139 research outputs found

    The g-mode Excitation in the Proto Neutron Star by the Standing Accretion Shock Instability

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    The so-called "acoustic revival mechanism" of core-collapse supernova proposed recently by the Arizona group is an interesting new possibility. Aiming to understand the elementary processes involved in the mechanism, we have calculated the eigen frequencies and eigen functions for the g-mode oscillations of a non-rotating proto neutron star. The possible excitation of these modes by the standing accretion shock instability, or SASI, is discussed based on these eigen functions. We have formulated the forced oscillations of gg-modes by the external pressure perturbations exerted on the proto neutron star surface. The driving pressure fluctuations have been adopted from our previous computations of the axisymmetric SASI in the non-linear regime. We have paid particular attention to low l modes, since these are the modes that are dominant in SASI and that the Arizona group claimed played an important role in their acoustic revival scenario. Here l is the index of the spherical harmonic functions, YlmY_l^m. Although the frequency spectrum of the non-linear SASI is broadened substantially by non-linear couplings, the typical frequency is still much smaller than those of g-modes, the fact leading to a severe impedance mismatch. As a result, the excitations of various gg-modes are rather inefficient and the energy of the saturated g-modes is 1050\sim 10^{50}erg or smaller, with the g_2-mode being the largest in our model. Here the g_2-mode has two radial nodes and is confined to the interior of the convection region. The energy transfer rate from the g-modes to out-going sound waves is estimated from the growth of the g-modes and found to be 1051\sim 10^{51}erg/s in the model studied in this paper.Comment: 24 pages, 6 figure

    Crocetin reduces the oxidative stress induced reactive oxygen species in the stroke-prone spontaneously hypertensive rats (SHRSPs) brain

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    Crocetin is a natural carotenoid compound of gardenia fruits and saffron, which has various effects in biological systems. In this study, we investigated the antioxidant effects of crocetin on reactive oxygen species such as hydroxyl radical using in vitro X-band electron spin resonance and spin trapping. Crocetin significantly inhibited hydroxyl radical generation compared with the control. Moreover, we performed electron spin resonance computed tomography ex vivo with the L-band electron spin resonance imaging system and determined the electron spin resonance signal decay rate in the isolated brain of stroke-prone spontaneously hypertensive rats, a high-oxidative stress model. Crocetin significantly reduced oxidative stress in the isolated brain by acting as a scavenger of reactive oxygen species, especially hydroxyl radical, as demonstrated by in vitro and ex vivo electron spin resonance analysis. The distribution of crocetin was also determined in the plasma and the brain of stroke-prone spontaneously hypertensive rats using high-performance liquid chromatography. After oral administration, crocetin was detected at high levels in the plasma and the brain. Our results suggest that crocetin may participate in the prevention of reactive oxygen species-induced disease due to a reduction of oxidative stress induced by reactive oxygen species in the brain

    Development of Bioactivity and Pull-out Torque Control Technology on Ti Implant Surface and its Application for Cold Thread Rolled Bone Screw

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    AbstractThe influence of cold thread rolling conditions and a production method of titania (TiO2) films on surface bioactivity and pull-out torque of a titanium bone screw was investigated. The bone screw with micro surface roughness distribution was formed by cold thread rolling with a pair of parallel dies. The die shape and surface roughness distribution were changed to the 3 grades. The TiO2 films were coated on the surface of the bone screw using anodizing in aqueous solutions (hydro-coating). We introduced the rolled bone screws into tibia of rats for two weeks and examined the effects of the combinations of the surface morphology and the TiO2 film on osteoconductivity in an in-vivo experiment. As the results, it is found that we could control the bioactivity and pull-out torque by controlling the surface roughness at the bottom of the screw root

    Splicing inhibition induces gene expression through canonical NF-κB pathway and extracellular signal-related kinase activation

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    AbstractSplicing, a process for mRNA maturation, is essential for correct gene expression after transcription. However, recent studies also suggest that splicing affects transcription, but its mechanism remains elusive. We previously reported that treatment with spliceostatin A (SSA), a specific splicing inhibitor targeting the splicing factor SF3b, leads to transcriptional activation of a small subset of genes. To investigate the underlying mechanism we utilized luciferase reporters driven by the Interleukin 8 (IL-8) and cytomegalovirus (CMV) promoters, as both recruit a similar set of transcription factors. We also found that SSA treatment led to increased extracellular signal-regulated protein kinase (ERK) activity and that chemical inhibition of ERK also led to decreased promoter activation. Systematic deletion studies suggested that NF-κB activation is mainly responsible for SSA-induced promoters activation

