Curvature formula for the space of 2-d conformal field theories

We derive a formula for the curvature tensor of the natural Riemannian metric on the space of two-dimensional conformal field theories and also a formula for the curvature tensor of the space of boundary conformal field theories.Comment: 36 pages, 1 figure; v2 references adde

Population genetics of trypanosoma brucei rhodesiense: clonality and diversity within and between foci

African trypanosomes are unusual among pathogenic protozoa in that they can undergo their complete morphological life cycle in the tsetse fly vector with mating as a non-obligatory part of this development. Trypanosoma brucei rhodesiense, which infects humans and livestock in East and Southern Africa, has classically been described as a host-range variant of the non-human infective Trypanosoma brucei that occurs as stable clonal lineages. We have examined T. b. rhodesiense populations from East (Uganda) and Southern (Malawi) Africa using a panel of microsatellite markers, incorporating both spatial and temporal analyses. Our data demonstrate that Ugandan T. b. rhodesiense existed as clonal populations, with a small number of highly related genotypes and substantial linkage disequilibrium between pairs of loci. However, these populations were not stable as the dominant genotypes changed and the genetic diversity also reduced over time. Thus these populations do not conform to one of the criteria for strict clonality, namely stability of predominant genotypes over time, and our results show that, in a period in the mid 1990s, the previously predominant genotypes were not detected but were replaced by a novel clonal population with limited genetic relationship to the original population present between 1970 and 1990. In contrast, the Malawi T. b. rhodesiense population demonstrated significantly greater diversity and evidence for frequent genetic exchange. Therefore, the population genetics of T. b. rhodesiense is more complex than previously described. This has important implications for the spread of the single copy T. b. rhodesiense gene that allows human infectivity, and therefore the epidemiology of the human disease, as well as suggesting that these parasites represent an important organism to study the influence of optional recombination upon population genetic dynamics

Members of the chloride intracellular ion channel protein family demonstrate glutaredoxin-like enzymatic activity

© 2015 Al Khamici et al. The Chloride Intracellular Ion Channel (CLIC) family consists of six evolutionarily conserved proteins in humans. Members of this family are unusual, existing as both monomeric soluble proteins and as integral membrane proteins where they function as chloride selective ion channels, however no function has previously been assigned to their soluble form. Structural studies have shown that in the soluble form, CLIC proteins adopt a glutathione S-transferase (GST) fold, however, they have an active site with a conserved glutaredoxin monothiol motif, similar to the omega class GSTs. We demonstrate that CLIC proteins have glutaredoxin-like glutathione-dependent oxidoreductase enzymatic activity. CLICs 1, 2 and 4 demonstrate typical glutaredoxin-like activity using 2-hydroxyethyl disulfide as a substrate. Mutagenesis experiments identify cysteine 24 as the catalytic cysteine residue in CLIC1, which is consistent with its structure. CLIC1 was shown to reduce sodium selenite and dehydroascorbate in a glutathione-dependent manner. Previous electrophysiological studies have shown that the drugs IAA-94 and A9C specifically block CLIC channel activity. These same compounds inhibit CLIC1 oxidoreductase activity. This work for the first time assigns a functional activity to the soluble form of the CLIC proteins. Our results demonstrate that the soluble form of the CLIC proteins has an enzymatic activity that is distinct from the channel activity of their integral membrane form. This CLIC enzymatic activity may be important for protecting the intracellular environment against oxidation. It is also likely that this enzymatic activity regulates the CLIC ion channel function

Massive type IIA string theory cannot be strongly coupled

Understanding the strong coupling limit of massive type IIA string theory is a longstanding problem. We argue that perhaps this problem does not exist; namely, there may be no strongly coupled solutions of the massive theory. We show explicitly that massive type IIA string theory can never be strongly coupled in a weakly curved region of space-time. We illustrate our general claim with two classes of massive solutions in AdS4xCP3: one, previously known, with N = 1 supersymmetry, and a new one with N = 2 supersymmetry. Both solutions are dual to d = 3 Chern-Simons-matter theories. In both these massive examples, as the rank N of the gauge group is increased, the dilaton initially increases in the same way as in the corresponding massless case; before it can reach the M-theory regime, however, it enters a second regime, in which the dilaton decreases even as N increases. In the N = 2 case, we find supersymmetry-preserving gauge-invariant monopole operators whose mass is independent of N. This predicts the existence of branes which stay light even when the dilaton decreases. We show that, on the gravity side, these states originate from D2-D0 bound states wrapping the vanishing two-cycle of a conifold singularity that develops at large N.Comment: 43 pages, 5 figures. v2: added reference

Keratinocyte growth factor for the treatment of the acute respiratory distress syndrome (KARE): a randomised, double-blind, placebo-controlled phase 2 trial

