The Camel's Nose Is in the Tent: Rules, Theories, and Slippery Slopes

Slippery slopes have been the topic of a spate of recent literature. In this Article, the authors provide a general theory for understanding and evaluating slippery slope arguments (SSAs) and their associated slippery slope events (SSEs). The central feature of the theory is a structure of discussion within which all arguments take place. The structure is multi-layered, consisting of decisions, rules, theories, and research programs. Each layer influences and shapes the layer beneath: rules influence decisions, theories influence the choice of rules, and research programs influence the choice of theories. In this structure, SSAs take the form of meta-arguments, as they purport to predict the future development of arguments in the structure. Evaluating such arguments requires having knowledge of the specific content of the structure of discussion itself. The Article then presents four viable types of slippery slope argument, draws attention to four different factors that (other things equal) tend to increase the likelihood of slippery slopes, and explores a variety of strategies for coping with slippery slopes.SLIPPERY SLOPE ARGUMENTS; STRUCTURE OF DISCUSSION (ARGUMENT); RULES; UNINTENDED CONSEQUENCES

The Morality of Profits, and The Struggle for Existence

ethics ; profit

Higgsless Electroweak Symmetry Breaking in Warped Backgrounds: Constraints and Signatures

We examine the phenomenology of a warped 5-dimensional model based on SU(2)$_L \times$ SU(2)$_R \times$ U(1)$_{B-L}$ model which implements electroweak symmetry breaking through boundary conditions, without the presence of a Higgs boson. We use precision electroweak data to constrain the general parameter space of this model. Our analysis includes independent $L$ and $R$ gauge couplings, radiatively induced UV boundary gauge kinetic terms, and all higher order corrections from the curvature of the 5-d space. We show that this setup can be brought into good agreement with the precision electroweak data for typical values of the parameters. However, we find that the entire range of model parameters leads to violation of perturbative unitarity in gauge boson scattering and hence this model is not a reliable perturbative framework. Assuming that unitarity can be restored in a modified version of this scenario, we consider the collider signatures. It is found that new spin-1 states will be observed at the LHC and measurement of their properties would identify this model. However, the spin-2 graviton Kaluza-Klein resonances, which are a hallmark of the Randall-Sundrum model, are too weakly coupled to be detected.Comment: More detailed analysis, added references, 43 pages, 15 figures, LaTe

The Genetic causal Tradition of Modern Economic History

Economic theory

Fundamental Issues in the Justification of Profits

ethics ; profit

Constraining the Littlest Higgs

Little Higgs models offer a new way to address the hierarchy problem, and give rise to a weakly-coupled Higgs sector. These theories predict the existence of new states which are necessary to cancel the quadratic divergences of the Standard Model. The simplest version of these models, the Littlest Higgs, is based on an $SU(5)/SO(5)$ non-linear sigma model and predicts that four new gauge bosons, a weak isosinglet quark, $t'$, with $Q=2/3$, as well as an isotriplet scalar field exist at the TeV scale. We consider the contributions of these new states to precision electroweak observables, and examine their production at the Tevatron. We thoroughly explore the parameter space of this model and find that small regions are allowed by the precision data where the model parameters take on their natural values. These regions are, however, excluded by the Tevatron data. Combined, the direct and indirect effects of these new states constrain the `decay constant' f\gsim 3.5 TeV and m_{t'}\gsim 7 TeV. These bounds imply that significant fine-tuning be present in order for this model to resolve the hierarchy problem.Comment: 31 pgs, 26 figures; bound on t' mass fixed to mt'>2f, conclusions unchange

Phenomenology of Randall-Sundrum Black Holes

We explore the phenomenology of microscopic black holes in the $S^1/Z_2$ Randall-Sundrum (RS) model. We consider the canonical framework in which both gauge and matter fields are confined to the brane and only gravity spills into the extra dimension. The model is characterized by two parameters, the mass of the first massive graviton $(m_1)$, and the curvature $1/\ell$ of the RS anti-de Sitter space. We compute the sensitivity of present and future cosmic ray experiments to various regions of $\ell$ and $m_1,$ and compare with that of Runs I and II at the Tevatron. As part of our phenomenological analysis, we examine constraints placed on $\ell$ by AdS/CFT considerations.Comment: Version to appear in Physical Review D; contains additional analysis on sensitivity of OW

b -> s gamma in the left-right supersymmetric model

The rare decay $b \to s \gamma$ is studied in the left-right supersymmetric model. We give explicit expressions for all the amplitudes associated with the supersymmetric contributions coming from gluinos, charginos and neutralinos in the model to one-loop level. The branching ratio is enhanced significantly compared to the standard model and minimal supersymmetric standard model values by contributions from the right-handed gaugino and squark sector. We give numerical results coming from the leading order contributions. If the only source of flavor violation comes from the CKM matrix, we constrain the scalar fermion-gaugino sector. If intergenerational mixings are allowed in the squark mass matrix, we constrain such supersymmetric sources of flavor violation. The decay $b \to s \gamma$ sets constraints on the parameters of the model and provides distinguishing signs from other supersymmetric scenarios.Comment: 12 figure

A Formally Verified NAT Stack

Prior work proved a stateful NAT network function to be semantically correct, crash-free, and memory safe. Their toolchain verifies the network function code while assuming the underlying kernel-bypass framework, drivers, operating system, and hardware to be correct. We extend the toolchain to verify the kernel-bypass framework and a NIC driver in the context of the NAT. We uncover bugs in both the framework and the driver. Our code is publicly available

The role of cytokine gene polymorphisms in the pathogenesis of abdominal aortic aneurysms: A case-control study

AbstractBackground: Cytokines are the primary mediators of inflammation and also influence matrix metalloproteinase expression, both of which are important in development of abdominal aortic aneurysm (AAA). A significant, but as yet unknown, familial factor contributes to the pathogenesis of AAA. Many cytokine genes contain polymorphic sites, some of which affect cytokine production in vitro. Cytokine gene polymorphisms may therefore influence the pathogenesis of AAA. The purpose of this study was to determine whether there is any association between cytokine gene polymorphisms and AAA. Methods and Results: This case-control study comprised 100 patients with AAA and 100 age-matched and sex-matched control subjects. For each case and control subject in the study, genotypes at the following cytokine gene polymorphic loci were determined: interleukin (IL)-1β +3953, IL-6 −174, IL-10 −1082, IL-10 −592, and tumor necrosis factors-α −308. Allele and genotype frequencies were compared between AAA and control groups, and odds ratios (OR) were calculated for the presence of AAA with each allele at each locus examined as risk factors. The IL-10 −1082 A allele was significantly more common in the AAA group than the control group (P =.03). The OR for the IL-10 −1082 A allele as a risk factor for AAA was 1.8 (95% confidence interval, 0.9-3.6). Discussion: These associations suggest a significant role for IL-10 in the pathogenesis of AAA. This association of AAA with the IL-10 −1082 A allele is also biologically plausible; the IL-10 −1082 A allele is associated with low IL-10 secretion, and it may be that AAA develops in patients who are unable to mount the same anti-inflammatory response as those who do not have AAA. (J Vasc Surg 2003;37:999-1005.