Figuring Out the Doha Round

The global economic and financial crisis has awakened protectionist sentiments around the world, and policymakers have failed to actively seek trade liberalization. In light of this, some have proposed abandoning the Doha Round and starting over with a new agenda. Figuring Out the Doha Round argues that this is far from the time to drop the Doha Round and that it is now more important than ever to sustain political support for the rules-based multilateral trade system. This important new study recommends modest increments in market access commitments by G-20 countries beyond tariff and subsidy cuts in agriculture and nonagricultural market access (NAMA), and policy reforms in customs procedures and related areas that slash red tape and cut transactions costs for exporting and importing goods and services. With additional effort by the G-20 countries, WTO countries can put together a Doha package that is both ambitious and balanced between the interests of developed and developing countries. The study finds that following these recommendations can lead to a world GDP gain of almost $300 billion a year.

Neuropsychiatric systemic lupus erythematosus: a diagnostic challenge

A 58-year-old woman presented to neuropsychiatric services with increased frequency of confusional episodes and intermittent psychotic symptoms. She had a 19-year history of atypical epileptic seizures and cognitive decline. Detailed review of history and clinical investigations revealed that she had accumulated sufficient features to meet diagnostic criteria for systemic lupus erythematosus (SLE). She had previously had lymphopenia and a malar rash; she had positive antinuclear, anti-Ro (anti-Sjögren's-syndrome-related antigen A) and anti-SM (anti-Smith Antibody) antibodies, and elevated erythrocyte sedimentation rate. The seizures, cognitive impairment and psychosis were attributable to neuropsychiatric SLE. Treatment with immune-modulating therapy, cyclophosphamide, resulted in significant improvement in subjective and objective clinical presentation. Neuropsychiatric SLE should be considered a potential differential diagnosis for patients presenting with seizures, psychotic symptoms or cognitive decline. A detailed clinical evaluation with review of the medical history and appropriate laboratory analyses allows this diagnosis to be made, and appropriate treatment to be initiated

The Quantized O(1,2)/O(2)×Z2O(1,2)/O(2)\times Z_2 Sigma Model Has No Continuum Limit in Four Dimensions. I. Theoretical Framework

The nonlinear sigma model for which the field takes its values in the coset space $O(1,2)/O(2)\times Z_2$ is similar to quantum gravity in being perturbatively nonrenormalizable and having a noncompact curved configuration space. It is therefore a good model for testing nonperturbative methods that may be useful in quantum gravity, especially methods based on lattice field theory. In this paper we develop the theoretical framework necessary for recognizing and studying a consistent nonperturbative quantum field theory of the $O(1,2)/O(2)\times Z_2$ model. We describe the action, the geometry of the configuration space, the conserved Noether currents, and the current algebra, and we construct a version of the Ward-Slavnov identity that makes it easy to switch from a given field to a nonlinearly related one. Renormalization of the model is defined via the effective action and via current algebra. The two definitions are shown to be equivalent. In a companion paper we develop a lattice formulation of the theory that is particularly well suited to the sigma model, and we report the results of Monte Carlo simulations of this lattice model. These simulations indicate that as the lattice cutoff is removed the theory becomes that of a pair of massless free fields. Because the geometry and symmetries of these fields differ from those of the original model we conclude that a continuum limit of the $O(1,2)/O(2)\times Z_2$ model which preserves these properties does not exist.Comment: 25 pages, no figure

Acid stress damage of DNA is prevented by Dps binding in Escherichia coli O157:H7

