The production process in basketball: Empirical evidence from Spanish league

The main objective of this paper is to provide an empirical assessment of the production process in a basketball team. We estimate a logit model in which the output produced by a team is the game outcome (win or loss) and the inputs are those play characteristics that impact on that outcome. From the results obtained it is clear that, on average, there is a substantial difference between the impact of each play characteristic on a basketball team’s winning probability and that probability varies as the quality/quantity of the inputs used changes, albeit not proportionally.sports economics, team sport, professional basketball, productive process, logit model

The economic geography of football success: empirical evidence from european cities

Introduction. – 1. The geography of successful football teams: an analytical framework – 2. Empirical analysis – 2.1. Data, model estimation and results – 2.2. Cities and teams: some remarks about market size and teams’ performance – 3. Conclusions – 4. Annex

β-(1,4)-Galactan remodelling in Arabidopsis cell walls affects the xyloglucan structure during elongation

Galactan turnover occurs during cell elongation and affects the cell wall xyloglucan structure which is involved in the interaction between cellulose and xyloglucan. β-(1,4)-Galactan is one of the main side chains of rhamnogalacturonan I. Although the specific function of this polymer has not been completely established, it has been related to different developmental processes. To study β-(1,4)-galactan function, we have generated transgenic Arabidopsis plants overproducing chickpea βI-Gal β-galactosidase under the 35S CaMV promoter (35S::βI-Gal) to reduce galactan side chains in muro. Likewise, an Arabidopsis double loss-of-function mutant for BGAL1 and BGAL3 Arabidopsis β-galactosidases (bgal1/bgal3) has been obtained to increase galactan levels. The characterization of these plants has confirmed the role of β-(1,4)-galactan in cell growth, and demonstrated that the turnover of this pectic side chain occurs during cell elongation, at least in Arabidopsis etiolated hypocotyls and floral stem internodes. The results indicate that BGAL1 and BGAL3 β-galactosidases act in a coordinate way during cell elongation. In addition, this work indicates that galactan plays a role in the maintenance of the cell wall architecture during this process. Our results point to an involvement of the β-(1,4)-galactan in the xyloglucan structure and the interaction between cellulose and xyloglucan

Sustained blood glutamate scavenging enhances protection in ischemic stroke

Stroke is a major cause of morbidity, mortality, and disability. During ischemic stroke, a marked and prolonged rise of glutamate concentration in the brain causes neuronal cell death. This study explores the protective effect of a bioconjugate form of glutamate oxaloacetate transaminase (hrGOT), which catalyzes the depletion of blood glutamate in the bloodstream for ~6 days following a single administration. When treated with this bioconjugate, a significant reduction of the infarct volume and a better retention of sensorimotor function was observed for ischemic rats compared to those treated with saline. Moreover, the equivalent dose of native hrGOT yielded similar results to the saline treated group for some tests. Targeting the bioconjugate to the blood-brain-barrier did not improve its performance. The data suggest that the bioconjugates draw glutamate out of the brain by displacing homeostasis between the different glutamate pools of the body

Load assessment and analysis of impacts in multibody systems

The evaluation of contact forces during an impact requires the use of continuous force-based methods. An accurate prediction of the impact force demands the identification of the contact parameters on a case-by-case basis. In this paper, the preimpact effective kinetic energy (Formula presented.) is put forward as an indicator of the intensity of the impact force along the contact normal direction. This represents a part of the total kinetic energy of the system that is associated with the subspace of constrained motion defined by the impact constraints at the moment of contact onset. Its value depends only on the mechanical parameters and the configuration of the system. We illustrate in this paper that this indicator can be used to characterize the impact force intensity. The suitability of this indicator is confirmed by numerical simulations and experimentsPostprint (author's final draft

Did Patagonia collide with Gondwana in the Late Paleozoic? Some insights from a multidisciplinary study of magmatic units of the North Patagonian Massif

The origin of Patagonia and its relations with the South American crustal blocks to the north have been a matter of debate for decades. We report results from a multidisciplinary study centered on Paleozoic granitoids exposed in the northeastern corner of the North Patagonian Massif. Microstructural and magnetofabric studies reveal two suites of granitoids. Late Carboniferous (?) granitoids (Yaminué Complex, Tardugno Granodiorite, Cabeza de Vaca leucogranite) were emplaced and subsequently deformed in a major NNE-SSW compressive stress regime that also provoked top-to-the-SW thrust deformation in shallow crustal levels. Gravity and geobarometric studies show that the same major deformation event has been recorded at different crustal levels. The age and type of deformation of this event recorded across the northern boundary of Patagonia strongly supports a Late Carboniferous - Early Permian frontal collision between Patagonia and Gondwana. This major deformation event ceased by 281 Ma when the Navarrete Plutonic Complex, which shows mainly magmatic fabrics, was emplaced under a far-field WNW-ESE stress regime. Crustal continuity between the North Patagonian Massif and the Pampia and Arequipa- Antofalla terranes is suggested by similar Late Paleoproterozoic crustal model ages, comparable detrital zircon ages in Early Paleozoic successions, the apparent continuity of an Early Ordovician continental magmatic arc and paleomagnetic data. Reconciliation of this evidence with the Late Paleozoic frontal collision is obtained in a tectonic model that suggests that the North Patagonian Massif is a parautochthonous crustal block

IL-21 production by CD4+ effector T cells and frequency of circulating follicular helper T cells are increased in type 1 diabetes patients.

