Robust warming pattern of global subtropical oceans and its mechanism

Author Posting. © American Meteorological Society, 2015. This article is posted here by permission of American Meteorological Society for personal use, not for redistribution. The definitive version was published in Journal of Climate 28 (2015): 8574–8584, doi:10.1175/JCLI-D-14-00809.1.The subsurface ocean response to anthropogenic climate forcing remains poorly characterized. From the Coupled Model Intercomparison Project (CMIP), a robust response of the lower thermocline is identified, where the warming is considerably weaker in the subtropics than in the tropics and high latitudes. The lower thermocline change is inversely proportional to the thermocline depth in the present climatology. Ocean general circulation model (OGCM) experiments show that sea surface warming is the dominant forcing for the subtropical gyre change in contrast to natural variability for which wind dominates, and the ocean response is insensitive to the spatial pattern of surface warming. An analysis based on a ventilated thermocline model shows that the pattern of the lower thermocline change can be interpreted in terms of the dynamic response to the strengthened stratification and downward heat mixing. Consequently, the subtropical gyres become intensified at the surface but weakened in the lower thermcline, consistent with results from CMIP experiments.The work was supported by the National Basic Research Program of China (2012CB955600), the National Natural Science Foundation of China (41125019, 41206021), and the U.S. National Science Foundation (AGS 1249145, 1305719).2016-05-0

Elevated CO2 and Warming Altered Grassland Microbial Communities in Soil Top-Layers.

As two central issues of global climate change, the continuous increase of both atmospheric CO2 concentrations and global temperature has profound effects on various terrestrial ecosystems. Microbial communities play pivotal roles in these ecosystems by responding to environmental changes through regulation of soil biogeochemical processes. However, little is known about the effect of elevated CO2 (eCO2) and global warming on soil microbial communities, especially in semiarid zones. We used a functional gene array (GeoChip 3.0) to measure the functional gene composition, structure, and metabolic potential of soil microbial communities under warming, eCO2, and eCO2 + warming conditions in a semiarid grassland. The results showed that the composition and structure of microbial communities was dramatically altered by multiple climate factors, including elevated CO2 and increased temperature. Key functional genes, those involved in carbon (C) degradation and fixation, methane metabolism, nitrogen (N) fixation, denitrification and N mineralization, were all stimulated under eCO2, while those genes involved in denitrification and ammonification were inhibited under warming alone. The interaction effects of eCO2 and warming on soil functional processes were similar to eCO2 alone, whereas some genes involved in recalcitrant C degradation showed no significant changes. In addition, canonical correspondence analysis and Mantel test results suggested that NO3-N and moisture significantly correlated with variations in microbial functional genes. Overall, this study revealed the possible feedback of soil microbial communities to multiple climate change factors by the suppression of N cycling under warming, and enhancement of C and N cycling processes under either eCO2 alone or in interaction with warming. These findings may enhance our understanding of semiarid grassland ecosystem responses to integrated factors of global climate change

Rapid identification of time-frequency domain gravitational wave signals from binary black holes using deep learning

Recent developments in deep learning techniques have offered an alternative and complementary approach to traditional matched filtering methods for the identification of gravitational wave (GW) signals. The rapid and accurate identification of GW signals is crucial for the progress of GW physics and multi-messenger astronomy, particularly in light of the upcoming fourth and fifth observing runs of LIGO-Virgo-KAGRA. In this work, we use the 2D U-Net algorithm to identify the time-frequency domain GW signals from stellar-mass binary black hole (BBH) mergers. We simulate BBH mergers with component masses from 5 to 80 $M_{\odot}$ and account for the LIGO detector noise. We find that the GW events in the first and second observation runs could all be clearly and rapidly identified. For the third observation run, about $80\%$ GW events could be identified and GW190814 is inferred to be a BBH merger event. Moreover, since the U-Net algorithm has advantages in image processing, the time-frequency domain signals obtained through U-Net can preliminarily determine the masses of GW sources, which could help provide the mass priors for future parameter inferences. We conclude that the U-Net algorithm could rapidly identify the time-frequency domain GW signals from BBH mergers and provide great help for future parameter inferences.Comment: 11 pages, 9 figure

Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.

Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling. Transiently or stably overexpression of mitochondria Omi/HtrA2 in H9C2 cells enhance apoptosis as evidenced by elevated caspase-3, -9 activity and TUNEL staining, which was completely blocked by Ucf-101, a specific Omi/HtrA2 inhibitor. Mechanistic studies revealed mitochondrial Omi/HtrA2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Ucf-101. Additionally, transfected cells overexpressing mitochondrial Omi/HtrA2 were more sensitive to hypoxia and reoxygenation (H/R) induced apoptosis. Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked translocation of Omi/HtrA2 from mitochondrial to cytoplasm, and protected transfected cells incompletely against H/R-induced caspase-3 activation. We report in vitro and in vivo overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. Thus, strategies to directly inhibit Omi/HtrA2 or its cytosolic translocation from mitochondria may protect against heart injury

Systematic Evolution and Study of UAGN Decoding tRNAs in a Genomically Recoded Bacteria

We report the first systematic evolution and study of tRNA variants that are able to read a set of UAGN (N = A, G, U, C) codons in a genomically recoded E. coli strain that lacks any endogenous in-frame UAGN sequences and release factor 1. Through randomizing bases in anticodon stem-loop followed by a functional selection, we identified tRNA mutants with significantly improved UAGN decoding efficiency, which will augment the current efforts on genetic code expansion through quadruplet decoding. We found that an extended anticodon loop with an extra nucleotide was required for a detectable efficiency in UAGN decoding. We also observed that this crucial extra nucleotide was converged to a U (position 33.5) in all of the top tRNA hits no matter which UAGN codon they suppress. The insertion of U33.5 in the anticodon loop likely causes tRNA distortion and affects anticodoncodon interaction, which induces +1 frameshift in the P site of ribosome. A new model was proposed to explain the observed features of UAGN decoding. Overall, our findings elevate our understanding of the +1 frameshift mechanism and provide a useful guidance for further efforts on the genetic code expansion using a non-canonical quadruplet reading frame

Systematic Evolution and Study of UAGN Decoding tRNAs in a Genomically Recoded Bacteria

We report the first systematic evolution and study of tRNA variants that are able to read a set of UAGN (N = A, G, U, C) codons in a genomically recoded E. coli strain that lacks any endogenous in-frame UAGN sequences and release factor 1. Through randomizing bases in anticodon stem-loop followed by a functional selection, we identified tRNA mutants with significantly improved UAGN decoding efficiency, which will augment the current efforts on genetic code expansion through quadruplet decoding. We found that an extended anticodon loop with an extra nucleotide was required for a detectable efficiency in UAGN decoding. We also observed that this crucial extra nucleotide was converged to a U (position 33.5) in all of the top tRNA hits no matter which UAGN codon they suppress. The insertion of U33.5 in the anticodon loop likely causes tRNA distortion and affects anticodoncodon interaction, which induces +1 frameshift in the P site of ribosome. A new model was proposed to explain the observed features of UAGN decoding. Overall, our findings elevate our understanding of the +1 frameshift mechanism and provide a useful guidance for further efforts on the genetic code expansion using a non-canonical quadruplet reading frame

5-Arc transitive cubic Cayley graphs on finite simple groups

AbstractIn this paper, we determine all connected 5-arc transitive cubic Cayley graphs on the alternating group A47; there are only two such graphs (up to isomorphism). By earlier work of the authors, these are the only two non-normal connected cubic arc-transitive Cayley graphs for finite nonabelian simple groups, and so this paper completes the classification of such non-normal Cayley graphs