Holographic QCD and Pion Mass

To realize massive pions, we study variations of the holographic model of massless QCD using the D4/D8/anti-D8 brane configuration proposed by Sakai and Sugimoto. We propose deformations which break the chiral symmetry explicitly and compute the mass of the pions and vector mesons. The observed value of the pion mass can be obtained. We also argue a chiral perturbation corresponding to our deformation.Comment: 23pages, minor changes, references adde

Holographic technicolor models and their S-parameter

We study the Peskin-Takeuchi S-parameter of holographic technicolor models. We present the recipe for computing the parameter in a generalized holographic setup. We then apply it to several holographic models that include: (a) the Sakai-Sugimoto model and (b) its non-compactified cousin, (c) a non-critical analog of (a) based on near extremal AdS_6 background, (d) the KMMW model which is similar to model (a) but with D6 and anti-D6 flavor branes replacing the D8 and anti-D8 branes, (e) a model based on D5 branes compactified on two S^1s with D7 and anti-7 probe branes and (f) the conifold model with the same probe branes as in (e). The models are gravity duals of gauge theories with U(N_{TC}) gauge theory and with a breakdown of a flavor symmetry U(N_{TF})xU(N_{TF}) to U_V(N_{TF}). The models (a), (c),(d) and (e) are duals of a confining gauge theories whereas (b) and (f) associate with non confining models. The S-parameter was found to be S=sN_{TC} where s is given by 0.017\lambda_{TC}, 0.016\lambda_{TC}, 0.095, 0.50 and 0.043 for the (a),(b),(c),(d), (f) models respectively and for model (e) s is divergent. These results are valid in the large N_{TC} and large \lambda_{TC} limit. We further derive the dependence of the S-parameter on the "string endpoint" mass of the techniquarks for the various models. We compute the masses of the low lying vector technimesons.Comment: 37 pages, 2 figures V2: 2 coerrections in sectionss 4 and 5, reference adde

Localized Backreacted Flavor Branes in Holographic QCD

We investigate the perturbative (in $g_s N_{D8}$) backreaction of localized D8 branes in D4-D8 systems including in particular the Sakai Sugimoto model. We write down the explicit expressions of the backreacted metric, dilaton and RR form. We find that the backreaction remains small up to a radial value of $u \ll \ell_s/(g_s N_{D8})$, and that the background functions are smooth except at the D8 sources. In this perturbative window, the original embedding remains a solution to the equations of motion. Furthermore, the fluctuations around the original embedding, describing scalar mesons, do not become tachyonic due to the backreaction in the perturbative regime. This is is due to a cancelation between the DBI and CS parts of the D8 brane action in the perturbed background.Comment: 1+48 pages (7 figures) + 15 pages, citations added & minor correction

Revisiting the physiological roles of SGLTs and GLUTs using positron emission tomography in mice.

Glucose transporters are central players in glucose homeostasis. There are two major classes of glucose transporters in the body, the passive facilitative glucose transporters (GLUTs) and the secondary active sodium-coupled glucose transporters (SGLTs). In the present study, we report the use of a non-invasive imaging technique, positron emission tomography, in mice aiming to evaluate the role of GLUTs and SGLTs in controlling glucose distribution and utilization. We show that GLUTs are most significant for glucose uptake into the brain and liver, whereas SGLTs are important in glucose recovery in the kidney. This work provides further support for the use of SGLT imaging in the investigation of the role of SGLT transporters in human physiology and diseases such as diabetes and cancer. The importance of sodium-coupled glucose transporters (SGLTs) and facilitative glucose transporters (GLUTs) in glucose homeostasis was studied in mice using fluorine-18 labelled glucose molecular imaging probes and non-invasive positron emission tomography (PET) imaging. The probes were: α-methyl-4-[F-18]-fluoro-4-deoxy-d-glucopyranoside (Me-4FDG), a substrate for SGLTs; 4-deoxy-4-[F-18]-fluoro-d-glucose (4-FDG), a substrate for SGLTs and GLUTs; and 2-deoxy-2-[F-18]-fluoro-d-glucose (2-FDG), a substrate for GLUTs. These radiolabelled imaging probes were injected i.v. into wild-type, Sglt1(-/-) , Sglt2(-/-) and Glut2(-/-) mice and their dynamic whole-body distribution was determined using microPET. The distribution of 2-FDG was similar to that reported earlier (i.e. it accumulated in the brain, heart, liver and kidney, and was excreted into the urinary bladder). There was little change in the distribution of 2-FDG in Glut2(-/-) mice, apart from a reduction in the rate of uptake into liver. The major differences between Me-4FDG and 2-FDG were that Me-4FDG did not enter the brain and was not excreted into the urinary bladder. There was urinary excretion of Me-4FDG in Sglt1(-/-) and Sglt2(-/-) mice. However, Me-4FDG was not reabsorbed in the kidney in Glut2(-/-) mice. There were no differences in Me-4FDG uptake into the heart of wild-type, Sglt1(-/-) and Sglt2(-/-) mice. We conclude that GLUT2 is important in glucose liver transport and reabsorption of glucose in the kidney along with SGLT2 and SGLT1. Complete reabsorption of Me-4FDG from the glomerular filtrate in wild-type mice and the absence of reabsorption in the kidney in Glut2(-/-) mice confirm the importance of GLUT2 in glucose absorption across the proximal tubule