Exploring soft constraints on effective actions

We study effective actions for simultaneous breaking of space-time and internal symmetries. Novel features arise due to the mixing of Goldstone modes under the broken symmetries which, in contrast to the usual Adler's zero, leads to non-vanishing soft limits. Such scenarios are common for spontaneously broken SCFT's. We explicitly test these soft theorems for $\mathcal{N}=4$ sYM in the Coulomb branch both perturbatively and non-perturbatively. We explore the soft constraints systematically utilizing recursion relations. In the pure dilaton sector of a general CFT, we show that all amplitudes up to order $s^{n} \sim \partial^{2n}$ are completely determined in terms of the $k$-point amplitudes at order $s^k$ with $k \leq n$. Terms with at most one derivative acting on each dilaton insertion are completely fixed and coincide with those appearing in the conformal DBI, i.e. DBI in AdS. With maximal supersymmetry, the effective actions are further constrained, leading to new non-renormalization theorems. In particular, the effective action is fixed up to eight derivatives in terms of just one unknown four-point coefficient and one more coefficient for ten-derivative terms. Finally, we also study the interplay between scale and conformal invariance in this context.Comment: 20+4 pages, 1 figure; v2: references added, typos corrected; v3: typos corrected, JHEP versio

Role of IRAK-M in Alcohol Induced Liver Injury

Increasing evidence suggests that innate immunity plays an important role in alcohol-induced liver injury and most studies have focused on positive regulation of innate immunity. The main objective of this study was to investigate the negative regulator of innate immunity, IL-1/Toll-like receptor (TLR) signaling pathways and interleukin receptor-associated kinase-M (IRAK-M) in alcoholic liver injury. We established an alcohol-induced liver injury model using wild type and IRAK-M deficient B6 mice and investigated the possible mechanisms. We found that in the absence of IRAK-M, liver damage by alcohol was worse with higher alanine transaminase (ALT), more immune cell infiltration and increased numbers of IFNγ producing cells. We also found enhanced phagocytic activity in CD68+ cells. Moreover, our results revealed altered gut bacteria after alcohol consumption and this was more striking in the absence of IRAK-M. Our study provides evidence that IRAK-M plays an important role in alcohol-induced liver injury and IRAK-M negatively regulates the innate and possibly the adaptive immune response in the liver reacting to acute insult by alcohol. In the absence of IRAK-M, the hosts developed worse liver injury, enhanced gut permeability and altered gut microbiota

Applications of simulation technique on debris-flow hazard zone delineation: a case study in Hualien County, Taiwan

Debris flows pose severe hazards to communities in mountainous areas, often resulting in the loss of life and property. Helping debris-flow-prone communities delineate potential hazard zones provides local authorities with useful information for developing emergency plans and disaster management policies. In 2003, the Soil and Water Conservation Bureau of Taiwan proposed an empirical model to delineate hazard zones for all creeks (1420 in total) with potential of debris flows and utilized the model to help establish a hazard prevention system. However, the model does not fully consider hydrologic and physiographical conditions for a given creek in simulation. The objective of this study is to propose new approaches that can improve hazard zone delineation accuracy and simulate hazard zones in response to different rainfall intensity. In this study, a two-dimensional commercial model FLO-2D, physically based and taking into account the momentum and energy conservation of flow, was used to simulate debris-flow inundated areas. <br><br> Sensitivity analysis with the model was conducted to determine the main influence parameters which affect debris flow simulation. Results indicate that the roughness coefficient, yield stress and volumetric sediment concentration dominate the computed results. To improve accuracy of the model, the study examined the performance of the rainfall-runoff model of FLO-2D as compared with that of the HSPF (Hydrological Simulation Program Fortran) model, and then the proper values of the significant parameters were evaluated through the calibration process. Results reveal that the HSPF model has a better performance than the FLO-2D model at peak flow and flow recession period, and the volumetric sediment concentration and yield stress can be estimated by the channel slope. The validation of the model for simulating debris-flow hazard zones has been confirmed by a comparison of field evidence from historical debris-flow disaster data. The model can successfully replicate the influence zone of the debris-flow disaster event with an acceptable error and demonstrate a better result than the empirical model adopted by the Soil and Water Conservation Bureau of Taiwan

At-Speed Logic BIST for IP Cores

This paper describes a flexible logic BIST scheme that features high fault coverage achieved by fault-simulation guided test point insertion, real at-speed test capability for multi-clock designs without clock frequency manipulation, and easy physical implementation due to the use of a low-speed SE signal. Application results of this scheme to two widely used IP cores are also reported.Design, Automation and Test in Europe (DATE05), 7-11 March 2005, Munich, German

Pseuduscalar Heavy Quarkonium Decays With Both Relativistic and QCD Radiative Corrections

