Methane emission by Camelids

Methane emissions from ruminant livestock have been intensively studied in order to reduce contribution to the greenhouse effect. Ruminants were found to produce more enteric methane than other mammalian herbivores. As camelids share some features of their digestive anatomy and physiology with ruminants, it has been proposed that they produce similar amounts of methane per unit of body mass. This is of special relevance for countrywide greenhouse gas budgets of countries that harbor large populations of camelids like Australia. However, hardly any quantitative methane emission measurements have been performed in camelids. In order to fill this gap, we carried out respiration chamber measurements with three camelid species (Vicugna pacos, Lama glama, Camelus bactrianus; n = 16 in total), all kept on a diet consisting of food produced from alfalfa only. The camelids produced less methane expressed on the basis of body mass (0.3260.11 L kg21 d21) when compared to literature data on domestic ruminants fed on roughage diets (0.5860.16 L kg21 d21). However, there was no significant difference between the two suborders when methane emission was expressed on the basis of digestible neutral detergent fiber intake (92.7633.9 L kg21 in camelids vs. 86.2612.1 L kg21 in ruminants). This implies that the pathways of methanogenesis forming part of the microbial digestion of fiber in the foregut are similar between the groups, and that the lower methane emission of camelids can be explained by their generally lower relative food intake. Our results suggest that the methane emission of Australia’s feral camels corresponds only to 1 to 2% of the methane amount produced by the countries’ domestic ruminants and that calculations of greenhouse gas budgets of countries with large camelid populations based on equations developed for ruminants are generally overestimating the actual levels

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

Methadone is a local anaesthetic-like inhibitor of neuronal Na+ channels and blocks excitability of mouse peripheral nerves

Background: Opioids enhance and prolong analgesia when applied as adjuvants to local anaesthetics (LAs). A possible molecular mechanism for this property is a direct inhibition of voltage-gated Na+ channels which was reported for some opioids. Methadone is an effective adjuvant to LA and was recently reported to inhibit cardiac Na+ channels. Here, we explore and compare LA properties of methadone and bupivacaine on neuronal Na+ channels, excitability of peripheral nerves, and cell viability. Methods: Effects of methadone were explored on compound action potentials (CAP) of isolated mouse saphenous nerves. Patch clamp recordings were performed on Na+ channels in ND7/23 cells, the α-subunits Nav1.2, Nav1.3, Nav1.7, and Nav1.8, and the hyperpolarization-activated cyclic nucleotide-gated channel 2 (HCN2). Cytotoxicity was determined using flow cytometry. Results: Methadone (IC50 86–119 µM) is a state-dependent and unselective blocker on Nav1.2, Nav1.3, Nav1.7, and Nav1.8 with a potency comparable with that of bupivacaine (IC50 177 µM). Both bupivacaine and methadone also inhibit C- and A-fibre CAPs in saphenous nerves in a concentration-dependent manner. Tonic block of Nav1.7 revealed a discrete stereo-selectivity with a higher potency for levomethadone than for dextromethadone. Methadone is also a weak blocker of HCN2 channels. Both methadone and bupivacaine induce a pronounced cytotoxicity at concentrations required for LA effects. Conclusions: Methadone induces typical LA effects by inhibiting Na+ channels with a potency similar to that of bupivacaine. This hitherto unknown property of methadone might contribute to its high efficacy when applied as an adjuvant to LA

European Record Efficiency Amorphous Crystalline Silicon Heterojunction Solar Cells Final Results from the HETSI Project

In this work, we present some of the main results obtained within the project Heterojunction Solar Cells based on a Si c Si HETSI [1], funded by the European Commission in the framework of the 7th Research Framework Program from 2008 to 2011. This project, based on the promising silicon heterojunction technology, represents a concerted effort of the consortium, a well balanced mix of universities, institutes of technology and industrial partners, to combine device modelling, material optimization and characterization, process development from texturization to metallization , PV cell and module process integration, while cost and environmental issues are addressed as well. Thanks to a better understanding of the device physics from advanced characterization tools and modeling, the results obtained by this consortium have put Europe on the map, with a record cell efficiency of 20,7 on large area n type c Si wafers. Moreover, a dedicated module process has been developed with low losses of only 1 absolute from cell to modul

Educational Differences in Smoking: Selection Versus Causation

We investigate sources of educational differences in smoking. Using a large German data set containing retrospective information on the age at smoking onset, we compare age-specific hazard rates of starting smoking between (future) low and high educated individuals. We and that up to 90% of the educational differences in smoking develop before the age of 16, i.e. before compulsory schooling is completed. This Education gap persists into adulthood. Further, we examine the role of health-related knowledge (proxied by working in health-related occupations) and it hardly explains smoking decisions. Our findings suggest that (unobserved) factors determining both the selection into smoking and education are almost exclusively responsible for educational differences in smoking. Only small parts of the education gap seem to be caused by general or health-specific education. The effectiveness of education policy to combat smoking is thus likely limited