Relativistic nuclear structure effects in quasielastic neutrino scattering

Charged-current cross sections are calculated for quasielastic neutrino and antineutrino scattering using a relativistic meson-nucleon model. We examine how nuclear-structure effects, such as relativistic random-phase-approximation (RPA) corrections and momentum-dependent nucleon self-energies, influence the extraction of the axial form factor of the nucleon. RPA corrections are important only at low-momentum transfers. In contrast, the momentum dependence of the relativistic self-energies changes appreciably the value of the axial-mass parameter, $M_A$, extracted from dipole fits to the axial form factor. Using Brookhaven's experimental neutrino spectrum we estimate the sensitivity of M$_A$ to various relativistic nuclear-structure effects.Comment: 26 pages, revtex, 6 postscript figures (available upon request

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

Background: When a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD. Methods: In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na+/K+ pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate. Results: We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na+/K+ ATPase elicits SD. Elevated K+ or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling. Conclusions: Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory. © 2022, The Author(s)

Hadron Collider Signatures for New Interactions of Top and Bottom Quarks

One of the main goals for hadron colliders is the study of the properties of the third generation quarks. We study the signatures for new TeV resonances that couple to top or bottom quarks both at the Tevatron Run II and at the LHC. We find that in the simplest production processes of Drell-Yan type at the Tevatron, the signals are overwhelmed by QCD backgrounds. We also find that it is possible to study these resonances when they are produced in association with a pair of heavy quarks or in association with a single top at the LHC.In particular, with an integrated luminosity of 300 fb$^{-1}$ at the LHC, it is possible to probe resonance masses up to around 2 TeV.Comment: 24 pages, 15 figures, Minor corrections, version to appear in Phys. Rev.

Chirality Correlation within Dirac Eigenvectors from Domain Wall Fermions

In the dilute instanton gas model of the QCD vacuum, one expects a strong spatial correlation between chirality and the maxima of the Dirac eigenvectors with small eigenvalues. Following Horvath, {\it et al.} we examine this question using lattice gauge theory within the quenched approximation. We extend the work of those authors by using weaker coupling, $\beta=6.0$, larger lattices, $16^4$, and an improved fermion formulation, domain wall fermions. In contrast with this earlier work, we find a striking correlation between the magnitude of the chirality density, $|\psi^\dagger(x)\gamma^5\psi(x)|$, and the normal density, $\psi^\dagger(x)\psi(x)$, for the low-lying Dirac eigenvectors.Comment: latex, 25 pages including 12 eps figure

Higgs production in gluon fusion at next-to-next-to-leading order QCD for finite top mass

The inclusive Higgs production cross section from gluon fusion is calculated through NNLO QCD, including its top quark mass dependence. This is achieved through a matching of the 1/mtop expansion of the partonic cross sections to the exact large s-hat limits which are derived from k_T-factorization. The accuracy of this procedure is estimated to be better than 1% for the hadronic cross section. The final result is shown to be within 1% of the commonly used effective theory approach, thus confirming earlier findings.Comment: 28 pages, 14 figure

Questioning Glutamate Excitotoxicity in Acute Brain Damage: The Importance of Spreading Depolarization

