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Abstract. Snowpits along a traverse from coastal East Antarctica to the summit of the ice sheet (Dome Argus) are used to investigate the post-depositional processing of nitrate (NO − 3 ) in snow. Seven snowpits from sites with accumulation rates between 24 and 172 kg m −2 a −1 were sampled to depths of 150 to 300 cm. At sites from the continental interior (low accumulation, < 55 kg m −2 a −1 ), nitrate mass fraction is generally > 200 ng g −1 in surface snow and decreases quickly with depth to < 50 ng g −1 . Considerably increasing values of δ 15 N of nitrate are also observed (16-461 ‰ vs. air N 2 ), particularly in the top 20 cm, which is consistent with predicted fractionation constants for the photolysis of nitrate. The δ 18 O of nitrate (17-84 ‰ vs. VSMOW (Vienna Standard Mean Ocean Water)), on the other hand, decreases with increasing δ 15 N, suggestive of secondary formation of nitrate in situ (following photolysis) with a low δ 18 O source. Previous studies have suggested that δ 15 N and δ 18 O of nitrate at deeper snow depths should be predictable based upon an exponential change derived near the surface. At deeper depths sampled in this study, however, the relationship between nitrate mass fraction and δ 18 O changes, with increasing δ 18 O of nitrate observed between 100 and 200 cm. Predicting the impact of post-depositional loss, and therefore changes in the isotopes with depth, is highly sensitive to the depth interval over which an exponential change is assumed. In the snowpits collected closer to the coast (accumulation > 91 kg m −2 a −1 ), there are no obvious trends detected with depth and instead seasonality in nitrate mass fraction and isotopic composition is found. In comparison to the interior sites, the coastal pits are lower in δ 15 N (−15-71 ‰ vs. air N 2 ) and higher in δ 18 O of nitrate (53-111 ‰ vs. VSMOW). The relationships found amongst mass fraction, δ 15 N, δ 18 O and 17 O ( 17 O = δ 17 O-0.52 × δ 18 O) of nitrate cannot be explained by local post-depositional processes alone, and are instead interpreted in the context of a primary atmospheric signal. Consistent with other Antarctic observational and modeling studies, the isotopic results are suggestive of an important influence of stratospheric ozone chemistry on nitrate formation during the cold season and a mix of tropospheric sources and chemistry during the warm season. Overall, the findings in this study speak to the sensitivity of nitrate isotopic composition to post-depositional processing and highlight the strength of combined use of the nitrogen and oxygen isotopes for a mechanistic understanding of this processing.

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A detailed history of volcanism covering the last 2840 years is reconstructed from the top 100.42 m of a 109.91 m ice core from Dome A (DA2005 ice core), East Antarctica. Using two known volcanic stratigraphic markers, the mean accumulation rate during the period AD 1260-1964 is found to be 23.2 mmw.e. a-1, consistent with the previously reported accumulation rate at Dome A. This mean accumulation rate is used to date the entire core. Volcanic eruptions in the period 840 BC-AD1998 are detected as outstanding sulphate events. Seventy-eight eruptions are identified, with a mean of 2.7 eruptions per century. Comparisons with previous Antarctic ice-core volcanic records are made to assess the quality of this new DA2005 record. In terms of dates for volcanic events, the DA2005 record is in good agreement with previous records in the second millennium ad (ad 1000-1998). A series of volcanic signatures found in both the DA2005 record and several other Antarctic ice-core records in the first millennium ad (ad 1-1000) appear to validate the DA2005 record during this time period. For the older periods, direct comparisons are difficult between the DA2005 record and other Antarctic ice-core records due to the lack of well-dated stratigraphic horizons.

BackgroundHeart failure (HF) is associated with increased arrhythmia risk and triggered activity. Abnormal Ca2+ handling is thought to underlie triggered activity, and mitochondria participate in Ca2+ homeostasis.Methods and ResultsA model of nonischemic HF was induced in C57BL/6 mice by hypertension. Computer simulations were performed using a mouse ventricular myocyte model of HF. Isoproterenol‐induced premature ventricular contractions and ventricular fibrillation were more prevalent in nonischemic HF mice than sham controls. Isolated myopathic myocytes showed decreased cytoplasmic Ca2+ transients, increased mitochondrial Ca2+ transients, and increased action potential duration at 90% repolarization. The alteration of action potential duration at 90% repolarization was consistent with in vivo corrected QT prolongation and could be explained by augmented L‐type Ca2+ currents, increased Na+‐Ca2+ exchange currents, and decreased total K+ currents. Of myopathic ventricular myocytes, 66% showed early afterdepolarizations (EADs) compared with 17% of sham myocytes (P<0.05). Intracellular application of 1 μmol/L Ru360, a mitochondrial Ca2+ uniporter–specific antagonist, could reduce mitochondrial Ca2+ transients, decrease action potential duration at 90% repolarization, and ameliorate EADs. Furthermore, genetic knockdown of mitochondrial Ca2+ uniporters inhibited mitochondrial Ca2+ uptake, reduced Na+‐Ca2+ exchange currents, decreased action potential duration at 90% repolarization, suppressed EADs, and reduced ventricular fibrillation in nonischemic HF mice. Computer simulations showed that EADs promoted by HF remodeling could be abolished by blocking either the mitochondrial Ca2+ uniporter or the L‐type Ca2+ current, consistent with the experimental observations.ConclusionsMitochondrial Ca2+ handling plays an important role in EADs seen with nonischemic cardiomyopathy and may represent a therapeutic target to reduce arrhythmic risk in this condition.