Process understanding of soil BVOC fluxes in natural ecosystems:a review

Biogenic volatile organic compounds (BVOCs) can be released from soils to the atmosphere through microbial decomposition of plant residues or soil organic carbon, root emission, evaporation of litter-stored BVOCs, and other physical processes. Soils can also act as a sink of BVOCs through biotic and abiotic uptake. Currently, the source and sink capabilities of soils have not been explicitly accounted for in global BVOC estimates from the terrestrial biosphere. In this review, we summarize the current knowledge of soil BVOC processes and aim to propose a generic framework for modelling soil BVOCs based on current understanding and data availability. To achieve this target, we start by reviewing measured sources and sinks of soil BVOCs and summarize commonly reported compounds. Next, we strive to disentangle the drivers for the underlying biotic and abiotic processes. We have ranked the list of compounds, known to be emitted from soils, based on our current understanding of how each process controls emission and uptake. We then present a modelling framework to describe soil BVOC emissions. The proposed framework is an important step toward initializing modelling exercises related to soil BVOC fluxes. Finally, we also provide suggestions for measurements needed to separate individual processes, as well as explore long-term and large-scale patterns in soil BVOC fluxes

Matrix Gla Protein involved in elastic fiber calcification in the dermis of pseudoxanthoma elasticum patients.

Mature MGP (Matrix gamma-carboxyglutamic acid protein) is known to inhibit soft connective tissues calcification. We investigated its possible involvement in pseudoxanthoma elasticum (PXE), a genetic disorder whose clinical manifestations are due to mineralization of elastic fibers. PXE patients have lower serum concentration of total MGP compared to controls (P<0.001). Antibodies specific for the noncarboxylated (Glu-MGP) and for the gamma-carboxylated (Gla-MGP) forms of MGP were assayed on ultrathin sections of dermis from controls and PXE patients. Normal elastic fibers in controls and patients were slightly positive for both forms of MGP, whereas Gla-MGP was more abundant within control's than within patient's elastic fibers (P<0.001). In patients' calcified elastic fibers, Glu-MGP intensively colocalized with mineral precipitates, whereas Gla-MGP precisely localized at the mineralization front. Data suggest that MGP is present within elastic fibers and is associated with calcification of dermal elastic fibers in PXE. To investigate whether local cells produce MGP, dermal fibroblasts were cultured in vitro and MGP was assayed at mRNA and protein levels. In spite of very similar MGP mRNA expression, cells from PXE patients produced 30% less of Gla-MGP compared to controls. Data were confirmed by immunocytochemistry on ultrathin sections. Normal fibroblasts in vitro were positive for both forms of MGP. PXE fibroblasts were positive for Glu-MGP and only barely positive for Gla-MGP (P<0.001). In conclusion, MGP is involved in elastic fiber calcification in PXE. The lower ratio of Gla-MGP over Glu-MGP in pathological fibroblasts compared to controls suggests these cells may play an important role in the ectopic calcification in PXE

Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study

Vitamin K-dependent proteins, including matrix Gla-protein, have been shown to inhibit vascular calcification. Activation of these proteins via carboxylation depends on the availability of vitamin K. We examined whether dietary intake of phylloquinone (vitamin K-1) and menaquinone (vitamin K-2) were related to aortic calcification and coronary heart disease (CHD) in the population-based Rotterdam Study. The analysis included 4807 subjects with dietary data and no history of myocardial infarction at baseline (1990-1993) who were followed until January 1, 2000. The risk of incident CHD, all-cause mortality, and aortic atherosclerosis was studied in tertiles of energy-adjusted vitamin K intake after adjustment for age, gender, BMI, smoking, diabetes, education, and dietary factors. The relative risk (RR) of CHD mortality was reduced in the mid and upper tertiles of dietary menaquinone compared to the lower tertile [RR = 0.73 (95% CI: 0.45, 1.17) and 0.43 (0.24, 0.77), respectively]. Intake of menaquinone was also inversely related to all-cause mortality [RR = 0.91 (0.75, 1.09) and 0.74 (0.59, 0.92), respectively] and severe aortic calcification [odds ratio of 0.71 (0.50, 1.00) and 0.48 (0.32, 0.71), respectively]. Phylloquinone intake was not related to any of the outcomes. These findings suggest tha

Magnesium but not nicotinamide prevents vascular calcification in experimental uraemia

BACKGROUND: Optimal phosphate control is an unmet need in chronic kidney disease (CKD). High serum phosphate increases calcification burden and is associated with mortality and cardiovascular disease in CKD. Nicotinamide (NA) alone or in combination with calcium-free phosphate binders might be a strategy to reduce phosphate levels and calcification and thus impact cardiovascular disease in CKD. METHODS: We studied the effect of NA alone and in combination with magnesium carbonate (MgCO3) as a potential no

Ucma/GRP inhibits phosphate-induced vascular smooth muscle cell calcification via SMAD-dependent BMP signalling

Vascular calcification (VC) is the process of deposition of calcium phosphate crystals in the blood vessel wall, with a central role for vascular smooth muscle cells (VSMCs). VC is highly prevalent in chronic kidney disease (CKD) patients and thought, in part, to be induced by phosphate imbalance. The molecular mechanisms that regulate VC are not fully known. Here we propose a novel role for the mineralisation regulator Ucma/GRP (Upper zone of growth plate and Cartilage Matrix Associated protein/Gla Rich Protein) in phosphate-induced VSMC calcification. We show that Ucma/GRP is present in calcified atherosclerotic plaques and highly expressed in calcifying VSMCs in vitro. VSMCs from Ucma/GRP(-/-) mice showed increased mineralisation and expression of osteo/chondrogenic markers (BMP-2, Runx2, beta-catenin, p-SMAD1/5/8, ALP, OCN), and decreased expression of mineralisation inhibitor MGP, suggesting that Ucma/GRP is an inhibitor of mineralisation. Using BMP signalling inhibitor noggin and SMAD1/5/8 signalling inhibitor dorsomorphin we showed that Ucma/GRP is involved in inhibiting the BMP-2-SMAD1/5/8 osteo/chondrogenic signalling pathway in VSMCs treated with elevated phosphate concentrations. Additionally, we showed for the first time evidence of a direct interaction between Ucma/GRP and BMP-2. These results demonstrate an important role of Ucma/GRP in regulating osteo/chondrogenic differentiation and phosphate-induced mineralisation of VSMCs.NWO ZonMw [MKMD 40-42600-98-13007]; FCT [SFRH/BPD/70277/2010]info:eu-repo/semantics/publishedVersio

Vitamin K supplementation increases vitamin K tissue levels but fails to counteract ectopic calcification in a mouse model for pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is an autosomal recessive disorder in which calcification of connective tissue leads to pathology in skin, eye and blood vessels. PXE is caused by mutations in ABCC6. High expression of this transporter in the basolateral hepatocyte membrane suggests that it secretes an as-yet elusive factor into the circulation which prevents ectopic calcification. Utilizing our Abcc6−/− mouse model for PXE, we tested the hypothesis that this factor is vitamin K (precursor) (Borst et al. 2008, Cell Cycle). For 3 months, Abcc6−/− and wild-type mice were put on diets containing either the minimum dose of vitamin K required for normal blood coagulation or a dose that was 100 times higher. Vitamin K was supplied as menaquinone-7 (MK-7). Ectopic calcification was monitored in vivo by monthly micro-CT scans of the snout, as the PXE mouse model develops a characteristic connective tissue mineralization at the base of the whiskers. In addition, calcification of kidney arteries was measured by histology. Results show that supplemental MK-7 had no effect on ectopic calcification in Abcc6−/− mice. MK-7 supplementation increased vitamin K levels (in skin, heart and brain) in wild-type and in Abcc6−/− mice. Vitamin K tissue levels did not depend on Abcc6 genotype. In conclusion, dietary MK-7 supplementation increased vitamin K tissue levels in the PXE mouse model but failed to counteract ectopic calcification. Hence, we obtained no support for the hypothesis that Abcc6 transports vitamin K and that PXE can be cured by increasing tissue levels of vitamin K

A Nonuniform Sensor Distribution Strategy for Avoiding Energy Holes in Wireless Sensor Networks

The energy hole problem exerts great impact on the energy efficiency and lifetime of wireless sensor networks (WSNs) based on many-to-one communication model. Unequal cluster emerged in recent years is a good way to alleviate the energy hole problem by dispersing cluster heads' burden. However, it fails to address this problem fundamentally due to its inherent characteristics. The single non-uniform nodes distribution strategy can alleviate the energy hole problem well by setting more nodes in networks to achieve energy balance, yet it may result in low energy efficiency and high cost of the networks. In this paper, by analyzing and minimizing intra- and inter-cluster energy consumption, we construct a suboptimal unequal cluster for WSNs. We propose a non-uniform sensor distribution strategy based on the previous unequal cluster in accordance with the energy balance principle. Simulation results show that our proposed non-uniform sensor nodes distribution strategy can not only achieve good energy efficiency as the unequal cluster method, but also ensure the network energy consumption balance and resolve the energy hole problem completely as the non-uniform sensor distribution approach. Furthermore, our algorithm needs fewer sensors to be settled than single non-uniform node distribution

Spinal codes

Spinal codes are a new class of rateless codes that enable wireless networks to cope with time-varying channel conditions in a natural way, without requiring any explicit bit rate selection. The key idea in the code is the sequential application of a pseudo-random hash function to the message bits to produce a sequence of coded symbols for transmission. This encoding ensures that two input messages that differ in even one bit lead to very different coded sequences after the point at which they differ, providing good resilience to noise and bit errors. To decode spinal codes, this paper develops an approximate maximum-likelihood decoder, called the bubble decoder, which runs in time polynomial in the message size and achieves the Shannon capacity over both additive white Gaussian noise (AWGN) and binary symmetric channel (BSC) models. Experimental results obtained from a software implementation of a linear-time decoder show that spinal codes achieve higher throughput than fixed-rate LDPC codes, rateless Raptor codes, and the layered rateless coding approach of Strider, across a range of channel conditions and message sizes. An early hardware prototype that can decode at 10 Mbits/s in FPGA demonstrates that spinal codes are a practical construction.Massachusetts Institute of Technology (Irwin and Joan Jacobs Presidential Fellowship)Massachusetts Institute of Technology (Claude E. Shannon Assistantship)Intel Corporation (Intel Fellowship