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Salt marshes are recognized as blue carbon ecosystems for their ability to rapidly sequester organic carbon (OC) via sedimentation. For this reason, there is growing interest in managing these systems to help mitigate climate change. However, in order for sediment accretion to offset ongoing CO2emissions, organic matter undergoing burial must be derived from contemporary primary production. To investigate the provenance of OC sequestered by salt marshes, we analyzed the concentration and isotope composition (δ13C and Δ14C) of sedimentary OC in two minerogenic marshes in San Francisco Bay, California, USA. Data from the low marsh dominated by Spartinaspp. show that autochthonous OC is entering the sediment matrix and may in part be stabilized through incorporation into the mineral‐bound pool. However, the sedimentary OC stock as a whole is dominated by material with low values of δ13C (~ −20 to −25‰) and Δ14C (~ 100 to −300‰) indicating a preponderance of allochthonous OC that was retained in other OC reservoirs for 102to 103years prior to deposition in the marsh. Diagenetic modeling of OC and its δ13C values further shows that autochthonous OC is lost from the sediment profile at a much faster rate than allochthonous OC. The rapid turnover of contemporary autochthonous OC (“fast carbon”) relative to the apparent stability of old allochthonous OC (“slow carbon”) suggest that carbon burial at these sites is largely decoupled from ongoing CO2emissions.

The fractional redistribution of cardiac output to bone in dietary calcium deficiency was studied in the immature rat, utilizing the86Rb method of Sapirstein. The results of the study indicated that there was a rapid and significant increase in the fraction of cardiac output to the femurs of the calcium-deficient rats relative to the control population. The increase in cardiac output fraction to bone occurred during the same general time period in which significant changes in the density, dry weight and ash content were detected. The increased fraction of the cardiac output to the femur in the calcium-deficient rats returned to normal after nine days, in spite of continuation of the calcium-deficient diet.