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Abstract. Regional land carbon budgets provide insights on the spatial distribution of the land uptake of atmospheric carbon dioxide, and can be used to evaluate carbon cycle models and to define baselines for land-based additional mitigation efforts. The scientific community has been involved in providing observation-based estimates of regional carbon budgets either by downscaling atmospheric CO2 observations into surface fluxes with atmospheric inversions, by using inventories of carbon stock changes in terrestrial ecosystems, by upscaling local field observations such as flux towers with gridded climate and remote sensing fields or by integrating data-driven or process-oriented terrestrial carbon cycle models. The first coordinated attempt to collect regional carbon budgets for nine regions covering the entire globe in the RECCAP-1 project has delivered estimates for the decade 2000–2009, but these budgets were not comparable between regions, due to different definitions and component fluxes reported or omitted. The recent recognition of lateral fluxes of carbon by human activities and rivers, that connect CO2 uptake in one area with its release in another also requires better definition and protocols to reach harmonized regional budgets that can be summed up to the globe and compared with the atmospheric CO2 growth rate and inversion results. In this study, for the international initiative RECCAP-2 coordinated by the Global Carbon Project, which aims as an update of regional carbon budgets over the last two decades based on observations, for 10 regions covering the globe, with a better harmonization that the precursor project, we provide recommendations for using atmospheric inversions results to match bottom-up carbon accounting and models, and we define the different component fluxes of the net land atmosphere carbon exchange that should be reported by each research group in charge of each region. Special attention is given to lateral fluxes, inland water fluxes and land use fluxes.

Aims The aim of this study was to determine whether the sequential application of povidone iodine-alcohol (PVI) followed by chlorhexidine gluconate-alcohol (CHG) would reduce surgical wound contamination to a greater extent than PVI applied twice in patients undergoing spinal surgery. Patients and Methods A single-centre, interventional, two arm, parallel group randomised controlled trial was undertaken, involving 407 patients who underwent elective spinal surgery. For 203 patients, the skin was disinfected before surgery using PVI (10% [w/w (1% w/w available iodine)] in 95% industrial denatured alcohol, povidone iodine; Videne Alcoholic Tincture) twice, and for 204 patients using PVI once followed by CHG (2% [w/v] chlorhexidine gluconate in 70% [v/v] isopropyl alcohol; Chloraprep with tint). The primary outcome measure was contamination of the wound determined by aerobic and anaerobic bacterial growth from samples taken after disinfection. Results The detection of viable bacteria in any one of the samples taken after disinfection (culture-positive) was significantly lower in the group treated with both PVI and CHG than in the group treated with PVI alone (59 (29.1%) versus 85 (41.7%), p = 0.009; odds ratio 0.574; 95% confidence interval, 0.380 to 0.866). Conclusions Antisepsis of the skin with the sequential application of PVI and CHG more effectively reduces the contamination of a surgical wound than PVI alone. Cite this article: Bone Joint J 2017;99-B:1354–65.

Abstract As the part of a study to develop buparvaquone (BPQ) formulations for the treatment of cutaneous leishmaniasis, the topical delivery of BPQ and one of its prodrugs from a range of formulations was evaluated. In previous studies, BPQ and its prodrugs were shown to be potent antileishmanials in-vitro, with ED50 values in the nanomolar range. 3-Phosphono-oxymethyl-buparvaquone (3-POM-BPQ) was the most potent antileishmanial and was chosen, together with the parent drug, for further investigation. The ability of the parent and prodrug formulations to cross human and murine skin was tested in-vitro using the Franz diffusion cells. Formulations intended for topical application containing either BPQ or 3-POM-BPQ were developed using excipients that were either acceptable for topical use (GRAS or FDA inactive ingredients) or currently going through the regulatory process. BPQ was shown to penetrate both human epidermal membranes and full thickness BALB/c skin from a range of formulations (gels, emulsions). Similarly, 3-POM-BPQ penetrated full-thickness BALB/c skin from several gel formulations. In-vitro binding studies showed that BPQ bound melanin in a dose-dependent manner and preferably bound to delipidized skin over untreated BALB/c skin (on a weight to weight basis). The results confirm that BPQ and its prodrug 3-POM-BPQ can penetrate the skin from several formulations, making them potentially interesting candidates for further investigation of topical formulations using in-vivo models of cutaneous leishmaniasis.

Cholesta-5,7,9(11)-trien-3β-ol and its oleate ester were incorporated into human low-density lipoprotein and reconstituted high-density lipoprotein. The unesterified sterol was more efficient than its ester in quenching tryptophan fluorescence, especially in low-density lipoprotein. The results, which indicate that in such lipoproteins unesterified sterols are more closely associated with peptide than are esterified sterols, are used to assess possible structures for the lipoproteins.

