More on N=1 Matrix Model Curve for Arbitrary N

Using both the matrix model prescription and the strong-coupling approach, we describe the intersections of n=0 and n=1 non-degenerated branches for quartic (polynomial of adjoint matter) tree-level superpotential in N=1 supersymmetric SO(N)/USp(2N) gauge theories with massless flavors. We also apply the method to the degenerated branch. The general matrix model curve on the two cases we obtain is valid for arbitrary N and extends the previous work from strong-coupling approach. For SO(N) gauge theory with equal massive flavors, we also obtain the matrix model curve on the degenerated branch for arbitrary N. Finally we discuss on the intersections of n=0 and n=1 non-degenerated branches for equal massive flavors.Comment: 36pp; to appear in JHE

Phases and geometry of the N=1 A_2 quiver gauge theory and matrix models

We study the phases and geometry of the N=1 A_2 quiver gauge theory using matrix models and a generalized Konishi anomaly. We consider the theory both in the Coulomb and Higgs phases. Solving the anomaly equations, we find that a meromorphic one-form sigma(z)dz is naturally defined on the curve Sigma associated to the theory. Using the Dijkgraaf-Vafa conjecture, we evaluate the effective low-energy superpotential and demonstrate that its equations of motion can be translated into a geometric property of Sigma: sigma(z)dz has integer periods around all compact cycles. This ensures that there exists on Sigma a meromorphic function whose logarithm sigma(z)dz is the differential. We argue that the surface determined by this function is the N=2 Seiberg-Witten curve of the theory.Comment: 41 pages, 2 figures, JHEP style. v2: references adde

Effective superpotential for U(N) with antisymmetric matter

We consider an N=1 U(N) gauge theory with matter in the antisymmetric representation and its conjugate, with a tree level superpotential containing at least quartic interactions for these fields. We obtain the effective glueball superpotential in the classically unbroken case, and show that it has a non-trivial N-dependence which does not factorize. We also recover additional contributions starting at order S^N from the dynamics of Sp(0) factors. This can also be understood by a precise map of this theory to an Sp(2N-2) gauge theory with antisymmetric matter.Comment: 22 pages. v2: comment (and a reference) added at the end of section 2 on low rank cases; minor typos corrected. v3: 2 footnotes added with additional clarifications; version to appear in journa

Phases of N=1 Supersymmetric SO/Sp Gauge Theories via Matrix Model

We extend the results of Cachazo, Seiberg and Witten to N=1 supersymmetric gauge theories with gauge groups SO(2N), SO(2N+1) and Sp(2N). By taking the superpotential which is an arbitrary polynomial of adjoint matter \Phi as a small perturbation of N=2 gauge theories, we examine the singular points preserving N=1 supersymmetry in the moduli space where mutually local monopoles become massless. We derive the matrix model complex curve for the whole range of the degree of perturbed superpotential. Then we determine a generalized Konishi anomaly equation implying the orientifold contribution. We turn to the multiplication map and the confinement index K and describe both Coulomb branch and confining branch. In particular, we construct a multiplication map from SO(2N+1) to SO(2KN-K+2) where K is an even integer as well as a multiplication map from SO(2N) to SO(2KN-2K+2) (K is a positive integer), a map from SO(2N+1) to SO(2KN-K+2) (K is an odd integer) and a map from Sp(2N) to Sp(2KN+2K-2). Finally we analyze some examples which show some duality: the same moduli space has two different semiclassical limits corresponding to distinct gauge groups.Comment: 55pp; two paragraphs in page 19 added to clarify the relation between confinement index and multiplication map index, refs added and to appear in JHEP; Konishi anomaly equations corrected and some comments on the degenerated cases for SO(7) and SO(8) adde

Constructing Gauge Theory Geometries from Matrix Models

We use the matrix model -- gauge theory correspondence of Dijkgraaf and Vafa in order to construct the geometry encoding the exact gaugino condensate superpotential for the N=1 U(N) gauge theory with adjoint and symmetric or anti-symmetric matter, broken by a tree level superpotential to a product subgroup involving U(N_i) and SO(N_i) or Sp(N_i/2) factors. The relevant geometry is encoded by a non-hyperelliptic Riemann surface, which we extract from the exact loop equations. We also show that O(1/N) corrections can be extracted from a logarithmic deformation of this surface. The loop equations contain explicitly subleading terms of order 1/N, which encode information of string theory on an orientifolded local quiver geometry.Comment: 52 page

