Resolving "dirty" effects around black holes by decoupling the Teukolsky equation

Detecting the environment around the supermassive black holes and tests of general relativity are important applications of extreme-mass-ratio inspirals (EMRIs). There is still a challenge to efficiently describe various "dirty" impacts on the inspirals like dark matter, gas, dipole radiation, electromagnetic interaction, and so on. In this Letter, we find the inherent linearity of the asymptotic solution of the inhomogeneous Teukolsky equation. Based on this property, we completely decouple the factors of the perturber and the background spacetime in the energy fluxes and waveforms. With the new decoupling form, the waveforms of EMRIs with non-geodesic motion in Kerr spacetime can be calculated conveniently. This will help to resolve the environment (including gas, field, dark matter, electromagnetic interaction, etc.) around the supermassive black holes and test general relativity.Comment: 6 pages + supplementary materials, 4 figure

Kidins220 and tumour development: Insights into a complexity of cross-talk among signalling pathways (Review)

The mechanistic complexes of kinase D-interacting substrate of 220 kDa/ankyrin repeat-rich membrane spanning (Kidins220/ARMS) bind and integrate a variety of cellular cues to mediate neuronal activities such as neuronal differentiation, survival, and cytoskeleton remodelling by interacting with a variety of binding partners. Accumulated evidence has also indicated its role in the regulation of vascular development. Mice with Kidins220 knockdown phenotypically present with cardiovascular abnormalities. Kidins220 also contributes to immunomodulation in combination with B cells and T cells. Moreover, emerging evidence has revealed that this protein regulates many crucial cellular processes and thus has been implicated in an increasing number of malignancies. Here, we review recent advances in our understanding of Kidins220 and its role in cancer development. Further investigation is warranted to shed light on the role played by Kidins220 in the dynamic arrangement of the cytoskeleton and epithelial–mesenchymal transition, and its implication in tumourigenesis and cancer progression

Clinical and therapeutic implications of follistatin in solid tumours

Follistatin (FST), as a single-chain glycosylated protein, has two major isoforms, FST288 and FST315. The FST315 isoform is the predominant form whilst the FST288 variant accounts for less than 5% of the encoded mRNA. FST is differentially expressed in human tissues and aberrant expression has been observed in a variety of solid tumours, including gonadal, gastric and lung cancer, hepatocellular carcinoma, basal cell carcinoma and melanoma. Based on the current evidence, FST is an antagonist of transforming growth factor beta family members, such as activin and bone morphogenetic proteins (BMPs). FST plays a role in tumourigenesis, metastasis and angiogenesis of solid tumours through its interaction with activin and BMPs, thus resulting in pathophysiological function. In terms of diagnosis, prognosis and therapy FST has shown strong promise. Through a better understanding of its biological functions, potential clinical applications may yet emerge

Total Nuclear Reaction Cross Section Induced by Halo Nuclei and Stable Nuclei

We develop the method for the calculation of the total reaction cross sections induced by the halo nuclei and stable nuclei. This approach is based on the Glauber theory, which is valid for nuclear reactions at high energy. It is extended for nuclear reactions at low energy and intermediate energy by including both the quantum correction and Coulomb correction under the assumption of the effective nuclear density distribution. The calculated results of the total reaction cross section induced by stable nuclei agree well with the 30 experimental data within 10 percent accuracy.The comparison between the numerical results and the 20 experimental data for the total nuclear reaction cross section induced by the neutron halo nuclei and the proton halo nuclei indicates a satisfactory agreement after considering the halo structure of these nuclei, which implies the quite different mean fields for the nuclear reactions induced by halo nuclei and stable nuclei. The halo nucleon distributions and the root mean square radii of these nuclei can be extracted from above comparison based on the improved Glauber model, which indicate clearly the halo structures of these nuclei. Especially, it is clear to see that the medium correction of the nucleon-nucleon collision has little effect on the total reaction cross sections induced by the halo nuclei due to the very weak binding and the very extended density distribution.Comment: 15 pages,2 figures. Communucations in Theoretical Physics, (2003) in pres

Bone morphogenetic proteins in tumour associated angiogenesis and implication in cancer therapies

Bone morphogenetic protein (BMP) belongs to transforming growth factor-β superfamily. To date, more than 20 BMPs have been identified in humans. BMPs play a critical role in embryonic and postnatal development, and also in maintaining homeostasis in different organs and tissues by regulating cell differentiation, proliferation, survival and motility. They play important roles in the development and progression of certain malignancies, including prostate cancer, breast cancer, lung cancer, etc. Recently, more evidence shows that BMPs are also involved in tumour associated angiogenesis. For example BMP can either directly regulate the functions of vascular endothelial cells or indirectly influence the angiogenesis via regulation of angiogenic factors, such as vascular endothelial growth factor (VEGF). Such crosstalk can also be reflected in the interaction with other angiogenic factors, like hepatocyte growth factor (HGF) and basic fibroblast growth factor (bFGF). All these factors are involved in the orchestration of the angiogenic process during tumour development and progression. Review of the relevant studies will provide a comprehensive prospective on current understanding and shed light on the corresponding therapeutic opportunity

Dual roles of protein tyrosine phosphatase kappa in coordinating angiogenesis induced by pro-angiogenic factors

