Understanding Anthropological Understanding: for a merological anthropology

In this paper I argue for a merological anthropology in which ideas of ‘partiality’ and ‘practical adequacy’ provide a way out of the impasse of relativism which is implied by post-modernism and the related abandonment of a concern with ‘truth’. Ideas such as ‘aptness’ and ‘faithfulness’ enable us to re-establish empirical foundations without having to espouse a simple realism which has been rightly criticised. Ideas taken from ethnomethodology, particularly the way we bootstrap from ‘practical adequacy’ to ‘warrants for confidence’ point to a merological anthropology in which we recognize that we do not and cannot know everything, but that we can have reasons for being confident in the little we know

The climatic challenge: which plants will people use in the next century?

More than 31,000 useful plant species have been documented to fulfil needs and services for humans or the animals and environment we depend on. Despite this diversity, humans currently satisfy most requirements with surprisingly few plant species; for example, just three crops – rice, wheat and maize – comprise more than 50% of plant derived calories. Here, we synthesize the projected impact of global climatic change on useful plants across the spectrum of plant domestication. We illustrate the demographic, spatial, ecophysiological, chemical, functional, evolutionary and cultural traits that are likely to characterise useful plants and their resilience in the next century. Using this framework, we consider a range of possible pathways for future human use of plants. These are centred on two trade-offs: i) diversification versus specialization in the range of species we utilize, and ii) substitutionof the species towards those better suited to future climate versus facilitating adaptation in our existing suite of dominant useful plants. In the coming century, major challenges to agriculture and biodiversity will be dominated by increased climatic variation, shifting species ranges, disruption to biotic interactions, nutrient limitation and emerging pests and pathogens. These challenges must be mitigated, whilst enhancing sustainable production to meet the needs of a growing population and a more resource intensive standard of living. With the continued erosion of biodiversity, our future ability to choose among these pathways and trade-offs is likely to be diminished

Measurement of νˉμ\bar{\nu}_{\mu} and νμ\nu_{\mu} charged current inclusive cross sections and their ratio with the T2K off-axis near detector

We report a measurement of cross section $\sigma(\nu_{\mu}+{\rm nucleus}\rightarrow\mu^{-}+X)$ and the first measurements of the cross section $\sigma(\bar{\nu}_{\mu}+{\rm nucleus}\rightarrow\mu^{+}+X)$ and their ratio $R(\frac{\sigma(\bar \nu)}{\sigma(\nu)})$ at (anti-)neutrino energies below 1.5 GeV. We determine the single momentum bin cross section measurements, averaged over the T2K $\bar{\nu}/\nu$-flux, for the detector target material (mainly Carbon, Oxygen, Hydrogen and Copper) with phase space restricted laboratory frame kinematics of $\theta_{\mu}$500 MeV/c. The results are $\sigma(\bar{\nu})=\left( 0.900\pm0.029{\rm (stat.)}\pm0.088{\rm (syst.)}\right)\times10^{-39}$ and $\sigma(\nu)=\left( 2.41\ \pm0.022{\rm{(stat.)}}\pm0.231{\rm (syst.)}\ \right)\times10^{-39}$in units of cm$^{2}$/nucleon and$R\left(\frac{\sigma(\bar{\nu})}{\sigma(\nu)}\right)= 0.373\pm0.012{\rm (stat.)}\pm0.015{\rm (syst.)}$.Comment: 18 pages, 8 figure

Indications of Linkage and Association of Gilles de la Tourette Syndrome in Two Independent Family Samples: 17q25 Is a Putative Susceptibility Region

Gilles de la Tourette syndrome (GTS) is characterized by multiple motor and phonic tics and high comorbidity rates with other neurobehavioral disorders. It is hypothesized that frontal-subcortical pathways and a complex genetic background are involved in the etiopathogenesis of the disorder. The genetic basis of GTS remains elusive. However, several genomic regions have been implicated. Among them, 17q25 appears to be of special interest, as suggested by various independent investigators. In the present study, we explored the possibility that 17q25 contributes to the genetic component of GTS. The initial scan of chromosome 17 performed on two large pedigrees provided a nonparametric LOD score of 2.41 near D17S928. Fine mapping with 17 additional microsatellite markers increased the peak to 2.61 (P=.002). The original families, as well as two additional pedigrees, were genotyped for 25 single-nucleotide polymorphisms (SNPs), with a focus on three genes in the indicated region that could play a role in the development of GTS, on the basis of their function and expression profile. Multiple three-marker haplotypes spanning all three genes studied provided highly significant association results (P<.001). An independent sample of 96 small families with one or two children affected with GTS was also studied. Of the 25 SNPs, 3 were associated with GTS at a statistically significant level. The transmission/disequilibrium test for a three-site haplotype moving window again provided multiple positive results. The background linkage disequilibrium (LD) of the region was studied in eight populations of European origin. A complicated pattern was revealed, with the pairwise tests producing unexpectedly high LD values at the telomeric TBCD gene. In conclusion, our findings warrant the further investigation of 17q25 as a candidate susceptibility region for GTS

Effects of sleep deprivation on neural functioning: an integrative review

Sleep deprivation has a broad variety of effects on human performance and neural functioning that manifest themselves at different levels of description. On a macroscopic level, sleep deprivation mainly affects executive functions, especially in novel tasks. Macroscopic and mesoscopic effects of sleep deprivation on brain activity include reduced cortical responsiveness to incoming stimuli, reflecting reduced attention. On a microscopic level, sleep deprivation is associated with increased levels of adenosine, a neuromodulator that has a general inhibitory effect on neural activity. The inhibition of cholinergic nuclei appears particularly relevant, as the associated decrease in cortical acetylcholine seems to cause effects of sleep deprivation on macroscopic brain activity. In general, however, the relationships between the neural effects of sleep deprivation across observation scales are poorly understood and uncovering these relationships should be a primary target in future research

First observation and amplitude analysis of the B- -> D+K-pi(-) decay

The B-→D+K-π- decay is observed in a data sample corresponding to 3.0 fb-1 of pp collision data recorded by the LHCb experiment during 2011 and 2012. Its branching fraction is measured to be B(B-→D+K-π-)=(7.31±0.19±0.22±0.39)×10-5 where the uncertainties are statistical, systematic and from the branching fraction of the normalization channel B-→D+π-π-, respectively. An amplitude analysis of the resonant structure of the B-→D+K-π- decay is used to measure the contributions from quasi-two-body B-→D0∗(2400)0K-, B-→D2∗(2460)0K-, and B-→DJ∗(2760)0K- decays, as well as from nonresonant sources. The DJ∗(2760)0 resonance is determined to have spin 1

First observation and amplitude analysis of the B−→D+K−π− decay

The B−→D+K−π− decay is observed in a data sample corresponding to 3.0  fb−1 of pp collision data recorded by the LHCb experiment during 2011 and 2012. Its branching fraction is measured to be B(B−→D+K−π−)=(7.31±0.19±0.22±0.39)×10−5 where the uncertainties are statistical, systematic and from the branching fraction of the normalization channel B−→D+π−π−, respectively. An amplitude analysis of the resonant structure of the B−→D+K−π− decay is used to measure the contributions from quasi-two-body B−→D∗0(2400)0K−, B−→D∗2(2460)0K−, and B−→D∗J(2760)0K− decays, as well as from nonresonant sources. The D∗J(2760)0 resonance is determined to have spin 1