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East Asian summer monsoon (EASM) rainfall impacts the world’s most populous regions. Accurate EASM rainfall prediction necessitates robust paleoclimate reconstructions from proxy data and quantitative linkage to modern climatic conditions. Many precisely dated oxygen isotope records from Chinese stalagmites have been interpreted as directly reflecting past EASM rainfall amount variability, but recent research suggests that such records instead integrate multiple hydroclimatic processes. Using a Lagrangian precipitation moisture source diagnostic, we demonstrate that EASM rainfall is primarily derived from the Indian Ocean. Conversely, Pacific Ocean moisture export peaks during winter, and the moisture uptake area does not differ significantly between summer and winter and is thus a minor contributor to monsoonal precipitation. Our results are substantiated by an accurate reproduction of summer and winter spatial rainfall distributions across China. We also correlate modern EASM rainfall oxygen isotope ratios with instrumental rainfall amount and our moisture source data. This analysis reveals that the strength of the source effect is geographically variable, and differences in atmospheric moisture transport may significantly impact the isotopic signature of EASM rainfall at the Hulu, Dongge, and Wanxiang Cave sites. These results improve our ability to isolate the rainfall amount signal in paleomonsoon reconstructions and indicate that precipitation across central and eastern China will directly respond to variability in Indian Ocean moisture supply.

© 2015 Elsevier Ltd. Several recent studies have used records of the radiocarbon (14C) bomb peak in speleothems to inversely model the soil a 14CO2 and the age distribution of soil organic material (SOM) above caves, in part to investigate the potential of speleothems as sensitive records of past SOM dynamics. The results of these modeling studies have suggested that soil CO2 at karst sites is derived primarily from the decomposition of SOM with turnover times on the order of decades to centuries. This result is in stark contrast with observations of soil a 14CO2 at non-karst sites, which indicate that soil CO2 is derived primarily from root respiration and decomposition of SOM with much shorter turnover times. This discrepancy suggests that SOM in karst settings may have a very different age distribution than sites that have been studied previously and/or that soil CO2 is not the main source of speleothem carbon. To help resolve this discrepancy, we present an improved inverse model which we use to estimate the age of CO2 above several caves. We also present results from a detailed case study of soil carbon dynamics at Heshang Cave, China. This work demonstrates that SOM in karst sites may be much older than SOM in non-karst soils that have been studied previously, but that CO2 produced in the shallow soil zone is unlikely to be the main source of speleothem carbon. A review of the literature suggests that the most likely explanation for the aforementioned discrepancy is that decomposition of down-washed SOM in the vadose zone is the dominant source of speleothem carbon.

In response to mechanical load, cardiac hypertrophy (myocyte enlargement) is initially compensatory, but becomes a maladaptive process that leads to the development of heart failure. The high prevalence of pathological myocardial hypertrophy in cardiovascular disease coupled with a lack of effective treatment highlights a need for novel therapeutic strategies in this area. Recently, a diverse family of scaffold proteins termed A-Kinase Anchoring Proteins have been identified and characterized, playing multiple important roles in the heart. In a recent study using a mouse model with a partial AKAPLbc (AKAP13) gene deletion, we demonstrate a crucial in vivo role for AKAP-Lbc-protein kinase D1 (PKD1) signaling in the development of compensatory hypertrophy in response to transverse aortic constriction (TAC)-induced pressure overload and neurohumoral stimulation by AT-II/PE treatment. Overall, our results show that AKAP-Lbc-PKD1 signaling is critical for transcriptional activation during the development of compensatory hypertrophy in vivo, under conditions of pathological hypertrophy. By defining and understanding regulation, downstream signaling and function of AKAP-Lbc- PKD1 signaling under pathological conditions, studies will determine whether AKAP-Lbc-PKD1 is a possible therapeutic target for treatment of cardiac dysfunction.