AIMS/HYPOTHESIS: Type 1 diabetes results from the autoimmune destruction of insulin-secreting pancreatic beta cells by T cells. Despite the established role of T cells in the pathogenesis of the disease, to date, with the exception of the identification of islet-specific T effector (Teff) cells, studies have mostly failed to identify reproducible alterations in the frequency or function of T cell subsets in peripheral blood from patients with type 1 diabetes. METHODS: We assessed the production of the proinflammatory cytokines IL-21, IFN-γ and IL-17 in peripheral blood mononuclear cells from 69 patients with type 1 diabetes and 61 healthy donors. In an additional cohort of 30 patients with type 1 diabetes and 32 healthy donors, we assessed the frequency of circulating T follicular helper (Tfh) cells in whole blood. IL-21 and IL-17 production was also measured in peripheral blood mononuclear cells (PBMCs) from a subset of 46 of the 62 donors immunophenotyped for Tfh. RESULTS: We found a 21.9% (95% CI 5.8, 40.2; p = 3.9 × 10(-3)) higher frequency of IL-21(+) CD45RA(-) memory CD4(+) Teffs in patients with type 1 diabetes (geometric mean 5.92% [95% CI 5.44, 6.44]) compared with healthy donors (geometric mean 4.88% [95% CI 4.33, 5.50]). Consistent with this finding, we found a 14.9% increase in circulating Tfh cells in the patients (95% CI 2.9, 26.9; p = 0.016). CONCLUSIONS/INTERPRETATION: These results indicate that increased IL-21 production is likely to be an aetiological factor in the pathogenesis of type 1 diabetes that could be considered as a potential therapeutic target.This work was supported by the JDRF UK Centre for Diabetes - Genes, Autoimmunity and Prevention (D-GAP; 4-2007-1003) in collaboration with M. Peakman and T. Tree at King’s College London, the JDRF, the Wellcome Trust (WT; WT061858/091157 and 083650/Z/07/Z) and the National Institute for Health Research Cambridge Biomedical Research Centre (CBRC). The Cambridge Institute for Medical Research (CIMR) is in receipt of a Wellcome Trust Strategic Award (100140). RCF is funded by a JDRF post-doctoral fellowship (3-2011-374). CW is funded by the Wellcome Trust (088998). The funding organisations had no involvement with the design and conduct of the study; collection,management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.This is the final published version. It first appeared at http://link.springer.com/article/10.1007%2Fs00125-015-3509-8

Pectic galactan affects cell wall architecture during secondary cell wall deposition

Despite recent advances regarding the role of pectic β-(1,4)-galactan neutral side chains in primary cell wall remodelling during growth and cell elongation, little is known about the specific function of this polymer in other developmental processes. We have used transgenic Arabidopsis plants overproducing chickpea βI-Gal β-galactosidase under the 35S CaMV promoter (35S::βI-Gal) with reduced galactan levels in the basal non-elongating floral stem internodes to gain insight into the role of β-(1,4)-galactan in cell wall architecture during the cessation of elongation and the beginning of secondary growth. The loss of galactan mediated by βI-Gal in 35S::βI-Gal plants is accompanied by a reduction in the levels of KOH-extracted xyloglucan and an increase in the levels of xyloglucan released by a cellulose-specific endoglucanase. These variations in cellulose–xyloglucan interactions cause an altered xylan and mannan deposition in the cell wall that in turn results in a deficient lignin deposition. Considering these results, we can state that β-(1,4)-galactan plays a key structural role in the correct organization of the different domains of the cell wall during the cessation of growth and the early events of secondary cell wall development. These findings reinforce the notion that there is a mutual dependence between the different polysaccharides and lignin polymers to form an organized and functional cell wall

Widespread seasonal gene expression reveals annual differences in human immunity and physiology.

Seasonal variations are rarely considered a contributing component to human tissue function or health, although many diseases and physiological process display annual periodicities. Here we find more than 4,000 protein-coding mRNAs in white blood cells and adipose tissue to have seasonal expression profiles, with inverted patterns observed between Europe and Oceania. We also find the cellular composition of blood to vary by season, and these changes, which differ between the United Kingdom and The Gambia, could explain the gene expression periodicity. With regards to tissue function, the immune system has a profound pro-inflammatory transcriptomic profile during European winter, with increased levels of soluble IL-6 receptor and C-reactive protein, risk biomarkers for cardiovascular, psychiatric and autoimmune diseases that have peak incidences in winter. Circannual rhythms thus require further exploration as contributors to various aspects of human physiology and disease.The Gambian study providing data for analysis was supported by core funding MC-A760-5QX00 to the International Nutrition Group by the UK Medical Research Council (MRC) and the UK Department for the International Development (DFID) under the MRC/DFID Concordat agreement. This work was supported by the JDRF UK Centre for Diabetes-Genes, Autoimmunity and Prevention (D-GAP; 4-2007-1003), the JDRF (9-2011-253), the Wellcome Trust (WT061858/091157), the National Institute for Health Research Cambridge Biomedical Research Centre (CBRC) and the Medical Research Council (MRC) Cusrow Wadia Fund. The research leading to these results has received funding from the European Union’s 7th Framework Programme (FP7/2007–2013) under grant agreement no.241447 (NAIMIT). The Cambridge Institute for Medical Research (CIMR) is in receipt of a Wellcome Trust Strategic Award (WT100140). X.C.D. was a University of Cambridge/Wellcome Trust Infection and Immunity PhD student. R.C.F. is funded by a JDRF post-doctoral fellowship (3-2011-374). C.W. and H.G are funded by the Wellcome Trust (WT089989). The BABYDIET study was supported by grants from the Deutsche Forschungsgemeinschaft (DFG ZI-310/14-1 to-4), the JDRF (JDRF 17-2012-16 and 1-2006-665) and the German Center for Diabetes Research (DZD e.V.). E.B. is supported by the DFG Research Center and Cluster of Excellence—Center for Regenerative Therapies Dresden (FZ 111).This is the final published version. It first appeared at http://www.nature.com/ncomms/2015/150512/ncomms8000/full/ncomms8000.html