Cyclic cosmology from Lagrange-multiplier modified gravity

We investigate cyclic and singularity-free evolutions in a universe governed by Lagrange-multiplier modified gravity, either in scalar-field cosmology, as well as in $f(R)$ one. In the scalar case, cyclicity can be induced by a suitably reconstructed simple potential, and the matter content of the universe can be successfully incorporated. In the case of $f(R)$-gravity, cyclicity can be induced by a suitable reconstructed second function $f_2(R)$ of a very simple form, however the matter evolution cannot be analytically handled. Furthermore, we study the evolution of cosmological perturbations for the two scenarios. For the scalar case the system possesses no wavelike modes due to a dust-like sound speed, while for the $f(R)$ case there exist an oscillation mode of perturbations which indicates a dynamical degree of freedom. Both scenarios allow for stable parameter spaces of cosmological perturbations through the bouncing point.Comment: 8 pages, 3 figures, references added, accepted for publicatio

Shortcuts through Colocation Facilities

Network overlays, running on top of the existing Internet substrate, are of perennial value to Internet end-users in the context of, e.g., real-time applications. Such overlays can employ traffic relays to yield path latencies lower than the direct paths, a phenomenon known as Triangle Inequality Violation (TIV). Past studies identify the opportunities of reducing latency using TIVs. However, they do not investigate the gains of strategically selecting relays in Colocation Facilities (Colos). In this work, we answer the following questions: (i) how Colo-hosted relays compare with other relays as well as with the direct Internet, in terms of latency (RTT) reductions; (ii) what are the best locations for placing the relays to yield these reductions. To this end, we conduct a large-scale one-month measurement of inter-domain paths between RIPE Atlas (RA) nodes as endpoints, located at eyeball networks. We employ as relays Planetlab nodes, other RA nodes, and machines in Colos. We examine the RTTs of the overlay paths obtained via the selected relays, as well as the direct paths. We find that Colo-based relays perform the best and can achieve latency reductions against direct paths, ranging from a few to 100s of milliseconds, in 76% of the total cases; 75% (58% of total cases) of these reductions require only 10 relays in 6 large Colos.Comment: In Proceedings of the ACM Internet Measurement Conference (IMC '17), London, GB, 201

Heterodimerization of apelin receptor and neurotensin receptor 1 induces phosphorylation of ERK1/2 and cell proliferation via Gαq-mediated mechanism

Dimerization of G protein-coupled receptors (GPCRs) is crucial for receptor function including agonist affinity, efficacy, trafficking and specificity of signal transduction, including G protein coupling. Emerging data suggest that the cardiovascular system is the main target of apelin, which exerts an overall neuroprotective role, and is a positive regulator of angiotensin-converting enzyme 2 (ACE2) in heart failure. Moreover, ACE2 cleaves off C-terminal residues of vasoactive peptides including apelin-13, and neurotensin that activate the apelin receptor (APJ) and neurotensin receptor 1 (NTSR1) respectively, that belong to the A class of GPCRs. Therefore, based on the similar mode of modification by ACE2 at peptide level, the homology at amino acid level and the capability of forming dimers with other GPCRs, we have been suggested that APJ and NTSR1 can form a functional heterodimer. Using co-immunoprecipitation, BRET and FRET, we provided conclusive evidence of heterodimerization between APJ and NTSR1 in a constitutive and induced form. Upon agonist stimulation, hetrodimerization enhanced ERK1/2 activation and increased proliferation via activation of Gq α-subunits. These novel data provide evidence for a physiological role of APJ/NTSR1 heterodimers in terms of ERK1/2 activation and increased intracellular calcium and induced cell proliferation and provide potential new pharmaceutical targets for cardiovascular disease. © 2014 The Authors