What Do We Really Know About Cosmic Acceleration?

Essentially all of our knowledge of the acceleration history of the Universe - including the acceleration itself - is predicated upon the validity of general relativity. Without recourse to this assumption, we use SNeIa to analyze the expansion history and find (i) very strong (5 sigma) evidence for a period of acceleration, (ii) strong evidence that the acceleration has not been constant, (iii) evidence for an earlier period of deceleration and (iv) only weak evidence that the Universe has not been decelerating since z~0.3.Comment: 9 pages, 8 figure

Geometry and Destiny

The recognition that the cosmological constant may be non-zero forces us to re-evaluate standard notions about the connection between geometry and the fate of our Universe. An open Universe can recollapse, and a closed Universe can expand forever. As a corollary, we point out that there is no set of cosmological observations we can perform that will unambiguously allow us to determine what the ultimate destiny of the Universe will be.Comment: 7 pages, Gravity Research Foundation Essa

Genetic overlap between autism, schizophrenia and bipolar disorder

There is strong evidence that genetic factors make substantial contributions to the etiology of autism, schizophrenia and bipolar disorders, with heritability estimates being at least 80% for each. These illnesses have complex inheritance, with multiple genetic and environmental factors influencing disease risk; however, in psychiatry, complex genetics is further compounded by phenotypic complexity. Autism, schizophrenia and bipolar disorder are effectively syndromic constellations of symptoms that define groups of patients with broadly similar outcomes and responses to treatment. As such the diagnostic categories are likely to be heterogeneous and the boundaries between them somewhat arbitrary. Recent applications of whole-genome technologies have discovered rare copy number variants and common single-nucleotide polymorphisms that are associated with risk of developing these disorders. Furthermore, these studies have shown an overlap between the genetic loci and even alleles that predispose to the different phenotypes. The findings have several implications. First, they show that copy number variations are likely to be important risk factors for autism and schizophrenia, whereas common single-nucleotide polymorphism alleles have a role in all disorders. Second, they imply that there are specific genetic loci and alleles that increase an individual's risk of developing any of these disorders. Finally, the findings suggest that some of the specific genetic loci implicated so far encode proteins, such as neurexins and neuroligins, that function in synaptic development and plasticity, and therefore may represent a common biological pathway for these disorders

Gravity Waves from a Cosmological Phase Transition: Gauge Artifacts and Daisy Resummations

The finite-temperature effective potential customarily employed to describe the physics of cosmological phase transitions often relies on specific gauge choices, and is manifestly not gauge-invariant at finite order in its perturbative expansion. As a result, quantities relevant for the calculation of the spectrum of stochastic gravity waves resulting from bubble collisions in first-order phase transitions are also not gauge-invariant. We assess the quantitative impact of this gauge-dependence on key quantities entering predictions for gravity waves from first order cosmological phase transitions. We resort to a simple abelian Higgs model, and discuss the case of R_xi gauges. By comparing with results obtained using a gauge-invariant Hamiltonian formalism, we show that the choice of gauge can have a dramatic effect on theoretical predictions for the normalization and shape of the expected gravity wave spectrum. We also analyze the impact of resumming higher-order contributions as needed to maintain the validity of the perturbative expansion, and show that doing so can suppress the amplitude of the spectrum by an order of magnitude or more. We comment on open issues and possible strategies for carrying out "daisy resummed" gauge invariant computations in non-Abelian models for which a gauge-invariant Hamiltonian formalism is not presently available.Comment: 25 pages, 10 figure

Metabolically exaggerated cardiac reactions to acute psychological stress: The effects of resting blood pressure status and possible underlying mechanisms

The study aimed to: confirm that acute stress elicits metabolically exaggerated increases in cardiac activity; test whether individuals with elevated resting blood pressure show more exaggerated cardiac reactions to stress than those who are clearly normotensive; and explore the underlying mechanisms. Cardiovascular activity and oxygen consumption were measured pre-, during, and post- mental stress, and during graded submaximal cycling exercise in 11 young men with moderately elevated resting blood pressure and 11 normotensives. Stress provoked increases in cardiac output that were much greater than would be expected from contemporary levels of oxygen consumption. Exaggerated cardiac reactions were larger in the relatively elevated blood pressure group. They also had greater reductions in total peripheral resistance, but not heart rate variability, implying that their more exaggerated cardiac reactions reflected greater β-adrenergic activation

Comments on Non-Commutative Phenomenology

It is natural to ask whether non-commutative geometry plays a role in four dimensional physics. By performing explicit computations in various toy models, we show that quantum effects lead to violations of Lorentz invariance at the level of operators of dimension three or four. The resulting constraints are very stringent.Comment: Correction of an error in the U(1) and U(N) calculation leads to stronger limits than those given previously Clarifying comments and reference adde

Laboratory divergence of Methylobacterium extorquens AM1 through unintended domestication and past selection for antibiotic resistance

Background: A common assumption of microorganisms is that laboratory stocks will remain genetically and phenotypically constant over time, and across laboratories. It is becoming increasingly clear, however, that mutations can ruin strain integrity and drive the divergence or “domestication” of stocks. Since its discovery in 1960, a stock of Methylobacterium extorquens AM1 (“AM1”) has remained in the lab, propagated across numerous growth and storage conditions, researchers, and facilities. To explore the extent to which this lineage has diverged, we compared our own “Modern” stock of AM1 to a sample archived at a culture stock center shortly after the strain’s discovery. Stored as a lyophilized sample, we hypothesized that this Archival strain would better reflect the first-ever isolate of AM1 and reveal ways in which our Modern stock has changed through laboratory domestication or other means. Results: Using whole-genome re-sequencing, we identified some 29 mutations – including single nucleotide polymorphisms, small indels, the insertion of mobile elements, and the loss of roughly 36 kb of DNA - that arose in the laboratory-maintained Modern lineage. Contrary to our expectations, Modern was both slower and less fit than Archival across a variety of growth substrates, and showed no improvement during long-term growth and storage. Modern did, however, outperform Archival during growth on nutrient broth, and in resistance to rifamycin, which was selected for by researchers in the 1980s. Recapitulating selection for rifamycin resistance in replicate Archival populations showed that mutations to RNA polymerase B (rpoB) substantially decrease growth in the absence of antibiotic, offering an explanation for slower growth in Modern stocks. Given the large number of genomic changes arising from domestication (28), it is somewhat surprising that the single other mutation attributed to purposeful laboratory selection accounts for much of the phenotypic divergence between strains. Conclusions: These results highlight the surprising degree to which AM1 has diverged through a combination of unintended laboratory domestication and purposeful selection for rifamycin resistance. Instances of strain divergence are important, not only to ensure consistency of experimental results, but also to explore how microbes in the lab diverge from one another and from their wild counterparts