Generating Evidence to Guide Merger Enforcement

The challenge of effective merger enforcement is tremendous. U.S. antitrust agencies must, by statute, quickly forecast the competitive effects of mergers that occur in virtually every sector of the economy to determine if mergers can proceed. Surprisingly, given the complexity of the regulators task, there is remarkably little empirical evidence on the effects of mergers to guide regulators. This paper describes the necessity of retrospective analysis of past mergers in building an empirical basis for antitrust enforcement, and provides guidance on the key measurement issues researchers confront in estimating the price effects of mergers. We also describe how evidence from merger retrospectives can be used to evaluate the economic models used to predict the competitive effects of mergers.Corporate mergers, antitrust enforcement

Black Hole Criticality in the Brans-Dicke Model

We study the collapse of a free scalar field in the Brans-Dicke model of gravity. At the critical point of black hole formation, the model admits two distinctive solutions dependent on the value of the coupling parameter. We find one solution to be discretely self-similar and the other to exhibit continuous self-similarity.Comment: 4 pages, REVTeX 3.0, 5 figures include

Generating Evidence to Guide Merger Enforcement

The challenge of effective merger enforcement is tremendous. U.S. antitrust agencies must, by statute, quickly forecast the competitive effects of mergers that occur in virtually every sector of the economy to determine if mergers can proceed. Surprisingly, given the complexity of the regulators task, there is remarkably little empirical evidence on the effects of mergers to guide regulators. This paper describes the necessity of retrospective analysis of past mergers in building an empirical basis for antitrust enforcement, and provides guidance on the key measurement issues researchers confront in estimating the price effects of mergers. We also describe how evidence from merger retrospectives can be used to evaluate the economic models used to predict the competitive effects of mergers.

Subcellular organization of UBE3A in human cerebral cortex.

BackgroundLoss of UBE3A causes Angelman syndrome, whereas excess UBE3A activity appears to increase the risk for autism. Despite this powerful association with neurodevelopmental disorders, there is still much to be learned about UBE3A, including its cellular and subcellular organization in the human brain. The issue is important, since UBE3A's localization is integral to its function.MethodsWe used light and electron microscopic immunohistochemistry to study the cellular and subcellular distribution of UBE3A in the adult human cerebral cortex. Experiments were performed on multiple tissue sources, but our results focused on optimally preserved material, using surgically resected human temporal cortex of high ultrastructural quality from nine individuals.ResultsWe demonstrate that UBE3A is expressed in both glutamatergic and GABAergic neurons, and to a lesser extent in glial cells. We find that UBE3A in neurons has a non-uniform subcellular distribution. In somata, UBE3A preferentially concentrates in euchromatin-rich domains within the nucleus. Electron microscopy reveals that labeling concentrates in the head and neck of dendritic spines and is excluded from the PSD. Strongest labeling within the neuropil was found in axon terminals.ConclusionsBy highlighting the subcellular compartments in which UBE3A is likely to function in the human neocortex, our data provide insight into the diverse functional capacities of this E3 ligase. These anatomical data may help to elucidate the role of UBE3A in Angelman syndrome and autism spectrum disorder

Acute Outcomes for the Full US Cohort of the FLASH Mechanical Thrombectomy Registry in Pulmonary Embolism

Background Evidence supporting interventional pulmonary embolism (PE) treatment is needed. Aims We aimed to evaluate the acute safety and effectiveness of mechanical thrombectomy for intermediate- and high-risk PE in a large real-world population. Methods FLASH is a multicentre, prospective registry enrolling up to 1,000 US and European PE patients treated with mechanical thrombectomy using the FlowTriever System. The primary safety endpoint is a major adverse event composite including device-related death and major bleeding at 48 hours, and intraprocedural adverse events. Acute mortality and 48-hour outcomes are reported. Multivariate regression analysed characteristics associated with pulmonary artery pressure and dyspnoea improvement. Results Among 800 patients in the full US cohort, 76.7% had intermediate-high risk PE, 7.9% had high-risk PE, and 32.1% had thrombolytic contraindications. Major adverse events occurred in 1.8% of patients. All-cause mortality was 0.3% at 48-hour follow-up and 0.8% at 30-day follow-up, with no device-related deaths. Immediate haemodynamic improvements included a 7.6 mmHg mean drop in mean pulmonary artery pressure (-23.0%; p Conclusions Mechanical thrombectomy with the FlowTriever System demonstrates a favourable safety profile, improvements in haemodynamics and functional outcomes, and low 30-day mortality for intermediate- and high-risk PE

