The low-energy limit of AdS(3)/CFT2 and its TBA

We investigate low-energy string excitations in AdS3 × S3 × T4. When the worldsheet is decompactified, the theory has gapless modes whose spectrum at low energies is determined by massless relativistic integrable S matrices of the type introduced by Al. B. Zamolodchikov. The S matrices are non-trivial only for excitations with identical worldsheet chirality, indicating that the low-energy theory is a CFT2. We construct a Thermodynamic Bethe Ansatz (TBA) for these excitations and show how the massless modes’ wrapping effects may be incorporated into the AdS3 spectral problem. Using the TBA and its associated Y-system, we determine the central charge of the low-energy CFT2 to be c = 6 from calculating the vacuum energy for antiperiodic fermions — with the vacuum energy being zero for periodic fermions in agreement with a supersymmetric theory — and find the energies of some excited states

Quark--anti-quark potential in N=4 SYM

We construct a closed system of equations describing the quark--anti-quark potential at any coupling in planar N=4 supersymmetric Yang-Mills theory. It is based on the Quantum Spectral Curve method supplemented with a novel type of asymptotics. We present a high precision numerical solution reproducing the classical and one-loop string predictions very accurately. We also analytically compute the first 7 nontrivial orders of the weak coupling expansion. Moreover, we study analytically the generalized quark--anti-quark potential in the limit of large imaginary twist to all orders in perturbation theory. We demonstrate how the QSC reduces in this case to a one-dimensional Schrodinger equation. In the process we establish a link between the Q-functions and the solution of the Bethe-Salpeter equation.Comment: 31 pages, 1 figure; v2: minor correcton

Clinical Utilities of Peripheral Blood Gene Expression Profiling in the Management of Cardiac Transplant Patients

Cardiac allografts induce host immune responses that lead to endomyocardial tissue injury and progressive graft dysfunction. Inflammatory cell infiltration and myocyte damage characterize acute cellular rejection (ACR) that presents episodically in either a subclinical or symptom-associated manner. Sampling of the endomyocardium by transvenous biopsy enables pathologic grading using light microscopic criteria to distinguish severity based on the focality or diffuseness of inflammation and associated myocyte injury. Monitoring for ACR utilizes endomyocardial biopsy in conjunction with history and physical examination and assessment of allograft function by echocardiography. However, procedural and interpretive issues limit the diagnostic certainty provided by endomyocardial biopsy. The dynamic profiling of genes expressed by peripheral blood mononuclear cells (PBMCs) enables quantitative assessments of intracellular mRNA whose levels fluctuate during systemic alloimmune responses. Gene expression profiling of PBMCs using a multi-gene ACR classifier enables the AlloMap® molecular expression test to distinguish moderate to severe ACR (p = 0.0018) in heart transplant patients. The AlloMap test provides molecular insights into a patient's risk for ACR by distilling the aggregate expression levels of its informative genes into a single score on a scale of 0 to 40. The selection of a score as a threshold value for clinical decision-making is based on its associated negative predictive value (NPV), which ranges from 98 to 99% for values in three post-transplant periods: >2 to ≤6 months, > 6to ≤ 12 months, and >12 months. Scores below the threshold value rule out ACR, while those above suggest increased ACR risk. Incorporating the AlloMap test into immunomonitoring protocols provides an opportunity for clinicians to enhance patient care and to define its role in immunodiagnostic strategies to optimize the clinical outcomes of heart transplant recipients. This summary highlights the concepts presented in an invited presentation at a conference focused on Immunodiagnostics and Immunomonitoring: From Research to Clinic, in San Diego, CA on November 7, 2006