<p>Abstract</p> <p>Background</p> <p>Acid tolerance in <it>Escherichia coli </it>O157:H7 contributes to persistence in its bovine host and is thought to promote passage through the gastric barrier of humans. Dps (DNA-binding protein in starved cells) mutants of <it>E. coli </it>have reduced acid tolerance when compared to the parent strain although the role of Dps in acid tolerance is unclear. This study investigated the mechanism by which Dps contributes to acid tolerance in <it>E. coli </it>O157:H7.</p> <p>Results</p> <p>The results from this study showed that acid stress lead to damage of chromosomal DNA, which was accentuated in <it>dps </it>and <it>recA </it>mutants. The use of <it>Bal</it>31, which cleaves DNA at nicks and single-stranded regions, to analyze chromosomal DNA extracted from cells challenged at pH 2.0 provided <it>in vivo </it>evidence of acid damage to DNA. The DNA damage in a <it>recA </it>mutant further corroborated the hypothesis that acid stress leads to DNA strand breaks. Under <it>in vitro </it>assay conditions, Dps was shown to bind plasmid DNA directly and protect it from acid-induced strand breaks. Furthermore, the extraction of DNA from Dps-DNA complexes required a denaturing agent at low pH (2.2 and 3.6) but not at higher pH (>pH4.6). Low pH also restored the DNA-binding activity of heat-denatured Dps. Circular dichroism spectra revealed that at pH 3.6 and pH 2.2 Dps maintains or forms α-helices that are important for Dps-DNA complex formation.</p> <p>Conclusion</p> <p>Results from the present work showed that acid stress results in DNA damage that is more pronounced in <it>dps </it>and <it>recA </it>mutants. The contribution of RecA to acid tolerance indicated that DNA repair was important even when Dps was present. Dps protected DNA from acid damage by binding to DNA. Low pH appeared to strengthen the Dps-DNA association and the secondary structure of Dps retained or formed α-helices at low pH. Further investigation into the precise interplay between DNA protection and damage repair pathways during acid stress are underway to gain additional insight.</p

Benzyl N0-[1-(3-pyridyl)ethylidene]-hydrazinecarbodithioate

The title compound, C15H5N2S2, crystallizes as a trans–cis conformer. The thione sulfur is in a trans position with the methyl pyridyl fragment with respect to the C—N bond but adopts a cis position with the benzyl ring across the C—S bond. The dihedral angle between the planar quinoline ring and the dithiocarbazate unit is 103.70 (1). The inclination of the dithiocarbazate unit with the benzyl group is 17.20 (1).There are strong – stacking interactions between pairs of dithiocarbazate units and also pairs of pyridine rings [3.27 (5)and 3.28 (5) A ° , respectively]. A long-distance intermolecular N—H N hydrogen bond [3.171 (2) A ° ] also stabilizes the structure

2,5-Bis(2-naphthylmethylsulfanyl)-1-thia-3,4 diazacyclopenta-2,5-diene

The title molecule, C24H18N2S3, consists of three essentially planar fragments viz. two methylnaphthalene groups and a five-membered thiadiazole ring. The dihedral angles between the two methylnaphthalene groups and the central 1-thia-3,4-diazacyclopenta-2,5-diene group are 78.9 (1) and 68.8 (1)°. In the crystal structure, - stacking interactions exist between pairs of symmetry-related naphthalene fragments with an interplanar separation of 3.35 Å. All bond lengths and angles are comparable with previous reports except that both C-S bond lengths are slightly longer than normal. In addition, the C-S-C and S-C-C bond angles appear to be smaller than normal and this could be due to the steric hindrance of the methylnaphthalene fragments

2-Quinolylmethyl N0-[1-(m-tolyl) ethylidene] hydrazinecarbodithioate

The title compound, C20H19N3S2, crystallized as a cis–trans conformer in which the quinoline ring system is cis across the C—S bond but adopts a trans geometry with respect to the C—N bond. The compound exists in the thione form with the presence of a C S bond

A simple example of "Quantum Darwinism": Redundant information storage in many-spin environments