We estimate the decay rates of $\eta_c\rightarrow 2\gamma$, $\eta_c'\rightarrow 2\gamma$, and $J/\psi\rightarrow e^+ e^-$, $\psi^\prime\rightarrow e^+e^-$, by taking into account both relativistic and QCD radiative corrections. The decay amplitudes are derived in the Bethe-Salpeter formalism. The Bethe-Salpeter equation with a QCD-inspired interquark potential are used to calculate the wave functions and decay widths for these $c\bar{c}$ states. We find that the relativistic correction to the ratio $R\equiv \Gamma (\eta_c \rightarrow 2\gamma)/ \Gamma (J/ \psi \rightarrow e^+ e^-)$ is negative and tends to compensate the positive contribution from the QCD radiative correction. Our estimate gives $\Gamma(\eta_c \rightarrow 2\gamma)=(6-7) ~keV$ and $\Gamma(\eta_c^\prime \rightarrow 2\gamma)=2 ~keV$, which are smaller than their nonrelativistic values. The hadronic widths $\Gamma(\eta_c \rightarrow 2g)=(17-23) ~MeV$ and $\Gamma(\eta_c^\prime \rightarrow 2g)=(5-7)~MeV$ are then indicated accordingly to the first order QCD radiative correction, if $\alpha_s(m_c)=0.26-0.29$. The decay widths for $b\bar b$ states are also estimated. We show that when making the assmption that the quarks are on their mass shells our expressions for the decay widths will become identical with that in the NRQCD theory to the next to leading order of $v^2$ and $\alpha_s$.Comment: 14 pages LaTex (2 figures included

Host-Guest Complexation of Amphiphilic Molecules at the Air-Water Interface Prevents Oxidation by Hydroxyl Radicals and Singlet Oxygen

The oxidation of antioxidants by oxidizers imposes great challenges to both living organisms and the food industry. Here we show that the host–guest complexation of the carefully designed, positively charged, amphiphilic guanidinocalix[5]arene pentadodecyl ether (GC5A‐12C) and negatively charged oleic acid (OA), a well‐known cell membrane antioxidant, prevents the oxidation of the complex monolayers at the air–water interface from two potent oxidizers hydroxyl radicals (OH) and singlet delta oxygen (SDO). OH is generated from the gas phase and attacks from the top of the monolayer, while SDO is generated inside the monolayer and attacks amphiphiles from a lateral direction. Field‐induced droplet ionization mass spectrometry results have demonstrated that the host–guest complexation achieves steric shielding and prevents both types of oxidation as a result of the tight and “sleeved in” physical arrangement, rather than the chemical reactivity, of the complexes

Host-Guest Complexation of Amphiphilic Molecules at the Air-Water Interface Prevents Oxidation by Hydroxyl Radicals and Singlet Oxygen

The oxidation of antioxidants by oxidizers imposes great challenges to both living organisms and the food industry. Here we show that the host–guest complexation of the carefully designed, positively charged, amphiphilic guanidinocalix[5]arene pentadodecyl ether (GC5A‐12C) and negatively charged oleic acid (OA), a well‐known cell membrane antioxidant, prevents the oxidation of the complex monolayers at the air–water interface from two potent oxidizers hydroxyl radicals (OH) and singlet delta oxygen (SDO). OH is generated from the gas phase and attacks from the top of the monolayer, while SDO is generated inside the monolayer and attacks amphiphiles from a lateral direction. Field‐induced droplet ionization mass spectrometry results have demonstrated that the host–guest complexation achieves steric shielding and prevents both types of oxidation as a result of the tight and “sleeved in” physical arrangement, rather than the chemical reactivity, of the complexes

Hadronic Annihilation Decay Rates of P-wave Heavy Quarkonia with Both Relativistic and QCD Radiative Corrections

Hadronic annihilation decay rates of P-wave heavy quarkonia are given to next-to-leading order in both $\alpha_s$ and $v^2$. They include ten nonperturbative parameters, which can be rigorously defined as the matrix elements of color-singlet and color-octet operators in NRQCD. We expect these papameters will be determined from lattice calculations in future.Comment: 5 Pages RevTex. The paper is withdraw

Nucleotide-binding oligomerization domain-containing protein 2 (Nod2) modulates T1DM susceptibility by gut microbiota

Nucleotide-binding oligomerization domain-containing protein 2 (Nod2) is an innate immune receptor. To investigate the role of Nod2 in susceptibility to the autoimmune disease, type 1 diabetes mellitus (T1DM), we generated Nod2-/- non-obese diabetic (NOD) mice. The Nod2-/-NOD mice had different composition of the gut microbiota compared to Nod2+/+NOD mice and were significantly protected from diabetes, but only when housed separately from Nod2+/+NOD mice. This suggested that T1DM susceptibility in Nod2-/-NOD mice is dependent on the alteration of gut microbiota, which modulated the frequency and function of IgA-secreting B-cells and IL-10 promoting T-regulatory cells. Finally, colonizing germ-free NOD mice with Nod2-/-NOD gut microbiota significantly reduced pro-inflammatory cytokine-secreting immune cells but increased T-regulatory cells. Thus, gut microbiota modulate the immune system and T1D susceptibility. Importantly, our study raises a critical question about the housing mode in the interpretation of the disease phenotype of genetically-modified mouse strains in T1DM studies