WKB analysis of relativistic Stern-Gerlach measurements

Spin is an important quantum degree of freedom in relativistic quantum information theory. This paper provides a first-principles derivation of the observable corresponding to a Stern-Gerlach measurement with relativistic particle velocity. The specific mathematical form of the Stern-Gerlach operator is established using the transformation properties of the electromagnetic field. To confirm that this is indeed the correct operator we provide a detailed analysis of the Stern-Gerlach measurement process. We do this by applying a WKB approximation to the minimally coupled Dirac equation describing an interaction between a massive fermion and an electromagnetic field. Making use of the superposition principle we show that the +1 and -1 spin eigenstates of the proposed spin operator are split into separate packets due to the inhomogeneity of the Stern-Gerlach magnetic field. The operator we obtain is dependent on the momentum between particle and Stern-Gerlach apparatus, and is mathematically distinct from two other commonly used operators. The consequences for quantum tomography are considered.Comment: 13 pages, no figures. Comments welcom

Decreased Axon Caliber Underlies Loss of Fiber Tract Integrity, Disproportional Reductions in White Matter Volume, and Microcephaly in Angelman Syndrome Model Mice

Angelman syndrome (AS) is a debilitating neurodevelopmental disorder caused by loss of function of the maternally inherited UBE3A allele. It is currently unclear how the consequences of this genetic insult unfold to impair neurodevelopment. We reasoned that by elucidating the basis of microcephaly in AS, a highly penetrant syndromic feature with early postnatal onset, we would gain new insights into the mechanisms by which maternal UBE3A loss derails neurotypical brain growth and function. Detailed anatomical analysis of both male and female maternal Ube3a-null mice reveals that microcephaly in the AS mouse model is primarily driven by deficits in the growth of white matter tracts, which by adulthood are characterized by densely packed axons of disproportionately small caliber. Our results implicate impaired axon growth in the pathogenesis of AS and identify noninvasive structural neuroimaging as a potentially valuable tool for gauging therapeutic efficacy in the disorder

Localized qubits in curved spacetimes

We provide a systematic and self-contained exposition of the subject of localized qubits in curved spacetimes. This research was motivated by a simple experimental question: if we move a spatially localized qubit, initially in a state |\psi_1>, along some spacetime path \Gamma from a spacetime point x_1 to another point x_2, what will the final quantum state |\psi_2> be at point x_2? This paper addresses this question for two physical realizations of the qubit: spin of a massive fermion and polarization of a photon. Our starting point is the Dirac and Maxwell equations that describe respectively the one-particle states of localized massive fermions and photons. In the WKB limit we show how one can isolate a two-dimensional quantum state which evolves unitarily along \Gamma. The quantum states for these two realizations are represented by a left-handed 2-spinor in the case of massive fermions and a four-component complex polarization vector in the case of photons. In addition we show how to obtain from this WKB approach a fully general relativistic description of gravitationally induced phases. We use this formalism to describe the gravitational shift in the COW 1975 experiment. In the non-relativistic weak field limit our result reduces to the standard formula in the original paper. We provide a concrete physical model for a Stern-Gerlach measurement of spin and obtain a unique spin operator which can be determined given the orientation and velocity of the Stern-Gerlach device and velocity of the massive fermion. Finally, we consider multipartite states and generalize the formalism to incorporate basic elements from quantum information theory such as quantum entanglement, quantum teleportation, and identical particles. The resulting formalism provides a basis for exploring precision quantum measurements of the gravitational field using techniques from quantum information theory.Comment: 53 pages, 7 figures; v2: published version with further corrections. v3: some references and equation typesetting fixe

GABAergic Neuron-Specific Loss of Ube3a Causes Angelman Syndrome-Like EEG Abnormalities and Enhances Seizure Susceptibility

Loss of maternal UBE3A causes Angelman syndrome (AS), a neurodevelopmental disorder associated with severe epilepsy. We previously implicated GABAergic deficits onto layer (L) 2/3 pyramidal neurons in the pathogenesis of neocortical hyperexcitability, and perhaps epilepsy, in AS model mice. Here we investigate consequences of selective Ube3a loss from either GABAergic or glutamatergic neurons, focusing on the development of hyperexcitability within L2/3 neocortex and in broader circuit and behavioral contexts. We find that GABAergic Ube3a loss causes AS-like increases in neocortical EEG delta power, enhances seizure susceptibility, and leads to presynaptic accumulation of clathrin-coated vesicles (CCVs) – all without decreasing GABAergic inhibition onto L2/3 pyramidal neurons. Conversely, glutamatergic Ube3a loss fails to yield EEG abnormalities, seizures, or associated CCV phenotypes, despite impairing tonic inhibition onto L2/3 pyramidal neurons. These results substantiate GABAergic Ube3a loss as the principal cause of circuit hyperexcitability in AS mice, lending insight into ictogenic mechanisms in AS