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Ocean–atmosphere gas exchange in the Arctic Ocean is sensitive to global warming because the decrease of sea‐ice covered area enhances the exchange. Melting sea ice affects the vertical transport of dissolved gases. Few reports of Arctic Ocean studies have described observations of dissolved N2O or temporal variation of sea‐to‐atmosphere N2O flux. Therefore, production mechanisms of this greenhouse gas and the stratospheric ozone depleting gas remain unclear. We measured dissolved N2O and its isotopic signatures in the western Arctic shelf region of the Chukchi Sea and surrounding areas during September in 2014 and 2015. In the Chukchi Sea shelf, the N2O concentration was slightly higher than the value expected under sea–air equilibrium in the surface water. It increased with depth to 23 nmol kg−1 in 2014, although it showed a vertically homogeneous distribution in 2015. Isotopocule ratios of N2O, which include 15N‐site preference in the N2O molecule as well as elemental N and O isotope ratios, indicate that N2O in the Chukchi Sea shelf is a mixture of N2O produced in the bottom water and that of atmospheric origin. The isotopic signature of excess N2O (δ15Nbulk = −3.6‰ to −1.4‰, δ18O = 61.5‰–63.0‰, SP = 38.7‰–49.0‰) suggests that it is produced by archeal or bacterial nitrification and that it is partly reduced by denitrification. Although further quantitative observations are necessary, the results confirmed that the western Arctic Ocean can act as a source of N2O to the atmosphere when sea‐ice cover retreats and the pycnocline is weakened. Key Points: Continental shelf region in the western Arctic (Chukchi Sea) can act as a N2O source to the atmosphere in the summerThe N2O, produced mainly by archeal or bacterial nitrification, is partly reduced by denitrification in bottom water or shelf sedimentsVertical distribution of N2O in the water column is affected strongly by the degree of stratification caused by sea ice melting [ABSTRACT FROM AUTHOR]

Identifying ocean acidification and its controlling mechanisms is an important priority within the broader question of understanding how sustained anthropogenic CO2 emissions are harming the health of the ocean. Through extensive analysis of observational data products for ocean inorganic carbon, here we quantify the rate at which acidification is proceeding in the western tropical Pacific Warm Pool, revealing −0.0013 ± 0.0001 year−1 for pH and −0.0083 ± 0.0007 year−1 for the saturation index of aragonite for the years 1985–2016. However, the mean rate of total dissolved inorganic carbon increase (+0.81 ± 0.06 μmol · kg−1 · year−1) sustaining acidification was ~20% slower than what would be expected if it were simply controlled by the rate of atmospheric CO2 increase and transmitted through local air‐sea CO2 equilibration. Joint Lagrangian and Eulerian model diagnostics indicate that the acidification of the Warm Pool occurs primarily through the anthropogenic CO2 that invades the ocean in the extra‐tropics is transported to the tropics through the thermocline shallow overturning circulation and then re‐emerges into surface waters within the tropics through the Equatorial Undercurrent from below. An interior residence time of several years to decades, acting in conjunction with the accelerating CO2 growth in the atmosphere, can be expected to contribute to modulating the rate of Warm Pool acidification. Key Points: Progress of ocean acidification in the western tropical Pacific Warm Pool was identified using the data of oceanic CO2 measurementsThe rate of oceanic CO2 increase here was ~20% lower than that expected from the growth rate of the mixing ratio of CO2 in the atmosphereIntergyre exchange of anthropogenic CO2 within the thermocline predominantly controls the rate of acidification in this region [ABSTRACT FROM AUTHOR]

In 2008, a 44-year-old woman with mild epigastralgia diagnosed as having Helicobacter pylori-positive chronic gastritis without peptic ulcer underwent eradication therapy with lansoprazole (LPZ), amoxicillin (AMPC) and clarithromycin (CAM) for 7 days, but it failed, so treatment with rabeprazole, AMPC, and metronidazole (MNZ) for another 7 days was given, but it also failed. She was then prescribed a modified, 14-day sequential therapy of LPZ and AMPC with an increased dose of CAM followed by MNZ supplement, but the infection was still not eradicated. The H. pylori was cultured and examined for antibiotic susceptibility with the agar dilution method and was found to be resistant to CAM, MNZ, and levofloxacin, and non-sensitive to AMPC, namely multiple-antibiotic-resistant, although sensitive to minocycline. The CYP2C19 genotype of the patient was an extensive metabolizer (G681A: G/A, G636A: G/G). In 2010, she gave informed consent for a 14-day, tailor-made, modified classical (or modified high-dose PPI + AMPC) quadruple therapy comprising 30 mg LPZ, 500 mg AMPC and 500 mg bismuth subnitrate, qid, and 100 mg minocycline, bid. Two months later, her urea breath test was negative. Histology and bacterial culture were still negative 1 year after the therapy. She did not have any adverse events during or after the novel therapy, nor did she feel any further epigastralgia. [ABSTRACT FROM AUTHOR]