Origin of the deep Bering Sea nitrate deficit : constraints from the nitrogen and oxygen isotopic composition of water column nitrate and benthic nitrate fluxes

Author Posting. © American Geophysical Union, 2005. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Global Biogeochemical Cycles 19 (2005): GB4005, doi:10.1029/2005GB002508.On the basis of the normalization to phosphate, a significant amount of nitrate is missing from the deep Bering Sea (BS). Benthic denitrification has been suggested previously to be the dominant cause for the BS nitrate deficit. We measured water column nitrate 15N/14N and 18O/16O as integrative tracers of microbial denitrification, together with pore water-derived benthic nitrate fluxes in the deep BS basin, in order to gain new constraints on the mechanism of fixed nitrogen loss in the BS. The lack of any nitrate isotope enrichment into the deep part of the BS supports the benthic denitrification hypothesis. On the basis of the nitrate deficit in the water column with respect to the adjacent North Pacific and a radiocarbon-derived ventilation age of ∼50 years, we calculate an average deep BS (>2000 m water depth) sedimentary denitrification rate of ∼230 μmol N m−2 d−1 (or 1.27 Tg N yr−1), more than 3 times higher than high-end estimates of the average global sedimentary denitrification rate for the same depth interval. Pore water-derived estimates of benthic denitrification were variable, and uncertainties in estimates were large. A very high denitrification rate measured from the base of the steep northern slope of the basin suggests that the elevated average sedimentary denitrification rate of the deep Bering calculated from the nitrate deficit is driven by organic matter supply to the base of the continental slope, owing to a combination of high primary productivity in the surface waters along the shelf break and efficient down-slope sediment focusing along the steep continental slopes that characterize the BS.This study was supported by NSF grants OCE-0136449 and OCE-9981479 to D. M. S., OCE-0118126 and OCE-0324987 to D. C. M., and DFG grant LE 1326/1-1 to M. F. L. The BS cruise was funded by grant OPP-9912122

Quantitative Analysis of Mechanisms That Govern Red Blood Cell Age Structure and Dynamics during Anaemia

Mathematical modelling has proven an important tool in elucidating and quantifying mechanisms that govern the age structure and population dynamics of red blood cells (RBCs). Here we synthesise ideas from previous experimental data and the mathematical modelling literature with new data in order to test hypotheses and generate new predictions about these mechanisms. The result is a set of competing hypotheses about three intrinsic mechanisms: the feedback from circulating RBC concentration to production rate of immature RBCs (reticulocytes) in bone marrow, the release of reticulocytes from bone marrow into the circulation, and their subsequent ageing and clearance. In addition we examine two mechanisms specific to our experimental system: the effect of phenylhydrazine (PHZ) and blood sampling on RBC dynamics. We performed a set of experiments to quantify the dynamics of reticulocyte proportion, RBC concentration, and erythropoietin concentration in PHZ-induced anaemic mice. By quantifying experimental error we are able to fit and assess each hypothesis against our data and recover parameter estimates using Markov chain Monte Carlo based Bayesian inference. We find that, under normal conditions, about 3% of reticulocytes are released early from bone marrow and upon maturation all cells are released immediately. In the circulation, RBCs undergo random clearance but have a maximum lifespan of about 50 days. Under anaemic conditions reticulocyte production rate is linearly correlated with the difference between normal and anaemic RBC concentrations, and their release rate is exponentially correlated with the same. PHZ appears to age rather than kill RBCs, and younger RBCs are affected more than older RBCs. Blood sampling caused short aperiodic spikes in the proportion of reticulocytes which appear to have a different developmental pathway than normal reticulocytes. We also provide evidence of large diurnal oscillations in serum erythropoietin levels during anaemia

Health, education, and social care provision after diagnosis of childhood visual disability

Aim: To investigate the health, education, and social care provision for children newly diagnosed with visual disability.Method: This was a national prospective study, the British Childhood Visual Impairment and Blindness Study 2 (BCVIS2), ascertaining new diagnoses of visual impairment or severe visual impairment and blindness (SVIBL), or equivalent vi-sion. Data collection was performed by managing clinicians up to 1-year follow-up, and included health and developmental needs, and health, education, and social care provision.Results: BCVIS2 identified 784 children newly diagnosed with visual impairment/SVIBL (313 with visual impairment, 471 with SVIBL). Most children had associated systemic disorders (559 [71%], 167 [54%] with visual impairment, and 392 [84%] with SVIBL). Care from multidisciplinary teams was provided for 549 children (70%). Two-thirds (515) had not received an Education, Health, and Care Plan (EHCP). Fewer children with visual impairment had seen a specialist teacher (SVIBL 35%, visual impairment 28%, χ2p < 0.001), or had an EHCP (11% vs 7%, χ2p < 0 . 01).Interpretation: Families need additional support from managing clinicians to access recommended complex interventions such as the use of multidisciplinary teams and educational support. This need is pressing, as the population of children with visual impairment/SVIBL is expected to grow in size and complexity.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited

Competitive one-to-one promotions

One-to-one promotions are possible when consumers are individually addressable and firms know something about each customer's preferences. We explore the competitive effects of one-to-one promotions in a model with two competing firms where the firms differ in size and consumers have heterogeneous brand loyalty. We find that one-to-one promotions always lead to an increase in price competition (average prices in the market decrease). However, we also find that one-to-one promotions affect market shares. This market-share effect may outweigh the effect of lower prices, benefiting the firm whose market share increases. Our results suggest that of two firms, the firm with the higher-quality product may gain from one-to-one promotions. Our model also has implications for the phenomenon of customer churn, where consumers switch to a less preferred brand due to targeted promotional incentives. We show that churning can arise optimally from firms pursuing a profit-maximizing strategy. Instead of trying to minimize it, the optimal way to manage customer churn is to engage in both offensive and defensive promotions with the relative mix depending on the marginal cost of targeting