Background: Within 2 min of severe ischemia, spreading depolarization (SD) propagates like a wave through compromised gray matter of the higher brain. More SDs arise over hours in adjacent tissue, expanding the neuronal damage. This period represents a therapeutic window to inhibit SD and so reduce impending tissue injury. Yet most neuroscientists assume that the course of early brain injury can be explained by glutamate excitotoxicity, the concept that immediate glutamate release promotes early and downstream brain injury. There are many problems with glutamate release being the unseen culprit, the most practical being that the concept has yielded zero therapeutics over the past 30 years. But the basic science is also flawed, arising from dubious foundational observations beginning in the 1950s Methods: Literature pertaining to excitotoxicity and to SD over the past 60 years is critiqued. Results: Excitotoxicity theory centers on the immediate and excessive release of glutamate with resulting neuronal hyperexcitation. This instigates poststroke cascades with subsequent secondary neuronal injury. By contrast, SD theory argues that although SD evokes some brief glutamate release, acute neuronal damage and the subsequent cascade of injury to neurons are elicited by the metabolic stress of SD, not by excessive glutamate release. The challenge we present here is to find new clinical targets based on more informed basic science. This is motivated by the continuing failure by neuroscientists and by industry to develop drugs that can reduce brain injury following ischemic stroke, traumatic brain injury, or sudden cardiac arrest. One important step is to recognize that SD plays a central role in promoting early neuronal damage. We argue that uncovering the molecular biology of SD initiation and propagation is essential because ischemic neurons are usually not acutely injured unless SD propagates through them. The role of glutamate excitotoxicity theory and how it has shaped SD research is then addressed, followed by a critique of its fading relevance to the study of brain injury. Conclusions: Spreading depolarizations better account for the acute neuronal injury arising from brain ischemia than does the early and excessive release of glutamate.Grants to RDA from the Canadian Heart & Stroke Foundation, National Science Engineering and Research Council and the New Frontiers in Research Fund, to E.F from the National Research, Development and Innovation Office of Hungary, grant no. K134377; and the EU’s Horizon 2020 research and innovation program under grant agreement No. 739593, and to JPD from the DFG (German research Council) (DFG DR323/5-1,DFG DR 323/10-1) BMBF Bundesministerium fuer Bildung und Forschung (Era-Net Neuron EBio2, with funds from BMBF 01EW2004)

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

Background: When a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD. Methods: In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na/K pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate. Results: We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na/K ATPase elicits SD. Elevated K or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling. Conclusions: Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory.This work was supported by grants from the Heart and Stroke Foundation of Canada and the National Science and Engineering Research Council of Canada to RDA, an NIH grant (NS106901) to CWS, a National Research, Development and Innovation Office of Hungary grant (K1343777) and EU Horizon 2020 research and innovation program (739953) to EF and from DFG Deutsche Forschungsgemeinschaft (German Research Council) (DFG DR 323/5-1), DFG DR 323/10-1, and BMBF Bundesministerium fuer Bildung und Forschung (EraNet Neuron EBio2, with funds from BMBF 01EW2004) to JPD

Quenched Lattice QCD with Domain Wall Fermions and the Chiral Limit

Quenched QCD simulations on three volumes, $8^3 \times$, $12^3 \times$ and $16^3 \times 32$ and three couplings, $\beta=5.7$, 5.85 and 6.0 using domain wall fermions provide a consistent picture of quenched QCD. We demonstrate that the small induced effects of chiral symmetry breaking inherent in this formulation can be described by a residual mass (\mres) whose size decreases as the separation between the domain walls ($L_s$) is increased. However, at stronger couplings much larger values of $L_s$ are required to achieve a given physical value of \mres. For $\beta=6.0$ and $L_s=16$, we find \mres/m_s=0.033(3), while for $\beta=5.7$, and $L_s=48$, \mres/m_s=0.074(5), where $m_s$ is the strange quark mass. These values are significantly smaller than those obtained from a more naive determination in our earlier studies. Important effects of topological near zero modes which should afflict an accurate quenched calculation are easily visible in both the chiral condensate and the pion propagator. These effects can be controlled by working at an appropriately large volume. A non-linear behavior of $m_\pi^2$ in the limit of small quark mass suggests the presence of additional infrared subtlety in the quenched approximation. Good scaling is seen both in masses and in $f_\pi$ over our entire range, with inverse lattice spacing varying between 1 and 2 GeV.Comment: 91 pages, 34 figure

t→bWt \to b W in NonCommutative Standard Model

We study the top quark decay to b quark and W boson in the NonCommutative Standard Model (NCSM). The lowest contribution to the decay comes from the terms quadratic in the matrix describing the noncommutative (NC) effects while the linear term is seen to identically vanish because of symmetry. The NC effects are found to be significant only for low values of the NC characteristic scale.Comment: 11 page Latex file containing 2 eps figures (redrawn). More discussion included. To appear in PR