MIT Open Access Articles
http://hdl.handle.net/1721.1/49433
2014-09-19T11:47:25ZOn the Spectrum of Lattice Massive SU(2) Yang–Mills
http://hdl.handle.net/1721.1/89821
On the Spectrum of Lattice Massive SU(2) Yang–Mills
Ferrari, Ruggero
On the basis of extended simulations, we provide some results concerning the spectrum of Massive SU(2) Yang–Mills on the lattice. We study the “time” correlator of local gauge invariant operators integrated over the remaining three dimensions. The energy gaps are measured in the isospin I = 0,1 and internal spin J = 0,1 channels. No correlation is found in the I = 1, J = 0 channel. In the I = 1, J = 1 channel and far from the critical mass value m[subscript c], the energy gap roughly follows the bare value m (vector mesons). In approaching the critical value m[subscript c] at β fixed, there is a bifurcation of the energy gap: one branch follows the value m, while the new is much larger and it shows a more and more dominant weight. This phenomenon might be the sign of two important features: the long range correlation near the fixed point at β →∞ implied by the low energy gap and the screening (or confining) mechanisms across the m = m[subscript c] associated to the larger gap. The I = 0, J = 0,1 gaps are of the same order of magnitude, typically larger than the I = 1, J = 1 gap (for m ≫ m[subscript c]). For m ∼ m[subscript c], both I = 0 gaps have a dramatic drop with minima near the value m. This behavior might correspond to the formation of I = 0 bound states both in the J = 0 and J = 1 channels.
2013-09-01T00:00:00ZThe SU(2) ⊗ U(1) Electroweak Model Based on the Nonlinearly Realized Gauge Group. II. Functional Equations and the Weak Power-Counting
http://hdl.handle.net/1721.1/89820
The SU(2) ⊗ U(1) Electroweak Model Based on the Nonlinearly Realized Gauge Group. II. Functional Equations and the Weak Power-Counting
Bettinelli, D.; Ferrari, Ruggero; Quadri, A.
In the present paper, that is the second part devoted to the construction of an electroweak model based on a nonlinear realization of the gauge group SU(2) ⊗ U(1), we study the tree-level vertex functional with all the sources necessary for the functional formulation of the relevant symmetries (Local Functional Equation, Slavnov–Taylor identity, Landau Gauge Equation) and for the symmetric removal of the divergences. The Weak Power Counting criterion is proven in the presence of the novel sources. The local invariant solutions of the functional equations are constructed in order to represent the counterterms for the one-loop subtractions. The bleaching technique is fully extended to the fermion sector. The neutral sector of the vector mesons is analyzed in detail in order to identify the physical fields for the photon and the Z boson. The identities necessary for the decoupling of the unphysical modes are fully analyzed. These latter results are crucially bound to the Landau gauge used throughout the paper.
2010-03-01T00:00:00Zebalance: A Stata Package for Entropy Balancing
http://hdl.handle.net/1721.1/89819
ebalance: A Stata Package for Entropy Balancing
Hainmueller, Jens; Su, Yiqing; Xu, Yiqing
The Stata package ebalance implements entropy balancing, a multivariate reweighting method described in Hainmueller (2012 ) that allows users to reweight a dataset such that the covariate distributions in the reweighted data satisfy a set of specified moment conditions. This can be useful to create balanced samples in observational studies with a binary treatment where the control group data can be reweighted to match the covariate moments in the treatment group. Entropy balancing can also be used to reweight a survey sample to known characteristics from a target population.
2012-08-01T00:00:00ZHypoxia shifts activity of neuropeptide Y in Ewing sarcoma from growth-inhibitory to growth-promoting effects
http://hdl.handle.net/1721.1/89818
Hypoxia shifts activity of neuropeptide Y in Ewing sarcoma from growth-inhibitory to growth-promoting effects
Lu, Congyi
Ewing sarcoma (ES) is an aggressive malignancy driven by an oncogenic fusion protein, EWS-FLI1. Neuropeptide Y (NPY), and two of its receptors, Y1R and Y5R are up-regulated by EWS-FLI1 and abundantly expressed in ES cells. Paradoxically, NPY acting via Y1R and Y5R stimulates ES cell death. Here, we demonstrate that these growth-inhibitory actions of NPY are counteracted by hypoxia, which converts the peptide to a growth-promoting factor. In ES cells, hypoxia induces another NPY receptor, Y2R, and increases expression of dipeptidyl peptidase IV (DPPIV), an enzyme that cleaves NPY to a shorter form, NPY3-36. This truncated peptide no longer binds to Y1R and, therefore, does not stimulate ES cell death. Instead, NPY3-36 acts as a selective Y2R/Y5R agonist. The hypoxia-induced increase in DPPIV activity is most evident in a population of ES cells with high aldehyde dehydrogenase (ALDH) activity, rich in cancer stem cells (CSCs). Consequently, NPY, acting via Y2R/Y5Rs, preferentially stimulates proliferation and migration of hypoxic ALDHhigh cells. Hypoxia also enhances the angiogenic potential of ES by inducing Y2Rs in endothelial cells and increasing the release of its ligand, NPY3-36, from ES cells. In summary, hypoxia acts as a molecular switch shifting NPY activity away from Y1R/Y5R-mediated cell death and activating the Y2R/Y5R/DPPIV/NPY3-36 axis, which stimulates ES CSCs and promotes angiogenesis. Hypoxia-driven actions of the peptide such as these may contribute to ES progression. Due to the receptor-specific and multifaceted nature of NPY actions, these findings may inform novel therapeutic approaches to ES.
2013-11-01T00:00:00Z