Improved matrix-model calculation of the N=2 prepotential

We present a matrix-model expression for the sum of instanton contributions to the prepotential of an N=2 supersymmetric U(N) gauge theory, with matter in various representations. This expression is derived by combining the renormalization-group approach to the gauge theory prepotential with matrix-model methods. This result can be evaluated order-by-order in matrix-model perturbation theory to obtain the instanton corrections to the prepotential. We also show, using this expression, that the one-instanton prepotential assumes a universal form.Comment: 20 pages, LaTeX, 2 figure

Orbiting Membranes in M-theory on AdS_7 x S^4 Background

We study classical solutions describing rotating and boosted membranes on AdS_7 x S^4 background in M-theory. We find the dependence of the energy on the spin and R-charge of these solutions. In the flat space limit we get E ~ S^{2/3}, while for AdS at leading order E-S grows as S^{1/3}. The membranes on AdS_4 x S^7 background have briefly been studied as well.Comment: 13 pages, latex, v2: a note and refs. added, some typos correcte

Gain-of-function Nav1.8 mutations in painful neuropathy

Painful peripheral neuropathy often occurs without apparent underlying cause. Gain-of-function variants of sodium channel Nav1.7 have recently been found in ~30% of cases of idiopathic painful small-fiber neuropathy. Here, we describe mutations in Nav1.8, another sodium channel that is specifically expressed in dorsal root ganglion (DRG) neurons and peripheral nerve axons, in patients with painful neuropathy. Seven Nav1.8 mutations were identified in 9 subjects within a series of 104 patients with painful predominantly small-fiber neuropathy. Three mutations met criteria for potential pathogenicity based on predictive algorithms and were assessed by voltage and current clamp. Functional profiling showed that two of these three Na v1.8 mutations enhance the channel's response to depolarization and produce hyperexcitability in DRG neurons. These observations suggest that mutations of Nav1.8 contribute to painful peripheral neuropathy

Polaronic Signatures in Mid-Infrared Spectra: Prediction for LaMnO3 and CaMnO3

Hole-doped LaMnO3 and electron-doped CaMnO3 form self-trapped electronic states. The spectra of these states have been calculated using a two orbital (Mn eg Jahn-Teller) model, from which the non-adiabatic optical conductivity spectra are obtained. In both cases the optical spectrum contains weight in the gap region, whose observation will indicate the self-trapped nature of the carrier states. The predicted spectra are proportional to the concentration of the doped carriers in the dilute regime, with coefficients calculated with no further model parameters.Comment: 6 pages with 3 figures imbedde

Clinical and genomic assessment of PD-L1 SP142 expression in triple-negative breast cancer

Purpose: The SP142 PD-L1 assay is a companion diagnostic for atezolizumab in metastatic triple-negative breast cancer (TNBC). We strove to understand the biological, genomic, and clinical characteristics associated with SP142 PD-L1 positivity in TNBC patients. Methods: Using 149 TNBC formalin-fixed paraffin-embedded tumor samples, tissue microarray (TMA) and gene expression microarrays were performed in parallel. The VENTANA SP142 assay was used to identify PD-L1 expression from TMA slides. We next generated a gene signature reflective of SP142 status and evaluated signature distribution according to TNBCtype and PAM50 subtypes. A SP142 gene expression signature was identified and was biologically and clinically evaluated on the TNBCs of TCGA, other cohorts, and on other malignancies treated with immune checkpoint inhibitors (ICI). Results: Using SP142, 28.9% of samples were PD-L1 protein positive. The SP142 PD-L1-positive TNBC had higher CD8+ T cell percentage, stromal tumor-infiltrating lymphocyte levels, and higher rate of the immunomodulatory TNBCtype compared to PD-L1-negative samples. The recurrence-free survival was prolonged in PD-L1-positive TNBC. The SP142-guided gene expression signature consisted of 94 immune-related genes. The SP142 signature was associated with a higher pathologic complete response rate and better survival in multiple TNBC cohorts. In the TNBC of TCGA, this signature was correlated with lymphocyte-infiltrating signature scores, but not with tumor mutational burden or total neoantigen count. In other malignancies treated with ICIs, the SP142 genomic signature was associated with improved response and survival. Conclusions: We provide multi-faceted evidence that SP142 PDL1-positive TNBC have immuno-genomic features characterized as highly lymphocyte-infiltrated and a relatively favorable survival