Advocating for Change? How a Civil Society-led Coalition Influences the Implementation of the Forest Rights Act in India

Forest policy implementation is a political endeavor involving both state and non-state actors. We observe that civil society organizations (CSOs) often federate into civil society-led coalitions (CSCs) in order to shape forest policies in their favor. They appear to be successful in doing this during the policy design phase but we know little about whether they are able to see through to implementation the changes they have put in motion. Analyzing CSC strategies during policy implementation could help to explain variation in the extent to which forest policies are successfully implemented. This paper analyzes the strategy choices and potential impact during policy implementation of a loose CSC comprised of CSOs, activists, people's movements, researchers, and lawyers that advocates for the full implementation of the Forest Rights Act in India. Drawing from the Advocacy Coalition Framework's focus on belief systems, complemented by insights from political ecology and civil society/social movements literature, we develop a framework to analyze CSC strategy choices. Our analysis is conducted at the national level and in two states, Andhra Pradesh and Odisha. We employ qualitative research methods, including 38 interviews with CSC and non-CSC members, and a comprehensive analysis of the main CSC listserv and 1000 relevant English language newspaper articles. Our study reveals that the CSC employs a range of conflictive and collaborative strategies in its attempts to influence state-led implementation processes, at both national and state levels. It draws on a loose, heterogeneous network with ability to connect internally and a clear moral justification of its involvement in FRA implementation. However the diverse range of views on the implementation issues held by CSC members, lack of dedicated funding for coordination, limited legitimacy in the eyes of some state actors and a constricting wider institutional setting, impedes the CSC's ability to make coalition-level strategy decisions. Our results lead us to argue that CSCs are undoubtedly active in forest policy implementation at the national level and in the two states analyzed, though limited coordination of strategies potentially restricts their impact on the policy implementation process

The elevated Curie temperature and half-metallicity in the ferromagnetic semiconductor Lax_{x}Eu1−x_{1-x}O

Here we study the effect of La doping in EuO thin films using SQUID magnetometry, muon spin rotation ($\mu$SR), polarized neutron reflectivity (PNR), and density functional theory (DFT). The $\mu$SR data shows that the La$_{0.15}$Eu$_{0.85}$O is homogeneously magnetically ordered up to its elevated $T_{\rm C}$. It is concluded that bound magnetic polaron behavior does not explain the increase in $T_{\rm C}$ and an RKKY-like interaction is consistent with the $\mu$SR data. The estimation of the magnetic moment by DFT simulations concurs with the results obtained by PNR, showing a reduction of the magnetic moment per La$_{x}$Eu$_{1-x}$O for increasing lanthanum doping. This reduction of the magnetic moment is explained by the reduction of the number of Eu-4$f$ electrons present in all the magnetic interactions in EuO films. Finally, we show that an upwards shift of the Fermi energy with La or Gd doping gives rise to half-metallicity for doping levels as high as 3.2 %.Comment: 7 pages, 11 figure

A Hierarchical Array of Integrable Models

Motivated by Harish-Chandra theory, we construct, starting from a simple CDD\--pole $S$\--matrix, a hierarchy of new $S$\--matrices involving ever ``higher'' (in the sense of Barnes) gamma functions.These new $S$\--matrices correspond to scattering of excitations in ever more complex integrable models.From each of these models, new ones are obtained either by ``$q$\--deformation'', or by considering the Selberg-type Euler products of which they represent the ``infinite place''. A hierarchic array of integrable models is thus obtained. A remarkable diagonal link in this array is established.Though many entries in this array correspond to familiar integrable models, the array also leads to new models. In setting up this array we were led to new results on the $q$\--gamma function and on the $q$\--deformed Bloch\--Wigner function.Comment: 18 pages, EFI-92-2

Causas de Morte em Doentes com Hemofilia: Estudo Retrospectivo de 1979 a 2007, no Serviço de Imunohemoterapia do HSJ

Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK2 receptors in animals and humans, and may be increased in asthma. Because beta(2)-adrenoceptor agonists are the most widely used bronchodilators in asthma, we investigated the effects of the beta(2)-adrenoceptor agonist fenoterol on NK2 receptor messenger RNA (mRNA) and receptor density as well as the functional responses of bovine tracheal smooth muscle to the NK2 receptor agonist [beta-Ala(8)]-NKA(4-10) in vitro, using Northern blot analysis, receptor binding, and organ bath studies. Incubation with fenoterol induced a time- and concentration-dependent upregulation of NK2 receptor mRNA (71% increase after 12 h at 10(-7) M fenoterol), which was abolished by propranolol (a nonselective beta-adrenoceptor agonist) and ICI118551 (a selective beta(2)-adrenoceptor antagonist), but not by CGP20712A (a selective beta(1)-adrenoceptor antagonist), indicating that fenoterol acts via beta(2)-adrenoceptors. These effects were mimicked by forskolin and prostaglandin E-2 (PGE,), both agents that increase cyclic adenosine monophosphate (cAMP), and by the cAMP analogue 8-bromo-cAMP. The upregulation was blocked by cycloheximide, indicating that it requires new protein synthesis, and was accompanied by an increase in both the stability of NK2 receptor mRNA and the rate of NK2 receptor gene transcription. Radioligand binding assay using the selective NK2 receptor antagonist [H-3]SR48968 showed a significant increase in the number of receptor binding sites after 12 h and 18 h, which was accompanied by an increased contractile responsiveness to the NK2 receptor agonist [beta-Ala(8)]-NKA(4-10). Dexamethasone completely prevented the fenoterol-induced increase in NK2 receptor mRNA and in the contractile response. We conclude that beta(2)-adrenoceptor agonists induce upregulation of functional NK2 receptors in airway smooth muscle by increasing cAMP, and that this can be prevented by a corticosteroid. The increased responsiveness could be relevant to asthma control and mortality

Failure to Detect Xenotropic Murine Leukemia Virus-Related Virus in Blood of Individuals at High Risk of Blood-Borne Viral Infections

A xenotropic murine leukemia virus-related virus (XMRV) has recently been reported in association with prostate cancer and chronic fatigue syndrome, with a prevalence of up to 3.7% in the healthy population. We looked for XMRV in 230 patients with human immunodeficiency virus type 1 or hepatitis C infection. XMRV was undetectable in plasma or peripheral blood mononuclear cells by polymerase chain reaction targeting XMRV gag or env. T cell responses to XMRV Gag were undetectable in peripheral blood mononuclear cells by ex vivo gamma interferon enzyme-linked immunospot assay. In our cohorts, XMRV was not enriched in patients with blood-borne or sexually transmitted infections fromthe United Kingdom and Western Europ

The fidelity of dynamic signaling by noisy biomolecular networks

This is the final version of the article. Available from Public Library of Science via the DOI in this record.Cells live in changing, dynamic environments. To understand cellular decision-making, we must therefore understand how fluctuating inputs are processed by noisy biomolecular networks. Here we present a general methodology for analyzing the fidelity with which different statistics of a fluctuating input are represented, or encoded, in the output of a signaling system over time. We identify two orthogonal sources of error that corrupt perfect representation of the signal: dynamical error, which occurs when the network responds on average to other features of the input trajectory as well as to the signal of interest, and mechanistic error, which occurs because biochemical reactions comprising the signaling mechanism are stochastic. Trade-offs between these two errors can determine the system's fidelity. By developing mathematical approaches to derive dynamics conditional on input trajectories we can show, for example, that increased biochemical noise (mechanistic error) can improve fidelity and that both negative and positive feedback degrade fidelity, for standard models of genetic autoregulation. For a group of cells, the fidelity of the collective output exceeds that of an individual cell and negative feedback then typically becomes beneficial. We can also predict the dynamic signal for which a given system has highest fidelity and, conversely, how to modify the network design to maximize fidelity for a given dynamic signal. Our approach is general, has applications to both systems and synthetic biology, and will help underpin studies of cellular behavior in natural, dynamic environments.We acknowledge support from a Medical Research Council and Engineering and Physical Sciences Council funded Fellowship in Biomedical Informatics (CGB) and a Scottish Universities Life Sciences Alliance chair in Systems Biology (PSS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Theorems on shear-free perfect fluids with their Newtonian analogues

In this paper we provide fully covariant proofs of some theorems on shear-free perfect fluids. In particular, we explicitly show that any shear-free perfect fluid with the acceleration proportional to the vorticity vector (including the simpler case of vanishing acceleration) must be either non-expanding or non-rotating. We also show that these results are not necessarily true in the Newtonian case, and present an explicit comparison of shear-free dust in Newtonian and relativistic theories in order to see where and why the differences appear.Comment: 23 pages, LaTeX. Submitted to GR

Large-Scale Spatial Cross-Calibration of Hinode/SOT-SP and SDO/HMI

We investigate the cross-calibration of the Hinode/SOT-SP and SDO/HMI instrument meta-data, specifically the correspondence of the scaling and pointing information. Accurate calibration of these datasets gives the correspondence needed by inter-instrument studies and learning-based magnetogram systems, and is required for physically-meaningful photospheric magnetic field vectors. We approach the problem by robustly fitting geometric models on correspondences between images from each instrument's pipeline. This technique is common in computer vision, but several critical details are required when using scanning slit spectrograph data like Hinode/SOT-SP. We apply this technique to data spanning a decade of the Hinode mission. Our results suggest corrections to the published Level 2 Hinode/SOT-SP data. First, an analysis on approximately 2,700 scans suggests that the reported pixel size in Hinode/SOT-SP Level 2 data is incorrect by around 1%. Second, analysis of over 12,000 scans show that the pointing information is often incorrect by dozens of arcseconds with a strong bias. Regression of these corrections indicates that thermal effects have caused secular and cyclic drift in Hinode/SOT-SP pointing data over its mission. We offer two solutions. First, direct co-alignment with SDO/HMI data via our procedure can improve alignments for many Hinode/SOT-SP scans. Second, since the pointing errors are predictable, simple post-hoc corrections can substantially improve the pointing. We conclude by illustrating the impact of this updated calibration on derived physical data products needed for research and interpretation. Among other things, our results suggest that the pointing errors induce a hemispheric bias in estimates of radial current density.Comment: Under revisions at ApJ

A Polymorphism Affecting MYB Binding within the Promoter of the PDCD4 Gene is Associated with Severe Asthma in Children

A previous genome-wide association study in asthma revealed putative associations that merit further investigation. In this study, the genome-wide significant associations of SNPs at the 5% false discovery rate were examined in independent groups of severe asthmatics. The panel consisted of 397 severe asthmatic adults, 116 severe asthmatic children, and a collection of 207 family-trios with an asthmatic proband. Three SNPs in the PDCD4 gene (rs6585018:G>A, rs1322997:C>A, and rs34104444:G>A) were significantly associated with severe childhood asthma (P values: 0.003, 0.002, 0.004) and total immunoglobulin E (IgE) levels (P values: 0.034, 0.041, 0.052). In an independent group of 234 asthmatic children and 652 controls, PDCD4 SNPs rs1407696:T>G and rs11195360:T>C were associated with total IgE levels (P values: 0.006, 0.014). In silico analysis of PDCD4 locus showed that rs6585018:G>A had the potential to affect MYB transcription factor binding, shown to act as a PDCD4-transcription inducer. Electromobility shift assays and reporter assays revealed that rs6585018:G>A alters MYB binding thereby influencing the expression of PDCD4. SNPs within MYB itself confer susceptibility to eosinophilia and asthma. Our association between a variant MYB binding site in PDCD4 and the severest form of childhood asthma therefore suggests that PDCD4 is a novel molecule of importance to asthmatic inflammatory responses