Supersymmetric Noncommutative QED and Lorentz Violation

We consider Lorentz-violating operators induced at the loop level in softly-broken supersymmetric noncommutative QED. Dangerous operators forbidden in the supersymmetric limit are generated via finite corrections, with the scale of supersymmetry breaking serving as a gauge-invariant regulator. We compare the most dangerous loop effects to those obtained in noncommutative theories truncated by a momentum-space cutoff, and find significantly improved bounds.Comment: 11 pages LaTeX, 4 eps figure

A No-Lose Theorem for Higgs Searches at a Future Linear Collider

Assuming perturbativity up to a high energy scale $\sim 10^{16}$ GeV, we demonstrate that a future $e^+e^-$ linear collider operating at $\sqrt{s} =$ 500 GeV with $\int{\cal L}=$ 500 fb$^{-1}$ per year (such as the recently proposed TESLA facility) will detect a Higgs boson signal regardless of the complexity of the Higgs sector and of how the Higgs bosons decay.Comment: 4 pages, LaTe

Theoretical Higgs Mass Bounds in the Standard Model and Supersymmetric Extensions

These lectures provide a very basic introduction to different theoretical limits on the mass of Higgs scalars. Particular attention is devoted to the pure Standard Model and its Minimal Supersymmetric extension (MSSM). [Lectures presented at the XXIV ITEP Winter School, Snegiri (Russia), February 96]Comment: 37 pages, TeX, 15 postscript figures include

BPS Monopole Equation in Omega-background

We study deformed supersymmetries in N=2 super Yang-Mills theory in the Omega-backgrounds characterized by two complex parameters $\epsilon_1, \epsilon_2$. When one of the $\epsilon$-parameters vanishes, the theory has extended supersymmetries. We compute the central charge of the algebra and obtain the deformed BPS monopole equation. We examine supersymmetries preserved by the equation.Comment: 14 pages, typos corrected, published version in JHE

The Status of the Minimal Supersymmetric Standard Model and Beyond

The minimal supersymmetric extension of the Standard Model (MSSM) is reviewed. In the most general framework with minimal field content and R-parity conservation, the MSSM is a 124-parameter model (henceforth called MSSM-124). An acceptable phenomenology occurs only at exceptional points (and small perturbations around these points) of MSSM-124 parameter space. Among the topics addressed in this review are: gauge coupling unification, precision electroweak data, phenomenology of the MSSM Higgs sector, and supersymmetry searches at present and future colliders. The implications of approaches beyond the MSSM are briefly addressed.Comment: 17 pages, LaTeX, with espcrc2.sty style file, to appear in the Proceedings of the 5th International Conference on Supersymmetries in Physics (SUSY 97

Neutrino-electron scattering in noncommutative space

Neutral particles can couple with the $U(1)$ gauge field in the adjoint representation at the tree level if the space-time coordinates are noncommutative (NC). Considering neutrino-photon coupling in the NC QED framework, we obtain the differential cross section of neutrino-electron scattering. Similar to the magnetic moment effect, one of the NC terms is proportional to $\frac 1 T$, where $T$ is the electron recoil energy. Therefore, this scattering provides a chance to achieve a stringent bound on the NC scale in low energy by improving the sensitivity to the smaller electron recoil energy.Comment: 12 pages, 2 figure

Complementarity of the CERN Large Hadron Collider and the e+e−e^+e^- International Linear Collider

The next-generation high-energy facilities, the CERN Large Hadron Collider (LHC) and the prospective $e^+e^-$ International Linear Collider (ILC), are expected to unravel new structures of matter and forces from the electroweak scale to the TeV scale. In this report we review the complementary role of LHC and ILC in drawing a comprehensive and high-precision picture of the mechanism breaking the electroweak symmetries and generating mass, and the unification of forces in the frame of supersymmetry.Comment: 14 pages, 17 figures, to be published in "Supersymmetry on the Eve of the LHC", a special volume of European Physical Journal C, Particles and Fields (EPJC) in memory of Julius Wes

TESLA Technical Design Report Part III: Physics at an e+e- Linear Collider

The TESLA Technical Design Report Part III: Physics at an e+e- Linear ColliderComment: 192 pages, 131 figures. Some figures have reduced quality. Full quality figures can be obtained from http://tesla.desy.de/tdr. Editors - R.-D. Heuer, D.J. Miller, F. Richard, P.M. Zerwa

Prostaglandin E2 Promotes Endothelial Differentiation from Bone Marrow-Derived Cells through AMPK Activation

Prostaglandin E2 (PGE2) has been reported to modulate angiogenesis, the process of new blood vessel formation, by promoting proliferation, migration and tube formation of endothelial cells. Endothelial progenitor cells are known as a subset of circulating bone marrow mononuclear cells that have the capacity to differentiate into endothelial cells. However, the mechanism underlying the stimulatory effects of PGE2 and its specific receptors on bone marrow-derived cells (BMCs) in angiogenesis has not been fully characterized. Treatment with PGE2 significantly increased the differentiation and migration of BMCs. Also, the markers of differentiation to endothelial cells, CD31 and von Willebrand factor, and the genes associated with migration, matrix metalloproteinases 2 and 9, were significantly upregulated. This upregulation was abolished by dominant-negative AMP-activated protein kinase (AMPK) and AMPK inhibitor but not protein kinase, a inhibitor. As a functional consequence of differentiation and migration, the tube formation of BMCs was reinforced. Along with altered BMCs functions, phosphorylation and activation of AMPK and endothelial nitric oxide synthase, the target of activated AMPK, were both increased which could be blocked by EP4 blocking peptide and simulated by the agonist of EP4 but not EP1, EP2 or EP3. The pro-angiogenic role of PGE2 could be repressed by EP4 blocking peptide and retarded in EP4+/− mice. Therefore, by promoting the differentiation and migration of BMCs, PGE2 reinforced their neovascularization by binding to the receptor of EP4 in an AMPK-dependent manner. PGE2 may have clinical value in ischemic heart disease