    Hysteretic Tricolor Electrochromic Systems Based on the Dynamic Redox Properties of Unsymmetrically Substituted Dihydrophenanthrenes and Biphenyl-2,2 '-Diyl Dications: Efficient Precursor Synthesis by a Flow Microreactor Method

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    A series of biphenyl-2, 2'-diylbis(diarylmethanol)s 3, which have two kinds of aryl groups at the bay region, were efficiently obtained by integrated flow microreactor synthesis. The diols 3NO/NX are the precursors of unsymmetric biphenylic dications 2NO/NX^[2+] which are transformed into the corresponding dihydrophenanthrenes 1NO/NX via 2NO/NX^[+•] upon reduction, when they exhibit two-stage color changes. On the other hand, the steady-state concentration of the intermediate 2NO/NX^[+•] is negligible during the oxidation of 1NO/NX to 2NO/NX^[2+], which reflects unique tricolor electrochromicity with a hysteretic pattern of color change [color 1→color 2→color 3→color 1]

    Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic Aneurysms

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    Background: Abdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPAR alpha) agonist, on AAA formation and rupture. Methods: Experimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in ApoE(-)(/)(-) mice for 4 weeks. Pemafibrate (0.1 mg/kg/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS). Results: The size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-alpha in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPAR alpha significantly attenuated the anti-oxidative effect of pemafibrate. Conclusion: Pemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells

    LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats

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    Doxorubicin (DOX)-based chemotherapy induces cardiotoxicity, which is considered the main bottleneck for its clinical application. In this study, we investigated the potential benefit of LCZ696, an angiotensin receptor-neprilysin inhibitor against DOX-induced cardiotoxicity in rats and H9c2 cells and determined whether the mechanism underlying any such effects involves its antioxidant activity. Male Sprague-Dawley rats were randomly separated into four groups, each consisting of 15 rats (DOX (1.5 mg/kg/day intraperitoneally for 10 days followed by non-treatment for 8 days); DOX + valsartan (31 mg/kg/day by gavage from day 1 to day 18); DOX + LCZ696 (68 mg/kg/day by gavage from day 1 to day 18); and control (saline intraperitoneally for 10 days). DOX-induced elevation of cardiac troponin T levels on day 18 was significantly reduced by LCZ696, but not valsartan. The DOX-induced increase in myocardial reactive oxygen species (ROS) levels determined using dihydroethidium was significantly ameliorated by LCZ696, but not valsartan, and was accompanied by the suppression of DOX-induced increase in p47phox. LCZ696 recovered the DOX-induced decrease in phosphorylation of adenosine monophosphate-activated protein kinase and increased the ratio of Bax and Bcl-2. In H9c2 cardiomyocytes, LCZ696 reduced DOX-induced mitochondrial ROS generation and improved cell viability more than valsartan. Our findings indicated that LCZ696 ameliorated DOX-induced cardiotoxicity in rat hearts in vivo and in vitro, possibly by mediating a decrease in oxidative stress

    Evaluation of platelet reactivity using P2Y12 reaction units in acute coronary syndrome with essential thrombocythemia: A case report

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    AbstractEssential thrombocythemia (ET) has been reported to cause acute coronary disease. However, the efficacy of anti-platelet therapy for ET is unclear since there are individual differences in the platelet function of ET patients. Here we report a case of a 62-year-old man with ET who was admitted to our hospital because of acute coronary syndrome. He underwent coronary angioplasty. Dual anti-platelet therapy with aspirin (81mg/day) and clopidogrel (75mg/day) was subsequently initiated. We evaluated platelet reactivity in P2Y12 reaction units, and subsequently determined anti-platelet drugs and corresponding doses.<Learning objective: Essential thrombocythemia (ET) is a myeloproliferative disorder that causes acute coronary disease. As there are individual differences in the platelet function of patients with ET, the efficacy of anti-platelet therapy for these patients varies. Evaluation of platelet reactivity using P2Y12 reaction units is useful in determining appropriate anti-platelet drugs and corresponding doses.
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