The drivers of projected North Atlantic sea level change

Sea level change predicted by the CMIP5 atmosphere–ocean general circulation models (AOGCMs) is not spatially homogeneous. In particular, the sea level change in the North Atlantic is usually characterised by a meridional dipole pattern with higher sea level rise north of 40°N and lower to the south. The spread among models is also high in that region. Here we evaluate the role of surface buoyancy fluxes by carrying out simulations with the FAMOUS low-resolution AOGCM forced by surface freshwater and heat flux changes from CO2-forced climate change experiments with CMIP5 AOGCMs, and by a standard idealised surface freshwater flux applied in the North Atlantic. Both kinds of buoyancy flux change lead to the formation of the sea level dipole pattern, although the effect of the heat flux has a greater magnitude, and is the main cause of the spread of results among the CMIP5 models. By using passive tracers in FAMOUS to distinguish between additional and redistributed buoyancy, we show that the enhanced sea level rise north of 40°N is mainly due to the direct steric effect (the reduction of sea water density) caused by adding heat or freshwater locally. The surface buoyancy forcing also causes a weakening of the Atlantic meridional overturning circulation, and the consequent reduction of the northward ocean heat transport imposes a negative tendency on sea level rise, producing the reduced rise south of 40°N. However, unlike previous authors, we find that this indirect effect of buoyancy forcing is generally less important than the direct one, except in a narrow band along the east coast of the US, where it plays a major role and leads to sea level rise, as found by previous authors.

Effect of maternal protein restriction during pregnancy and postweaning high-fat feeding of diet-induced thermogenesis in adult mouse offspring

Purpose Prenatal undernutrition followed by postweaning feeding of a high-fat diet results in obesity in the adult offspring. In this study, we investigated whether diet-induced thermogenesis is altered as a result of such nutritional mismatch. Methods Female MF-1 mice were fed a normal protein (NP, 18 % casein) or a protein-restricted (PR, 9 % casein) diet throughout pregnancy and lactation. After weaning, male offspring of both groups were fed either a high-fat diet (HF; 45 % kcal fat) or standard chow (C, 7 % kcal fat) to generate the NP/C, NP/HF, PR/C and PR/HF adult offspring groups (n = 7–11 per group). Results PR/C and NP/C offspring have similar body weights at 30 weeks of age. Postweaning HF feeding resulted in significantly heavier NP/HF offspring (P < 0.01), but not in PR/HF offspring, compared with their chow-fed counterparts. However, the PR/HF offspring exhibited greater adiposity (P < 0.01) v the NP/HF group. The NP/HF offspring had increased energy expenditure and increased mRNA expression of uncoupling protein-1 and β-3 adrenergic receptor in the interscapular brown adipose tissue (iBAT) compared with the NP/C mice (both at P < 0.01). No such differences in energy expenditure and iBAT gene expression were observed between the PR/HF and PR/C offspring. Conclusions These data suggest that a mismatch between maternal diet during pregnancy and lactation, and the postweaning diet of the offspring, can attenuate diet-induced thermogenesis in the iBAT, resulting in the development of obesity in adulthood.

Cardiac myocyte gene expression profiling during H2O2-induced apoptosis

High levels of oxidative stress promote cardiac myocyte death, though lower levels are potentially cytoprotective/anabolic. We examined the changes in gene expression in rat neonatal cardiac myocytes exposed to apoptotic (0.2 mM) or nontoxic (0.04 mM) concentrations of H2O2 (2, 4, or 24 h) using Affymetrix microarrays. Using U34B arrays, we identified a ubiquitously expressed, novel H2O2-responsive gene [putative peroxide-inducible transcript 1 (Perit1)], which generates two alternatively spliced transcripts. Using 230 2.0 arrays, H2O2 (0.04 mM) promoted significant changes in expression of only 32 genes, all of which were seen with 0.2 mM H2O2. We failed to detect any increase in the rate of protein synthesis in cardiac myocytes exposed to <0.1 mM H2O2, further suggesting that global, low concentrations of H2O2 are not anabolic in this system. H2O2 (0.2 mM) promoted significant (P < 0.05, >1.75-fold) changes in expression of 649 mRNAs and 187 RNAs corresponding to no established gene. Of the mRNAs, 114 encoded transcriptional regulators including Krüppel-like factors (Klfs). Quantitative PCR independently verified the changes in Klf expression. Thus, H2O2-induced cardiac myocyte apoptosis is associated with dynamic changes in gene expression. The expression of these genes and their protein products potentially influences the progression of the apoptotic response.

Soft balancing in the Americas: Latin American opposition to U.S. intervention, 1898–1936

In the aftermath of the 2003 U.S.-led invasion of Iraq, scholars of international relations debated how to best characterize the rising tide of global opposition. The concept of “soft balancing” emerged as an influential, though contested, explanation of a new phenomenon in a unipolar world: states seeking to constrain the ability of the United States to deploy military force by using multinational organizations, international law, and coalition building. Soft balancing can also be observed in regional unipolar systems. Multinational archival research reveals how Argentina, Mexico, and other Latin American countries responded to expanding U.S. power and military assertiveness in the early twentieth century through coordinated diplomatic maneuvering that provides a strong example of soft balancing. Examination of this earlier case makes an empirical contribution to the emerging soft-balancing literature and suggests that soft balancing need not lead to hard balancing or open conflict.