), and this increase was blunted during HINS/HI. We observed a linear decrease in plasma palmitate clearance with increasing plasma NEFA appearance independent of insulin levels. Plasma NEFA levels increased exponentially with increase in plasma NEFA appearance. We conclude that insulin stimulates plasma NEFA clearance by reducing the endogenous appearance rate of NEFA. The relationship between plasma NEFA level and appearance rate is nonlinear.