A potential role may be played by receptor-type protein tyrosine phosphatase kappa (PTPRK) in angiogenesis due to its critical function in coordinating intracellular signal transduction from various receptors reliant on tyrosine phosphorylation. In the present study, we investigated the involvement of PTPRK in the cellular functions of vascular endothelial cells (HECV) and its role in angiogenesis using in vitro assays and a PTPRK knockdown vascular endothelial cell model. PTPRK knockdown in HECV cells (HECVPTPRKkd) resulted in a decrease of cell proliferation and cell-matrix adhesion; however, increased cell spreading and motility were seen. Reduced focal adhesion kinase (FAK) and paxillin protein levels were seen in the PTPRK knockdown cells which may contribute to the inhibitory effect on adhesion. HECVPTPRKkd cells were more responsive to the treatment of fibroblast growth factor (FGF) in their migration compared with the untreated control and cells treated with VEGF. Moreover, elevated c-Src and Akt1 were seen in the PTPRK knockdown cells. The FGF-promoted cell migration was remarkably suppressed by an addition of PLCγ inhibitor compared with other small inhibitors. Knockdown of PTPRK suppressed the ability of HECV cells to form tubules and also impaired the tubule formation that was induced by FGF and conditioned medium of cancer cells. Taken together, it suggests that PTPRK plays dual roles in coordinating angiogenesis. It plays a positive role in cell proliferation, adhesion and tubule formation, but suppresses cell migration, in particular, the FGF-promoted migration. PTPRK bears potential to be targeted for the prevention of tumour associated angiogenesis

Mutual Composite Fermion and composite Boson approaches to balanced and imbalanced bilayer quantum Hall system: an electronic analogy of the Helium 4 system

We use both Mutual Composite Fermion (MCF) and Composite Boson (CB) approach to study balanced and im-balanced Bi-Layer Quantum Hall systems (BLQH) and make critical comparisons between the two approaches. We find the CB approach is superior to the MCF approach in studying ground states with different kinds of broken symmetries. In the phase representation of the CB theory, we first study the Excitonic superfluid state (ESF). The theory puts spin and charge degree freedoms in the same footing, explicitly bring out the spin-charge connection and classify all the possible excitations in a systematic way. Then in the dual density representation of the CB theory, we study possible intermediate phases as the distance increases. We propose there are two critical distances $d_{c1} < d_{c2}$ and three phases as the distance increases. When $0 < d < d_{c1}$, the system is in the ESF state which breaks the internal $U(1)$ symmetry, when $d_{c1} < d < d_{c2}$, the system is in an Pseudo-spin density wave (PSDW) state which breaks the translational symmetry, there is a first order transition at $d_{c1}$ driven by the collapsing of magneto-roton minimum at a finite wavevector in the pseudo-spin channel. When $d_{c2} < d < \infty$, the system becomes two weakly coupled $\nu =1/2$ Composite Fermion Fermi Liquid (FL) state. There is also a first order transition at $d= d_{c2}$. We construct a quantum Ginzburg Landau action to describe the transition from ESF to PSDW which break the two completely different symmetries. By using the QGL action, we explicitly show that the PSDW takes a square lattice and analyze in detail the properties of the PSDW at zero and finite temperature.Comment: 29 PRB pages, 18 figures, 2 tables, REVTEX

Bone morphogenetic proteins, breast cancer, and bone metastases: striking the right balance

Bone morphogenetic proteins (BMPs) belong to the TGF-β super family, and are essential for regulation of foetal development, tissue differentiation and homeostasis, and a multitude of cellular functions. Naturally, this has led to the exploration of aberrance in this highly regulated system as a key factor in tumourigenesis. Originally identified for their role in osteogenesis and bone turnover, attention has been turned to the potential role of BMPs in tumour metastases to, and progression within, the bone niche. This is particularly pertinent to breast cancer, which commonly metastasises to bone, and in which studies have revealed aberrations of both BMP expression and signalling which correlate clinically with breast cancer progression. Ultimately a BMP profile could provide new prognostic disease markers. As the evidence suggests a role for BMPs in regulating breast tumour cellular function, in particular interactions with tumour stroma and the bone metastatic microenvironment, there may be novel therapeutic potential in targeting BMP signalling in breast cancer. This review provides an update on the current knowledge of BMP abnormalities and their implication in the development and progression of breast cancer, particularly in the disease specific bone metastasis

Key factors in breast cancer dissemination and establishment at the bone: past, present and future perspectives

Bone metastases associated with breast cancer remain a clinical challenge due to their associated morbidity, limited therapeutic intervention and lack of prognostic markers. With a continually evolving understanding of bone biology and its dynamic microenvironment, many potential new targets have been proposed. In this chapter, we discuss the roles of well-established bone markers and how their targeting, in addition to tumour-targeted therapies, might help in the prevention and treatment of bone metastases. There are a vast number of bone markers, of which one of the best-known families is the bone morphogenetic proteins (BMPs). This chapter focuses on their role in breast cancer-associated bone metastases, associated signalling pathways and the possibilities for potential therapeutic intervention. In addition, this chapter provides an update on the role receptor activator of nuclear factor-κB (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) play on breast cancer development and their subsequent influence during the homing and establishment of breast cancer-associated bone metastases. Beyond the well-established bone molecules, this chapter also explores the role of other potential factors such as activated leukocyte cell adhesion molecule (ALCAM) and its potential impact on breast cancer cells’ affinity for the bone environment, which implies that ALCAM could be a promising therapeutic target