Resonantly enhanced and diminished strong-field gravitational-wave fluxes

The inspiral of a stellar mass ($1 - 100\,M_\odot$) compact body into a massive ($10^5 - 10^7\,M_\odot$) black hole has been a focus of much effort, both for the promise of such systems as astrophysical sources of gravitational waves, and because they are a clean limit of the general relativistic two-body problem. Our understanding of this problem has advanced significantly in recent years, with much progress in modeling the "self force" arising from the small body's interaction with its own spacetime deformation. Recent work has shown that this self interaction is especially interesting when the frequencies associated with the orbit's $\theta$ and $r$ motions are in an integer ratio: $\Omega_\theta/\Omega_r = \beta_\theta/\beta_r$, with $\beta_\theta$ and $\beta_r$ both integers. In this paper, we show that key aspects of the self interaction for such "resonant" orbits can be understood with a relatively simple Teukolsky-equation-based calculation of gravitational-wave fluxes. We show that fluxes from resonant orbits depend on the relative phase of radial and angular motions. The purpose of this paper is to illustrate in simple terms how this phase dependence arises using tools that are good for strong-field orbits, and to present a first study of how strongly the fluxes vary as a function of this phase and other orbital parameters. Future work will use the full dissipative self force to examine resonant and near resonant strong-field effects in greater depth, which will be needed to characterize how a binary evolves through orbital resonances.Comment: 25 pages, 6 figures, 4 tables. Accepted to Phys Rev D; accepted version posted here, including referee feedback and other useful comment

Functional interaction between BMPR-II and Tctex-1, a light chain of Dynein, is isoform-specific and disrupted by mutations underlying primary pulmonary hypertension

Diverse heterozygous mutations of bone morphogenetic receptor type II (BMPR-II) underlie the inherited form of the vascular disorder primary pulmonary hypertension (PPH). As yet, the molecular detail of how such defects contribute to the pathogenesis of PPH remains unclear. BMPR-II is a member of the transforming growth factor-beta cell signalling superfamily. Ligand binding induces cell surface receptor complex formation and activates a cascade of phosphorylation events of intracellular intermediaries termed Smads, which initiate transcriptional regulation. Some 30% of PPH-causing mutations localize to exon 12, which may be spliced out forming an isoform depleted of the unusually long BMPR-II cytoplasmic tail. To further elucidate the consequences of BMPR2 mutation, we sought to characterize aspects of the cytoplasmic domain function by seeking intracellular binding partners. We now report that Tctex-1, a light chain of the motor complex dynein, interacts with the cytoplasmic domain of BMPR-II and demonstrate that Tctex-1 is phosphorylated by BMPR-II, a function disrupted by PPH disease causing mutations within exon 12. Finally we show that BMPR-II and Tctex-1 co-localize to endothelium and smooth muscle within the media of pulmonary arterioles, key sites of vascular remodelling in PPH. Taken together, these data demonstrate a discrete function for the cytoplasmic domain of BMPR-II and justify further investigation of whether the interaction with and phosphorylation of Tctex-1 contributes to the pathogenesis of PPH

Loss-of-function analysis of EphA receptors in retinotectal mapping

Peer reviewedPublisher PD

Gravitational radiation reaction and inspiral waveforms in the adiabatic limit

We describe progress evolving an important limit of binary orbits in general relativity, that of a stellar mass compact object gradually spiraling into a much larger, massive black hole. These systems are of great interest for gravitational wave observations. We have developed tools to compute for the first time the radiated fluxes of energy and angular momentum, as well as instantaneous snapshot waveforms, for generic geodesic orbits. For special classes of orbits, we compute the orbital evolution and waveforms for the complete inspiral by imposing global conservation of energy and angular momentum. For fully generic orbits, inspirals and waveforms can be obtained by augmenting our approach with a prescription for the self force in the adiabatic limit derived by Mino. The resulting waveforms should be sufficiently accurate to be used in future gravitational-wave searches.Comment: Accepted for publication in Phys. Rev. Let

Identification of a non-purple tartrate-resistant acid phosphatase: an evolutionary link to Ser/Thr protein phosphatases?

BACKGROUND Tartrate-resistant acid phosphatases (TRAcPs), also known as purple acid phosphatases (PAPs), are a family of binuclear metallohydrolases that have been identified in plants, animals and fungi. The human enzyme is a major histochemical marker for the diagnosis of bone-related diseases. TRAcPs can occur as a small form possessing only the ~35 kDa catalytic domain, or a larger ~55 kDa form possessing both a catalytic domain and an additional N-terminal domain of unknown function. Due to its role in bone resorption the 35 kDa TRAcP has become a promising target for the development of anti-osteoporotic chemotherapeutics. FINDINGS A new human gene product encoding a metallohydrolase distantly related to the ~55 kDa plant TRAcP was identified and characterised. The gene product is found in a number of animal species, and is present in all tissues sampled by the RIKEN mouse transcriptome project. Construction of a homology model illustrated that six of the seven metal-coordinating ligands in the active site are identical to that observed in the TRAcP family. However, the tyrosine ligand associated with the charge transfer transition and purple color of TRAcPs is replaced by a histidine. CONCLUSION The gene product identified here may represent an evolutionary link between TRAcPs and Ser/Thr protein phosphatases. Its biological function is currently unknown but is unlikely to be associated with bone metabolism.This work was funded by the Royal Society of Tropical Medicine and Hygiene through a Dennis Burkitt Fellowship to JJM. ARD is supported by the Economic and Social Research Council. JJM is supported by a Wellcome Trust Research Training Fellowship (GR074833MA)