The oxidative metabolism of ethanol by the cytochrome P450 2E1 (CYP2E1) has been recognized to contribute to the ethanol-induced deleterious effects through the induction of oxidative stress. This study compared the effect of ethanol and acetaldehyde in the induction of oxidative stress and activation of transcription factors nuclear factor-κB (NF-κB) and activating protein 1 (AP-1) in HepG2 cells, which do not express CYP2E1, and HepG2 cells transfected with CYP2E1 (E47 cells). Neither ethanol (80 mmol/L) nor acetaldehyde (25-200 μmol/L) caused oxidative stress in HepG2 cells, an effect that was independent of blocking reduced glutathione (GSH) synthesis with buthionine-l -sulfoximine (BSO). However, BSO preincubation caused an overproduction of peroxides and activation of NF-κB and AP-1 in E47 cells even in the absence of ethanol. Furthermore, the incubation of E47 cells with ethanol (80 mmol/L for up to 5 days) depleted cellular GSH stores in both cytosol and mitochondria, reflecting the induction of oxidative stress. Ethanol activated NF-κB and AP-1 in E47 cells, an effect that was prevented by 4-methylpyrazole, potentiated by cyanamide, and attenuated by trolox C. Interestingly, however, despite the inability of acetaldehyde to induce oxidative stress in HepG2, acetaldehyde activated NF-κB and AP-1; in contrast, ethanol failed to activate these transcription factors in HepG2. Thus, our findings indicate that activation of NF-κB and AP-1 by ethanol and acetaldehyde occurs through distinct mechanisms. CYP2E1 is indispensable in the induction of oxidative stress from ethanol, whereas the activation of NF-κB and AP-1 by acetaldehyde is independent of oxidative stress.

Schrödinger [Schrödinger, E., 1944. What is Life? Cambridge University Press, Cambridge] marvelled at how the organism is able to use metabolic energy to maintain and even increase its organisation, which could not be understood in terms of classical statistical thermodynamics. Ho [Ho, M.W., 1993. The Rainbow and the Worm, The Physics of Organisms, World Scientific, Singapore; Ho, M.W., 1998a. The Rainbow and the Worm, The Physics of Organisms, 2nd (enlarged) ed., reprinted 1999, 2001, 2003 (available online from ISIS website www.i-sis.org.uk)] outlined a novel "thermodynamics of organised complexity" based on a nested dynamical structure that enables the organism to maintain its organisation and simultaneously achieve non-equilibrium and equilibrium energy transfer at maximum efficiency. This thermodynamic model of the organism is reminiscent of the dynamical structure of steady state ecosystems identified by Ulanowicz [Ulanowicz, R.E., 1983. Identifying the structure of cycling in ecosystems. Math. Biosci. 65, 210-237; Ulanowicz, R.E., 2003. Some steps towards a central theory of ecosystem dynamics. Comput. Biol. Chem. 27, 523-530]. The healthy organism excels in maintaining its organisation and keeping away from thermodynamic equilibrium--death by another name--and in reproducing and providing for future generations. In those respects, it is the ideal sustainable system. We propose therefore to explore the common features between organisms and ecosystems, to see how far we can analyse sustainable systems in agriculture, ecology and economics as organisms, and to extract indicators of the system's health or sustainability. We find that looking at sustainable systems as organisms provides fresh insights on sustainability, and offers diagnostic criteria for sustainability that reflect the system's health. In the case of ecosystems, those diagnostic criteria of health translate into properties such as biodiversity and productivity, the richness of cycles, the efficiency of energy use and minimum dissipation. In the case of economic systems, they translate into space-time differentiation or organised heterogeneity, local autonomy and sufficiency at appropriate levels, reciprocity and equality of exchange, and most of all, balancing the exploitation of natural resources--real input into the system--against the ability of the ecosystem to regenerate itself.

Abstract: Five groups of NMRI mice were fed ethanol or sucrose in a nutritionally adequate liquid diet for 9 days. The dietary fat consisted of olive oil with the fatty acid composition 18:1 77%, 18:2 10%, 18:0 and 16:0 12%. The ethanol treated groups received 5% w/v ethanol (E) or isocaloric sucrose (S). Two groups (S‐ and E‐) received the diet without supplement. In two groups (S+ and E +) 7% of the fat was exchanged for arachidonic acid (20:4). In a fifth group (IE +) treated with ethanol and arachidonic acid the diet also contained indomethacin (10 mg/1). The mean intake of ethanol was about 20 g/kg/day. After 9 days animals were killed and liver lipids analyzed after Folch extraction. The post mortem accumulation of prostaglandin E2 in the kidney was measured by GC‐MS. Dietary 20:4 was found to protect mice against fatty liver caused both by a high fat diet alone and in combination with ethanol. The liver triglycerides were 30.7 + 4.3 (S ‐), 46.1+6.9 (E ‐), 6.8 + 0.4 (S +) and 19.4 ±1.8 (E +). Prostaglandin levels in the kidney were depressed by ethanol treatment. Indomethacin gave variable degrees of PG synthesis inhibition. The degree of liver triglyceride accumulation in the IE+ group was inversely propotional to the degree of PG synthesis. The data suggest a role for liver 20:4 cyclooxyganase metabolites in fatty liver caused by high fat diets and ethanol.