Self-consistent picture of the mass ejection from a one second-long binary neutron star merger leaving a short-lived remnant in general-relativistic neutrino-radiation magnetohydrodynamic simulation

We perform a general-relativistic neutrino-radiation magnetohydrodynamicsimulation of a one second-long binary neutron star merger on Japanesesupercomputer Fugaku using about $72$ million CPU hours with $20,736$ CPUs. Weconsider an asymmetric binary neutron star merger with masses of $1.2$ and$1.5M_\odot$ and a `soft' equation of state SFHo. It results in a short-livedremnant with the lifetime of $\approx 0.017$\,s, and subsequent massive torusformation with the mass of $\approx 0.05M_\odot$ after the remnant collapses toa black hole. For the first time, we confirm that after the dynamical massejection, which drives the fast tail and mildly relativistic components, thepost-merger mass ejection from the massive torus takes place due to themagnetorotational instability-driven turbulent viscosity and the two ejectacomponents are seen in the distributions of the electron fraction and velocitywith distinct features.<br

General-relativistic neutrino-radiation magnetohydrodynamics simulation of black hole-neutron star mergers for seconds

Seconds-long numerical-relativity simulations for black hole-neutron star mergers are performed for the first time to obtain a self-consistent picture of the merger and post-merger evolution processes. To investigate the case that tidal disruption takes place, we choose the initial mass of the black hole to be $5.4M_\odot$ or $8.1M_\odot$ with the dimensionless spin of 0.75. The neutron-star mass is fixed to be $1.35M_\odot$. We find that after the tidal disruption, dynamical mass ejection takes place spending $\lesssim 10\,{\rm ms}$ together with the formation of a massive accretion disk. Subsequently, the magnetic field in the disk is amplified by the magnetic winding and magnetorotational instability, establishing a turbulent state and inducing the angular momentum transport. The post-merger mass ejection by the magnetically-induced viscous effect sets in at $\sim 300$-$500\,{\rm ms}$ after the tidal disruption, at which the neutrino luminosity drops below $\sim 10^{51.5}\,{\rm erg/s}$, and continues for several hundreds ms. A magnetosphere near the rotational axis of the black hole is developed after the matter and magnetic flux fall into the black hole from the accretion disk, and high-intensity Poynting flux generation sets in at a few hundreds ms after the tidal disruption. The intensity of the Poynting flux becomes low after the significant post-merger mass ejection, because the opening angle of the magnetosphere increases. The lifetime for the stage with the strong Poynting flux is $1$-$2\,{\rm s}$, which agrees with the typical duration of short-hard gamma-ray bursts

Study of double pion photoproduction on the deuteron

AbstractThe π+π− photoproductions on the proton and deuteron have been studied in a photon energy range of 0.8–1.1 GeV at the Laboratory of Nuclear Science, Tohoku University. Charged pions and protons were detected using Neutral Kaon Spectrometer. We obtained the cross sections for the p(γ,pπ+π−) and d(γ,pπ+π−)n. The quasi-free process with a neutron spectator was extracted by the neutron momentum cut of pn>0.3 GeV/c. The cross section for the Δ++Δ− production was deduced in the non-quasi-free process of the γd→pnπ+π−. It was 13.4±0.4 μb at Eγ=0.82 GeV

In Vivo Imaging of HIF-Active Tumors by an Oxygen-Dependent Degradation Protein Probe with an Interchangeable Labeling System

Hypoxia-inducible factor (HIF) functions as a master transcriptional regulator for adaptation to hypoxia by inducing adaptive changes in gene expression for regulation of proliferation, angiogenesis, apoptosis and energy metabolism. Cancers with high expression of the alpha subunit of HIF (HIFα) are often malignant and treatment-resistant. Therefore, the development of a molecular probe that can detect HIF activity has great potential value for monitoring tumor hypoxia. HIF prolyl hydroxylases (HPHDs) act as oxygen sensors that regulate the fate of HIFα protein through its oxygen-dependent degradation (ODD) domain. We constructed a recombinant protein PTD-ODD-HaloTag (POH) that is under the same ODD regulation as HIFα and contains protein transduction domain (PTD) and an interchangeable labeling system. Administration of near-infrared fluorescently labeled POH (POH-N) to mouse models of cancers allowed successful monitoring of HIF-active regions. Immunohistochemical analysis for intratumoral localization of POH probe revealed its specificity to HIF-active cells. Furthermore, lack of the PTD domain or a point mutation in the ODD domain abrogated the specificity of POH-N to HIF-active cells. Overall results indicate that POH is a practical probe specific to HIF-active cell in cancers and suggest its large potential for imaging and targeting of HIF-related diseases

Intricate macrophage-colorectal cancer cell communication in response to radiation

Both cancer and tumour-associated host cells are exposed to ionizing radiation when a tumour is subjected to radiotherapy. Macrophages frequently constitute the most abundant tumour-associated immune population, playing a role in tumour progression and response to therapy. The present work aimed to evaluate the importance of macrophage-cancer cell communication in the cellular response to radiation. To address this question, we established monocultures and indirect co-cultures of human monocyte-derived macrophages with RKO or SW1463 colorectal cancer cells, which exhibit higher and lower radiation sensitivity, respectively. Mono- and co-cultures were then irradiated with 5 cumulative doses, in a similar fractionated scheme to that used during cancer patients' treatment (2 Gy/fraction/day). Our results demonstrated that macrophages sensitize RKO to radiation-induced apoptosis, while protecting SW1463 cells. Additionally, the co-culture with macrophages increased the mRNA expression of metabolism- and survival-related genes more in SW1463 than in RKO. The presence of macrophages also upregulated glucose transporter 1 expression in irradiated SW1463, but not in RKO cells. In addition, the influence of cancer cells on the expression of pro- and anti-inflammatory macrophage markers, upon radiation exposure, was also evaluated. In the presence of RKO or SW1463, irradiated macrophages exhibit higher levels of pro-inflammatory TNF, IL6, CCL2 and CCR7, and of anti-inflammatory CCL18. However, RKO cells induce an increase of macrophage pro-inflammatory IL1B, while SW1463 cells promote higher pro-inflammatory CXCL8 and CD80, and also anti-inflammatory VCAN and IL10 levels. Thus, our data demonstrated that macrophages and cancer cells mutually influence their response to radiation. Notably, conditioned medium from irradiated co-cultures increased non-irradiated RKO cell migration and invasion and did not impact on angiogenesis in a chicken embryo chorioallantoic membrane assay. Overall, the establishment of primary human macrophage-cancer cell co-cultures revealed an intricate cell communication in response to ionizing radiation, which should be considered when developing therapies adjuvant to radiotherapy