The collimation of relativistic jets in post-neutron star binary merger simulations

The gravitational waves from the binary neutron star merger GW170817 were accompanied by a multi-wavelength electromagnetic counterpart, which confirms the association of the merger with a short gamma-ray burst (sGRB). The afterglow observations implied that the event was accompanied by a narrow, $\sim 5~$deg, and powerful, $\sim 10^{50}$ erg, jet. We study the propagation of a Poynting flux-dominated jet within the merger ejecta (kinematic, neutrino-driven and MRI turbulence-driven) of a neutrino-radiation-GR-MHD simulation of two coalescing neutron stars. We find that the presence of a post-merger low-density/low-pressure polar cavity, that arose due to angular momentum conservation, is crucial to let the jet break out. At the same time the ejecta collimates the jet to a narrow opening angle. The collimated jet has a narrow opening angle of $\sim 4$-$7$ deg and an energy of $10^{49}$-$10^{50}~$erg, in line with the observations of GW170817 and other sGRBs.Comment: 10 pages, 5 figures, 2 tables, accepted to ApJ Letter

Involvement of 4-hydroxy-2-nonenal Accumulation in Multiple System Atrophy

Recent studies have suggested implications for α-synuclein cytotoxicity in the pathomechanism of multiple system atrophy (MSA). Given in vitro evidence that α-synuclein generates oxidative stress, it is proposed that lipid peroxidation may be accelerated in MSA. To address this issue, we performed an immunohistochemical analysis of protein-bound 4-hydroxy-2-nonenal (P-HNE) in sections of archival, formalin-fixed, paraffin-embedded pontine materials of eight sporadic MSA patients and eight age-matched control subjects. In the MSA cases, P-HNE immunoreactivity was localized in all of the neuronal cytoplasmic inclusions and glial cytoplasmic inclusions, both of them identified with α-synuclein and ubiquitin. It was also detectable in reactive astrocytes and phagocytic microglia but undetectable in activated microglia. By contrast, P-HNE immunoreactivity in the control cases was only very weak or not at all in the parenchyma including neurons and glia. The present results provide in vivo evidence that HNE participates in α-synuclein-induced cytotoxicity and neuroinflammation in MSA

Numerical Examination of the Stability of an Exact Two-dimensional Solution for Flux Pile-up Magnetic Reconnection

The Kelvin--Helmholtz (KH) and tearing instabilities are likely to be important for the process of fast magnetic reconnection that is believed to explain the observed explosive energy release in solar flares. Theoretical studies of the instabilities, however, typically invoke simplified initial magnetic and velocity fields that are not solutions of the governing magnetohydrodynamic (MHD) equations. In the present study, the stability of a reconnecting current sheet is examined using a class of exact global MHD solutions for steady state incompressible magnetic reconnection, discovered by Craig & Henton. Numerical simulation indicates that the outflow solutions where the current sheet is formed by strong shearing flows are subject to the KH instability. The inflow solutions where the current sheet is formed by a fast and weakly sheared inflow are shown to be tearing unstable. Although the observed instability of the solutions can be interpreted qualitatively by applying standard linear results for the KH and tearing instabilities, the magnetic field and plasma flow, specified by the Craig--Henton solution, lead to the stabilization of the current sheet in some cases. The sensitivity of the instability growth rate to the global geometry of magnetic reconnection may help in solving the trigger problem in solar flare research.Comment: Accepted for publication in ApJ. Associated movie files and a PDF with high-resolution figures are available at http://www.pha.jhu.edu/~shirose/Craig

Ultrafast single-molecule imaging reveals focal adhesion nano-architecture and molecular dynamics

細胞膜上の分子がバレエの群舞のように見えてきた： 1蛍光分子の感度で、究極速度で撮像できるカメラを開発. 京都大学プレスリリース. 2023-06-06.Using our newly developed ultrafast camera described in the companion paper, we reduced the data acquisition periods required for photoactivation/photoconversion localization microscopy (PALM, using mEos3.2) and direct stochastic reconstruction microscopy (dSTORM, using HMSiR) by a factor of ≈30 compared with standard methods, for much greater view-fields, with localization precisions of 29 and 19 nm, respectively, thus opening up previously inaccessible spatiotemporal scales to cell biology research. Simultaneous two-color PALM-dSTORM and PALM-ultrafast (10 kHz) single fluorescent-molecule imaging-tracking has been realized. They revealed the dynamic nanoorganization of the focal adhesion (FA), leading to the compartmentalized archipelago FA model, consisting of FA-protein islands with broad diversities in size (13–100 nm; mean island diameter ≈30 nm), protein copy numbers, compositions, and stoichiometries, which dot the partitioned fluid membrane (74-nm compartments in the FA vs. 109-nm compartments outside the FA). Integrins are recruited to these islands by hop diffusion. The FA-protein islands form loose ≈320 nm clusters and function as units for recruiting FA proteins

Pipeline scheduling with input port constraints for an FPGA-based biochemical simulator

This paper discusses design methodology of high-throughput arithmetic pipeline modules for an FPGA-based biochemical simulator. Since limitation of data-input bandwidth caused by port constraints often has a negative impact on pipeline scheduling results, we propose a priority assignment method of input data which enables efficient arithmetic pipeline scheduling under given input port constraints. Evaluation results with frequently used rate-law functions in biochemical models revealed that the proposed method achieved shorter latency compared to ASAP and ALAP scheduling with random input orders, reducing hardware costs by 17.57% and by 27.43% on average, respectively.The original publication is available at www.springerlink.co