<p>(<b>A</b>) Immunofluorescence signal for dystrophin is significantly reduced in the SSI heart (bottom left panel) compared with the immunofluorescent signal in the SHAM heart (upper left panel), and the SHAM+ALLN (upper right panel) and SSI+ALLN (bottom right panel) myocardium. (<b>B</b>) Protein levels of dystrophin in the SHAM, SSI, SHAM+ALLN and SSI+ALLN hearts were measured 24 h after the CLP procedure and were expressed in arbitrary units (AUs). α-Tubulin was used to determine equivalent loading conditions. The results (n = 6 per group) are representative of three different experiments. Scale bars indicate 50 μm.</p

Daily life stress and the cortisol awakening response : testing the anticipation hypothesis

Acknowledgments We thank Paul Stewart for his contribution to data collection and Dr Matthew Jones for programming the handheld computers. Author Contributions Conceived and designed the experiments: WS DJP. Performed the experiments: DJP. Analyzed the data: WS. Wrote the paper: WS DJP.Peer reviewedPublisher PD

6D supergravity without tensor multiplets

We systematically investigate the finite set of possible gauge groups and matter content for N = 1 supergravity theories in six dimensions with no tensor multiplets, focusing on nonabelian gauge groups which are a product of SU(N) factors. We identify a number of models which obey all known low-energy consistency conditions, but which have no known string theory realization. Many of these models contain novel matter representations, suggesting possible new string theory constructions. Many of the most exotic matter structures arise in models which precisely saturate the gravitational anomaly bound on the number of hypermultiplets. Such models have a rigid symmetry structure, in the sense that there are no moduli which leave the full gauge group unbroken.Comment: 31 pages, latex; v2, v3: minor corrections, references adde

Space-like (vs. time-like) collinear limits in QCD: is factorization violated?

We consider the singular behaviour of QCD scattering amplitudes in kinematical configurations where two or more momenta of the external partons become collinear. At the tree level, this behaviour is known to be controlled by factorization formulae in which the singular collinear factor is universal (process independent). We show that this strict (process-independent) factorization is not valid at one-loop and higher-loop orders in the case of the collinear limit in space-like regions (e.g., collinear radiation from initial-state partons). We introduce a generalized version of all-order collinear factorization, in which the space-like singular factors retain some dependence on the momentum and colour charge of the non-collinear partons. We present explicit results on one-loop and two-loop amplitudes for both the two-parton and multiparton collinear limits. At the level of square amplitudes and, more generally, cross sections in hadron--hadron collisions, the violation of strict collinear factorization has implications on the non-abelian structure of logarithmically-enhanced terms in perturbative calculations (starting from the next-to-next-to-leading order) and on various factorization issues of mass singularities (starting from the next-to-next-to-next-to-leading order).Comment: 81 pages, 5 figures, typos corrected in the text, few comments added and inclusion of NOTE ADDED on recent development

Accelerated in vivo proliferation of memory phenotype CD4+ T-cells in human HIV-1 infection irrespective of viral chemokine co-receptor tropism.

CD4(+) T-cell loss is the hallmark of HIV-1 infection. CD4 counts fall more rapidly in advanced disease when CCR5-tropic viral strains tend to be replaced by X4-tropic viruses. We hypothesized: (i) that the early dominance of CCR5-tropic viruses results from faster turnover rates of CCR5(+) cells, and (ii) that X4-tropic strains exert greater pathogenicity by preferentially increasing turnover rates within the CXCR4(+) compartment. To test these hypotheses we measured in vivo turnover rates of CD4(+) T-cell subpopulations sorted by chemokine receptor expression, using in vivo deuterium-glucose labeling. Deuterium enrichment was modeled to derive in vivo proliferation (p) and disappearance (d*) rates which were related to viral tropism data. 13 healthy controls and 13 treatment-naive HIV-1-infected subjects (CD4 143-569 cells/ul) participated. CCR5-expression defined a CD4(+) subpopulation of predominantly CD45R0(+) memory cells with accelerated in vivo proliferation (p = 2.50 vs 1.60%/d, CCR5(+) vs CCR5(-); healthy controls; P<0.01). Conversely, CXCR4 expression defined CD4(+) T-cells (predominantly CD45RA(+) naive cells) with low turnover rates. The dominant effect of HIV infection was accelerated turnover of CCR5(+)CD45R0(+)CD4(+) memory T-cells (p = 5.16 vs 2.50%/d, HIV vs controls; P<0.05), naïve cells being relatively unaffected. Similar patterns were observed whether the dominant circulating HIV-1 strain was R5-tropic (n = 9) or X4-tropic (n = 4). Although numbers were small, X4-tropic viruses did not appear to specifically drive turnover of CXCR4-expressing cells (p = 0.54 vs 0.72 vs 0.44%/d in control, R5-tropic, and X4-tropic groups respectively). Our data are most consistent with models in which CD4(+) T-cell loss is primarily driven by non-specific immune activation