Bounds on negative energy densities in flat spacetime

We generalise results of Ford and Roman which place lower bounds -- known as quantum inequalities -- on the renormalised energy density of a quantum field averaged against a choice of sampling function. Ford and Roman derived their results for a specific non-compactly supported sampling function; here we use a different argument to obtain quantum inequalities for a class of smooth, even and non-negative sampling functions which are either compactly supported or decay rapidly at infinity. Our results hold in $d$-dimensional Minkowski space ($d\ge 2$) for the free real scalar field of mass $m\ge 0$. We discuss various features of our bounds in 2 and 4 dimensions. In particular, for massless field theory in 2-dimensional Minkowski space, we show that our quantum inequality is weaker than Flanagan's optimal bound by a factor of 3/2.Comment: REVTeX, 13 pages and 2 figures. Minor typos corrected, one reference adde

Quantum Inequalities on the Energy Density in Static Robertson-Walker Spacetimes

Quantum inequality restrictions on the stress-energy tensor for negative energy are developed for three and four-dimensional static spacetimes. We derive a general inequality in terms of a sum of mode functions which constrains the magnitude and duration of negative energy seen by an observer at rest in a static spacetime. This inequality is evaluated explicitly for a minimally coupled scalar field in three and four-dimensional static Robertson-Walker universes. In the limit of vanishing curvature, the flat spacetime inequalities are recovered. More generally, these inequalities contain the effects of spacetime curvature. In the limit of short sampling times, they take the flat space form plus subdominant curvature-dependent corrections.Comment: 18 pages, plain LATEX, with 3 figures, uses eps

Post-traumatic stress during pregnancy and the postpartum period

Research on PTSD in pregnancy and postpartum is relatively new but clearly demonstrates the importance of recognising and treating women with PTSD at this time. Women with PTSD in pregnancy are at greater risk of pregnancy complications and health behaviours that have a negative impact on the woman and fetus. In addition, approximately 1 to 3% of women develop PTSD as a direct response to the events of birth; and rates are increased in high risk groups such as women who have preterm or stillborn infants or life-threatening complications during pregnancy or labour. Models of the etiology of postpartum PTSD focus on the interaction between individual vulnerability, risk, and protective factors during and after birth. To date, there is strongest evidence for the role of previous psychiatric problems, a history of trauma, severe complications during birth, support, and women’s subjective experience of birth in postpartum PTSD. Very little research has examined screening or intervention, although intervention is possible at many levels. Midwife debriefing is commonly provided in the UK but there is inconsistent evidence of its efficacy. Further research is therefore desperately needed and we highlight key research topics that need addressing

Gene expression patterns following unilateral traumatic brain injury reveals a local pro-inflammatory and remote anti-inflammatory response.

BackgroundTraumatic brain injury (TBI) results in irreversible damage at the site of impact and initiates cellular and molecular processes that lead to secondary neural injury in the surrounding tissue. We used microarray analysis to determine which genes, pathways and networks were significantly altered using a rat model of TBI. Adult rats received a unilateral controlled cortical impact (CCI) and were sacrificed 24 h post-injury. The ipsilateral hemi-brain tissue at the site of the injury, the corresponding contralateral hemi-brain tissue, and naïve (control) brain tissue were used for microarray analysis. Ingenuity Pathway Analysis (IPA) software was used to identify molecular pathways and networks that were associated with the altered gene expression in brain tissues following TBI.ResultsInspection of the top fifteen biological functions in IPA associated with TBI in the ipsilateral tissues revealed that all had an inflammatory component. IPA analysis also indicated that inflammatory genes were altered on the contralateral side, but many of the genes were inversely expressed compared to the ipsilateral side. The contralateral gene expression pattern suggests a remote anti-inflammatory molecular response. We created a network of the inversely expressed common (i.e., same gene changed on both sides of the brain) inflammatory response (IR) genes and those IR genes included in pathways and networks identified by IPA that changed on only one side. We ranked the genes by the number of direct connections each had in the network, creating a gene interaction hierarchy (GIH). Two well characterized signaling pathways, toll-like receptor/NF-kappaB signaling and JAK/STAT signaling, were prominent in our GIH.ConclusionsBioinformatic analysis of microarray data following TBI identified key molecular pathways and networks associated with neural injury following TBI. The GIH created here provides a starting point for investigating therapeutic targets in a ranked order that is somewhat different than what has been presented previously. In addition to being a vehicle for identifying potential targets for post-TBI therapeutic strategies, our findings can also provide a context for evaluating the potential of therapeutic agents currently in development

Quantum Inequalities and Singular Energy Densities

There has been much recent work on quantum inequalities to constrain negative energy. These are uncertainty principle-type restrictions on the magnitude and duration of negative energy densities or fluxes. We consider several examples of apparent failures of the quantum inequalities, which involve passage of an observer through regions where the negative energy density becomes singular. We argue that this type of situation requires one to formulate quantum inequalities using sampling functions with compact support. We discuss such inequalities, and argue that they remain valid even in the presence of singular energy densities.Comment: 18 pages, LaTex, 2 figures, uses eps

Restrictions on Negative Energy Density in Flat Spacetime

In a previous paper, a bound on the negative energy density seen by an arbitrary inertial observer was derived for the free massless, quantized scalar field in four-dimensional Minkowski spacetime. This constraint has the form of an uncertainty principle-type limitation on the magnitude and duration of the negative energy density. That result was obtained after a somewhat complicated analysis. The goal of the current paper is to present a much simpler method for obtaining such constraints. Similar ``quantum inequality'' bounds on negative energy density are derived for the electromagnetic field, and for the massive scalar field in both two and four-dimensional Minkowski spacetime.Comment: 17 pages, including two figures, uses epsf, minor revisions in the Introduction, conclusions unchange

A Search for Hard X-Ray Emission from Globular Clusters - Constraints from BATSE

We have monitored a sample of 27 nearby globular clusters in the hard X-ray band (20-120 keV) for approximately 1400 days using the BATSE instrument on board the Compton Gamma-Ray Observatory. Globular clusters may contain a large number of compact objects (e.g., pulsars or X-ray binaries containing neutron stars) which can produce hard X-ray emission. Our search provides a sensitive (~50 mCrab) monitor for hard X-ray transient events on time scales of >1 day and a means for observing persistent hard X-ray emission. We have discovered no transient events from any of the clusters and no persistent emission. Our observations include a sensitive search of four nearby clusters containing dim X-ray sources: 47 Tucanae, NGC 5139, NGC 6397, and NGC 6752. The non-detection in these clusters implies a lower limit for the recurrence time of transients of 2 to 6 years for events with luminosities >10^36 erg s^-1 (20-120 keV) and ~20 years if the sources in these clusters are taken collectively. This suggests that the dim X-ray sources in these clusters are not transients similar to Aql~X-1. We also place upper limits on the persistent emission in the range 2-10*10^34 erg s^-1 (2 sigma, 20-120 keV) for these four clusters. For 47 Tuc the upper limit is more sensitive than previous measurements by a factor of 3. We find a model dependent upper limit of 19 isolated millisecond pulsars (MSPs) producing gamma-rays in 47 Tuc, compared to the 11 observed radio MSPs in this cluster.Comment: 20 pages; accepted, ApJ; uu encoded tar file; 7 figure