Nicotiana benthamiana RanBP1-1 Is Involved in the Induction of Disease Resistance via Regulation of Nuclear-Cytoplasmic Transport of Small GTPase Ran

Plant cells enhance the tolerances to abiotic and biotic stresses via recognition of the stress, activation and nuclear import of signaling factors, up-regulation of defense genes, nuclear export of mRNA and translation of defense proteins. Nuclear pore-mediated transports should play critical roles in these processes, however, the regulatory mechanisms of nuclear-cytoplasmic transport during stress responses are largely unknown. In this study, a regulator of nuclear export of RNA and proteins, NbRanBP1-1 (Ran-binding protein1-1), was identified as an essential gene for the resistance of Nicotiana benthamiana to potato blight pathogen Phytophthora infestans. NbRanBP1-1-silenced plants showed delayed accumulation of capsidiol, a sesquiterpenoid phytoalexin, in response to elicitor treatment, and reduced resistance to P. infestans. Abnormal accumulation of mRNA was observed in NbRanBP1-1-silenced plants, indicating that NbRanBP1-1 is involved in the nuclear export of mRNA. In NbRanBP1-1-silenced plants, elicitor-induced expression of defense genes, NbEAS and NbWIPK, was not affected in the early stage of defense induction, but the accumulation of NbWIPK protein was reduced. Nuclear export of the small G-protein NbRan1a was activated during the induction of plant defense, whereas this process was compromised in NbRanBP1-1-silenced plants. Silencing of genes encoding the nuclear pore proteins, Nup75 and Nup160, also caused abnormal nuclear accumulation of mRNA, defects in the nuclear export of NbRan1a, and reduced production of capsidiol, resulting in decreased resistance to P. infestans. These results suggest that nuclear export of NbRan is a key event for defense induction in N. benthamiana, and both RanBP1-1 and nucleoporins play important roles in the process

Extracellular vesicles from senescent hepatic stellate cells promote cell viability of hepatoma cells through increasing EGF secretion from differentiated THP?1 cells

Since the discovery of the senescence-associated secretory phenotype, the role of senescent hepatic stellate cells (HSCs) in hepatocellular carcinoma (HCC) development has gained increasing attention. Similar to cytokines, extracellular vesicles (EVs) are essential for intercellular communication. However, the function of EVs derived from senescent HSCs in HCC progression has not been extensively studied. The aims of the present study were to characterize the EVs derived from senescent HSCs and determine their role in the tumor microenvironment. Cellular senescence was induced in human hepatic stellate cells (HHSteCs) with various concentrations of etoposide. Induction was confirmed using EdU staining and 53BP1 and p21 immunostaining. EVs were isolated by ultracentrifugation and analyzed by nanoparticle tracking analysis. Multiplex immunoassays were used to compare the levels of growth factors secreted from hepatoma cell lines and macrophage cells pretreated with EVs derived from senescent HHSteCs (senescent EVs) with those pretreated with EVs derived from normal cultured HHSteCs (normal EVs). Treatment with 25 μM etoposide for 3 days was the most effective at inducing senescence in HHSteCs. This finding was confirmed by induction of irreversible cell-cycle arrest, upregulation of 53BP1 and p21 expression, and increased SA-β-gal staining. Senescent HHSteCs released increased quantities of EV particles compared with normally cultured HHSteCs. Multiplex analysis revealed that there was no difference between hepatoma cell lines treated with normal EVs and those treated with senescent EVs in growth factor secretion. In contrast, the secretion of epidermal growth factor (EGF) was increased by macrophage cells treated with senescent EVs compared with those treated with normal EVs. Furthermore, senescent EVs did not affect the viability of hepatoma cells but increased the viability of hepatoma cells co-cultured with macrophage cells. In conclusion, the release of EVs from senescent HSCs was higher compared with normal HSCs. Furthermore, senescent EVs promoted HCC development by upregulating EGF secretion from macrophages

Dynamic Meso-Scale Anchorage of GPI-Anchored Receptors in the Plasma Membrane: Prion Protein vs. Thy1

The central mechanism for the transmission of the prion protein misfolding is the structural conversion of the normal cellular prion protein to the pathogenic misfolded prion protein, by the interaction with misfolded prion protein. This process might be enhanced due to the homo-dimerization/oligomerization of normal prion protein. However, the behaviors of normal prion protein in the plasma membrane have remained largely unknown. Here, using single fluorescent-molecule imaging, we found that both prion protein and Thy1, a control glycosylphosphatidylinositol-anchored protein, exhibited very similar intermittent transient immobilizations lasting for a few seconds within an area of 24.2 and 3.5 nm in diameter in CHO-K1 and hippocampal neurons cultured for 1- and 2-weeks, respectively. Prion protein molecules were immobile during 72% of the time, approximately 1.4× more than Thy1, due to prion protein’s higher immobilization frequency. When mobile, prion protein diffused 1.7× slower than Thy1. Prion protein’s slower diffusion might be caused by its transient interaction with other prion protein molecules, whereas its brief immobilization might be due to temporary association with prion protein clusters. Prion protein molecules might be newly recruited to prion protein clusters all the time, and simultaneously, prion protein molecules in the cluster might be departing continuously. Such dynamic interactions of normal prion protein molecules would strongly enhance the spreading of misfolded prion protein