As quantum information science approaches the goal of constructing quantum computers, understanding loss of information through decoherence becomes increasingly important. The information about a system that can be obtained from its environment can facilitate quantum control and error correction. Moreover, observers gain most of their information indirectly, by monitoring (primarily photon) environments of the "objects of interest." Exactly how this information is inscribed in the environment is essential for the emergence of "the classical" from the quantum substrate. In this paper, we examine how many-qubit (or many-spin) environments can store information about a single system. The information lost to the environment can be stored redundantly, or it can be encoded in entangled modes of the environment. We go on to show that randomly chosen states of the environment almost always encode the information so that an observer must capture a majority of the environment to deduce the system's state. Conversely, in the states produced by a typical decoherence process, information about a particular observable of the system is stored redundantly. This selective proliferation of "the fittest information" (known as Quantum Darwinism) plays a key role in choosing the preferred, effectively classical observables of macroscopic systems. The developing appreciation that the environment functions not just as a garbage dump, but as a communication channel, is extending our understanding of the environment's role in the quantum-classical transition beyond the traditional paradigm of decoherence.Comment: 21 pages, 6 figures, RevTex 4. Submitted to Foundations of Physics (Asher Peres Festschrift

Contribution of the μ-opioid receptor system to affective disorders in temporal lobe epilepsy: A bidirectional relationship?

OBJECTIVE Affective disorders are frequent comorbidities of temporal lobe epilepsy (TLE). The endogenous opioid system has been implicated in both epilepsy and affective disorders, and may play a significant role in their bidirectional relationship. In this cross-sectional study, we investigated the association between μ-opioid receptor binding and affective disorders in patients with TLE. METHODS Nine patients with TLE and depression/anxiety underwent $^{11}$ C-carfentanil positron emission tomography (CFN PET) and neuropsychiatric assessment, including the Hospital Anxiety and Depression Scale and the Positive and Negative Affect Schedule. The normalized CFN PET scans were compared with those of 26 age-matched healthy controls. Correlation analyses with affective symptoms were performed by region of interest-based analysis focusing on the limbic circuit and orbitofrontal cortex. RESULTS We observed widely reduced CFN binding potential (BP) in bilateral frontal lobes and striata in patients with TLE compared to healthy controls. In the TLE group, more severe anxiety and negative affect were associated with decreased CFN BP in the posterior cingulate gyrus. SIGNIFICANCE In patients with TLE, interictally reduced binding in the opioid system was associated with higher levels of anxiety and negative affect. We speculate that seizure-related agonist-driven desensitization and downregulation of opioid receptors could be a potential underlying pathomechanism

Serotonin transporter in the temporal lobe, hippocampus and amygdala in SUDEP

Several lines of evidence link deficient serotonin function and SUDEP. Chronic treatment with serotonin reuptake inhibitors (SRIs) reduces ictal central apnoea, a risk factor for SUDEP. Reduced medullary serotonergic neurones, modulators of respiration in response to hypercapnia, were reported in a SUDEP post-mortem series. The amygdala and hippocampus have high serotonergic innervation and are functionally implicated in seizure-related respiratory dysregulation. We explored serotonergic networks in mesial temporal lobe structures in a surgical and post-mortem epilepsy series in relation to SUDEP risk. We stratified 75 temporal lobe epilepsy patients with hippocampal sclerosis (TLE/HS) into high (16), medium (11) and low risk (48) groups for SUDEP based on generalised seizure frequency. We also included the amygdala in 35 post-mortem cases, including SUDEP (17), epilepsy controls (10) and non-epilepsy controls (8). The immunohistochemistry labelling index (LI) and axonal length (AL) of serotonin transporter (SERT)-positive axons were quantified in 13 regions of interest with image analysis. SERT LI was highest in amygdala and subiculum regions. In the surgical series, higher SERT LI was observed in high risk than low risk cases in the dentate gyrus, CA1 and subiculum (p<0.05). In the post-mortem cases higher SERT LI and AL was observed in the basal and accessory basal nuclei of the amygdala and peri-amygdala cortex in SUDEP compared to epilepsy controls (p<0.05). Patients on SRI showed higher SERT in the dentate gyrus (p<0.005) and CA4 (p<0.05) but there was no difference in patients with or without a psychiatric history. Higher SERT in hippocampal subfields in TLE/HS cases with SUDEP risk factors and higher amygdala SERT in post-mortem SUDEP cases than epilepsy controls supports a role for altered serotonergic networks involving limbic regions in SUDEP. This may be of functional relevance through reduced 5-HT availability