Matrix Models and D-branes in Twistor String Theory

We construct two matrix models from twistor string theory: one by dimensional reduction onto a rational curve and another one by introducing noncommutative coordinates on the fibres of the supertwistor space P^(3|4)->CP^1. We comment on the interpretation of our matrix models in terms of topological D-branes and relate them to a recently proposed string field theory. By extending one of the models, we can carry over all the ingredients of the super ADHM construction to a D-brane configuration in the supertwistor space P^(3|4). Eventually, we present the analogue picture for the (super) Nahm construction.Comment: 1+37 pages, reference added, JHEP style, published versio

Drinfeld-Twisted Supersymmetry and Non-Anticommutative Superspace

We extend the analysis of hep-th/0408069 on a Lorentz invariant interpretation of noncommutative spacetime to field theories on non-anticommutative superspace with half the supersymmetries broken. By defining a Drinfeld-twisted Hopf superalgebra, it is shown that one can restore twisted supersymmetry and therefore obtain a twisted version of the chiral rings along with certain Ward-Takahashi identities. Moreover, we argue that the representation content of theories on the deformed superspace is identical to that of their undeformed cousins and comment on the consequences of our analysis concerning non-renormalization theorems.Comment: 1+17 pages; typos fixed, minor correction

N=1/2 Super Yang-Mills Theory on Euclidean AdS2xS2

We study D-branes in the background of Euclidean AdS2xS2 with a graviphoton field turned on. As the background is not Ricci flat, the graviphoton field must have both self-dual and antiself-dual parts. This, in general, will break all the supersymmetries on the brane. However, we show that there exists a limit for which one can restore half of the supersymmetries. Further, we show that in this limit, the N=1/2 SYM Lagrangian on flat space can be lifted on to the Euclidean AdS2xS2 preserving the same amount of supersymmetries as in the flat case. We observe that without the C-dependent terms present in the action this lift is not possible.Comment: 12 pages, latex file; v2: minor corrections, references adde

Instantons in N=1/2 Super Yang-Mills Theory via Deformed Super ADHM Construction

We study an extension of the ADHM construction to give deformed anti-self-dual (ASD) instantons in N=1/2 super Yang-Mills theory with U(n) gauge group. First we extend the exterior algebra on superspace to non(anti)commutative superspace and show that the N=1/2 super Yang-Mills theory can be reformulated in a geometrical way. By using this exterior algebra, we formulate a non(anti)commutative version of the super ADHM construction and show that the curvature two-form superfields obtained by our construction do satisfy the deformed ASD equations and thus we establish the deformed super ADHM construction. We also show that the known deformed U(2) one instanton solution is obtained by this construction.Comment: 32 pages, LaTeX, v2: typos corrected, references adde

On Non-linear Action for Gauged M2-brane

We propose a non-linear extension of U(1) \times U(1) (abelian) ABJM model including T_{M2} (higher derivative) corrections. The action proposed here is expected to describe a single M2-brane proving C^4/Z_k target space. The model includes couplings with the 3-form background in the eleven-dimensional supergravity which is consistent with the orbifold projection. We show that the novel higgs mechanism proposed by Mukhi and Papageorgakis does work even in the presence of higher derivative corrections and couplings with the background field, giving the correct structure of the Dirac-Born-Infeld action with Wess-Zumino term for a D2-brane. We also find half BPS solutions in the full non-linear theory which is interpreted as an another M2-brane intersecting with the original M2-brane. A possible generalization to U(N) \times U(N) gauge group is briefly discussed.Comment: 19 pages, no figure, references added, typos correcte

Vertex Operators for Closed Superstrings

We construct an iterative procedure to compute the vertex operators of the closed superstring in the covariant formalism given a solution of IIA/IIB supergravity. The manifest supersymmetry allows us to construct vertex operators for any generic background in presence of Ramond-Ramond (RR) fields. We extend the procedure to all massive states of open and closed superstrings and we identify two new nilpotent charges which are used to impose the gauge fixing on the physical states. We solve iteratively the equations of the vertex for linear x-dependent RR field strengths. This vertex plays a role in studying non-constant C-deformations of superspace. Finally, we construct an action for the free massless sector of closed strings, and we propose a form for the kinetic term for closed string field theory in the pure spinor formalism.Comment: TeX, harvmac, amssym.tex, 41 pp; references adde

D=2, N=2 Supersymmetric sigma models on Non(anti)commutative Superspace

We extend the results of hep-th/0310137 to show that a general classical action for D=2, N=2 sigma models on a non(anti)commutative superspace is not standard and contains infinite number of terms, which depend on the determinant of the non(anti)commutativity parameter, C^{\alpha\beta}. We show that using Kahler normal coordinates the action can be written in a manifestly covariant manner. We introduce vector multiplets and obtain the N=1/2 supersymmetry transformations of the theory in the Wess-Zumino gauge. By explicitly deriving the expressions for vector and twisted superfields on non(anti)commutative superspace, we study the classical aspects of Gauged linear sigma models.Comment: 38 pages, Latex; v3: Minor changes in the text, correction in eqns. (2.22) and (4.8), added references, version to appear in Phys. Rev.

The Role of Toll-Like Receptor 2 in Inflammation and Fibrosis during Progressive Renal Injury

Tissue fibrosis and chronic inflammation are common causes of progressive organ damage, including progressive renal disease, leading to loss of physiological functions. Recently, it was shown that Toll-like receptor 2 (TLR2) is expressed in the kidney and activated by endogenous danger signals. The expression and function of TLR2 during renal fibrosis and chronic inflammation has however not yet been elucidated. Therefore, we studied TLR2 expression in human and murine progressive renal diseases and explored its role by inducing obstructive nephropathy in TLR2−/− or TLR2+/+ mice. We found that TLR2 is markedly upregulated on tubular and tubulointerstitial cells in patients with chronic renal injury. In mice with obstructive nephropathy, renal injury was associated with a marked upregulation and change in distribution of TLR2 and upregulation of murine TLR2 danger ligands Gp96, biglycan, and HMGB1. Notably, TLR2 enhanced inflammation as reflected by a significantly reduced influx of neutrophils and production of chemokines and TGF-β in kidneys of TLR2−/− mice compared with TLR2+/+ animals. Although, the obstructed kidneys of TLR2−/− mice had less interstitial myofibroblasts in the later phase of obstructive nephropathy, tubular injury and renal matrix accumulation was similar in both mouse strains. Together, these data demonstrate that TLR2 can initiate renal inflammation during progressive renal injury and that the absence of TLR2 does not affect the development of chronic renal injury and fibrosis

Genetic architecture of subcortical brain structures in 38,851 individuals

Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease