Response of the ammonia oxidation activity of microorganisms in surface sediment to a controlled sub-seabed release of CO2

The impact of a sub-seabed CO2 leak from geological sequestration on the microbial process of ammonia oxidation was investigated in the field. Sediment samples were taken before, during and after a controlled sub-seabed CO2 leak at four zones differing in proximity to the CO2 source (epicentre, and 25m, 75m, and 450m distant). The impact of CO2 release on benthic microbial ATP levels was compared to ammonia oxidation rates and the abundance of bacterial and archaeal ammonia amoA genes and transcripts, and also to the abundance of nitrite oxidize (nirS) and anammox hydrazine oxidoreductase (hzo) genes and transcripts. The major factor influencing measurements was seasonal: only minor differences were detected at the zones impacted by CO2 (epicentre and 25m distant). This included a small increase to ammonia oxidation after 37daysof CO2 release which was linked to an increase in ammonia availability as a result of mineral dissolution. A CO2 leak on the scale used within this study (<1tonneday−1) would have very little impact to ammonia oxidation within coastal sediments. However, seawater containing 5% CO2 did reduce rates of ammonia oxidation. This was linked to the buffering capacity of the sediment, suggesting that the impact of a sub-seabed leak of stored CO2 on ammonia oxidation would be dependent on both the scale of the CO2 release and sediment type.

Global oceanic emission of ammonia: Constraints from seawater and atmospheric observations

Current global inventories of ammonia emissions identify the ocean as the largest natural source. This source depends on seawater pH, temperature, and the concentration of total seawater ammonia (NHx(sw)), which reflects a balance between remineralization of organic matter, uptake by plankton, and nitrification. Here we compare [NHx(sw)] from two global ocean biogeochemical models (BEC and COBALT) against extensive ocean observations. Simulated [NHx(sw)] are generally biased high. Improved simulation can be achieved in COBALT by increasing the plankton affinity for NHx within observed ranges. The resulting global ocean emissions is 2.5 TgN a−1, much lower than current literature values (7–23 TgN a−1), including the widely used Global Emissions InitiAtive (GEIA) inventory (8 TgN a−1). Such a weak ocean source implies that continental sources contribute more than half of atmospheric NHx over most of the ocean in the Northern Hemisphere. Ammonia emitted from oceanic sources is insufficient to neutralize sulfate aerosol acidity, consistent with observations. There is evidence over the Equatorial Pacific for a missing source of atmospheric ammonia that could be due to photolysis of marine organic nitrogen at the ocean surface or in the atmosphere. Accommodating this possible missing source yields a global ocean emission of ammonia in the range 2–5 TgN a−1, comparable in magnitude to other natural sources from open fires and soils.

The spectrum of endogenous human chromogranin A-derived peptides identified using a modified proteomic strategy.

The hypothesis that chromogranin A (CgA), a protein of neuroendocrine cell secretory granules, may be a precursor of biologically active peptides, rests on observed activities of peptide fragments largely produced by exogenous protease digestion of the bovine protein. Here we have adopted a modified proteomic strategy to isolate and characterise human CgA-derived peptides produced by endogenous prohormone convertases. Initial focus was on an insulinoma as previous studies have shown that CgA is rapidly processed in pancreatic beta cells and that tumours arising from these express appropriate prohormone convertases. Eleven novel peptides were identified arising from processing at both monobasic and dibasic sites and processing was most evident in the C-terminal domain of the protein. Some of these peptides were identified in endocrine tumours, such as mid-gut carcinoid and phaeochromocytoma, which arise from endocrine cells of different phenotype and in different anatomical sites. Two of the most interesting peptides, GR-44 and ER-37, representing the C-terminal region of CgA, were found to be amidated. These data would imply that the intact protein is C-terminally amidated and that these peptides are probably biologically active. The spectrum of novel CgA-derived peptides, described in the present study, should provide a basis for biological evaluation of authentic entities.

Differences in expression of junctional adhesion molecule-A and beta catenin in multiple sclerosis brain tissue: increasing evidence for the role of tight junction pathology

Previously we have employed antibodies to the tight junction (TJ)-associated proteins ZO-1 and occludin to describe endothelial tight junction abnormalities, in lesional and normal appearing white matter, in primary and secondary progressive multiple sclerosis (MS). This work is extended here by use of antibodies to the independent TJ-specific proteins and junctional adhesion molecule A & B (JAM-A, JAM-B). We have also assessed the expression in MS of ß-catenin, a protein specific to the TJ-associated adherens junction. Immunocytochemistry and semiquantitative confocal microscopy for JAM-A and ß-catenin was performed on snap-frozen sections from MS cases (n = 11) and controls (n = 6). Data on 1,443 blood vessels was acquired from active lesions (n = 13), inactive lesions (n = 13), NAWM (n = 20) and control white matter (n = 13). In MS abnormal JAM-A expression was found in active (46%) and inactive lesions (21%), comparable to previous data using ZO-1. However, a lower level of TJ abnormality was found in MS NAWM using JAM-A (3%) compared to ZO-1 (13%). JAM-B was strongly expressed on a small number of large blood vessels in control and MS tissues but at too low a level for quantitative analysis. By comparison with the high levels of abnormality observed with the TJ proteins, the adherens junction protein ß-catenin was normally expressed in all MS and control tissue categories. These results confirm, by use of the independent marker JAM-A, that TJ abnormalities are most frequent in active white matter lesions. Altered expression of JAM-A, in addition to affecting junctional tightness may also both reflect and affect leukocyte trafficking, with implications for immune status within the diseased CNS. Conversely, the adherens junction component of the TJ, as indicated by ß-catenin expression is normally expressed in all MS and control tissue categories.

How optimal life history changes with the community size-spectrum

This paper derives optimal life histories for fishes or other animals in relation to the size spectrum of the ecological community in which they are both predators and prey. Assuming log-linear size-spectra and well known scaling laws for feeding and mortality, we first construct the energetics of the individual. From these we find, using dynamic programming, the optimal allocation of energy between growth and reproduction as well as the trade-off between offspring size and numbers. Optimal strategies were found to be strongly dependent on size spectrum slope. For steep size spectra (numbers declining rapidly with size), determinate growth was optimal and allocation to somatic growth increased rapidly with increasing slope. However, restricting reproduction to a fixed mating season changed optimal allocations to give indeterminate growth approximating a von Bertalanffy trajectory. The optimal offspring size was as small as possible given other restrictions such as newborn starvation mortality. For shallow size spectra, finite optimal maturity size required a decline in fitness for large size or age. All the results are compared with observed size spectra of fish communities to show their consistency and relevance.