Cosmological contribution from population III stars in ultracompact minihalos

In this work, we investigate the effect of Population~III~(Pop.~III) stars in ultracompact minihalos~(UCMHs) on the cosmic ionization history using the Planck observation data. Although high-redshift astrophysics is not understood yet, UCMHs could host the Pop.~III stars like the halos formed in the standard structure formation scenario. Such Pop.~III stars would emit ionizing photons during their main sequence and facilitate cosmic reionization in high redshifts. To study their effects on the global ionization, we model the cosmic reionization evolution based on the ``tanh"-type reionization model which is expressed by $z_{\mathrm{reio}}$ with additional two parameters characterizing the initial mass of UCMHs and the number density of UCMHs. We implement the Monte Carlo Markov Chain analysis with the latest Planck observation data for our reionization model. As the result, we found that if the UCMH initial mass is larger than $10^{8.4}\mathrm{M}_{\odot}$, the number density of UCMHs is strictly limited. Then we obtained the constraint on the amplitude of the primordial power spectrum through the constraint on the UCMH number density like $\mathcal{A}_{\zeta}\lesssim 10^{-8}$ in the scales, $k\lesssim 50\mathrm{Mpc}^{-1}$, when we assume that the standard ``tanh"-type reionization occurs by $z=3$, so that we set $z_{\mathrm{reio}}>3$.Comment: 12 pages, 7 figure

Translating nano-Hertz gravitational wave background into primordial perturbations taking account of the cosmological QCD phase transition

The evidence of the nano-Hertz stochastic gravitational wave (GW) background is reported by multiple pulsar timing array collaborations. While a prominent candidate of the origin is astrophysical from supermassive black hole binaries, alternative models involving GWs induced by primordial curvature perturbations can explain the inferred GW spectrum. Serendipitously, the nano-Hertz range coincides with the Hubble scale during the cosmological quantum chromodynamics (QCD) phase transition. The influence of the QCD phase transition can modify the spectrum of induced GWs within the nano-Hertz frequency range, necessitating careful analysis. We estimate GWs induced by power-law power spectra of primordial curvature perturbations taking account of the QCD phase transition. Then we translate the implication of the NANOGrav data into the constraint on the power spectrum of the primordial curvature perturbation, which suggests that one may miss the correct interpretation if neglecting the QCD effect. We also derive fitting formulae for their amplitude and scale dependence, helping to update the constraint in future experiments.Comment: 7 pages, 5 figure

Cbl-b regulates macrophage activation

Aging and overnutrition cause obesity in rodents and humans. It is well-known that obesity causes various diseases by producing insulin resistance (IR). Macrophages infiltrate the adipose tissue (AT) of obese individuals and cause chronic low-level inflammation associated with IR. Macrophage infiltration is regulated by the chemokines that are released from hypertrophied adipocytes and the immune cells in AT. Saturated fatty acids are recognized by toll-like receptor 4 (TLR4) and induce inflammatory responses in AT macrophages (ATMs). The inflammatory cytokines that are released from activated ATMs promote IR in peripheral organs, such as the liver, skeletal muscle and AT. Therefore, ATM activation is a therapeutic target for IR in obesity. The ubiquitin ligase Casitas b-lineage lymphoma-b (Cbl-b) appears to potently suppress macrophage migration and activation. Cbl-b is highly expressed in leukocytes and negatively regulates signals associated with migration and activation. Cbl-b deficiency enhances ATM accumulation and IR in aging- and diet-induced obese mice. Cbl-b inhibits migration-related signals and SFA-induced TLR4 signaling in ATMs. Thus, targeting Cbl-b may be a potential therapeutic strategy to reduce the IR induced by ATM activation. In this review, we summarize the regulatory functions of Cbl-b in ATMs

Primordial black holes and gravitational waves induced by exponential-tailed perturbations

Primordial black holes (PBHs) whose masses are in $\sim[10^{-15}M_\odot,10^{-11}M_{\odot}]$ have been extensively studied as a candidate of whole dark matter (DM). One of the probes to test such a PBH-DM scenario is scalar-induced stochastic gravitational waves (GWs) accompanied with the enhanced primordial fluctuations to form the PBHs with frequency peaked in the mHz band being targeted by the LISA mission. In order to utilize the stochastic GWs for checking the PBH-DM scenario, it needs to exactly relate the PBH abundance and the amplitude of the GWs spectrum. Recently in Kitajima et al., the impact of the non-Gaussianity of the enhanced primordial curvature perturbations on the PBH abundance has been investigated based on the peak theory, and they found that a specific non-Gaussian feature called the exponential tail significantly increases the PBH abundance compared with the Gaussian case. In this work, we investigate the spectrum of the induced stochastic GWs associated with PBH DM in the exponential-tail case. In order to take into account the non-Gaussianity properly, we employ the diagrammatic approach for the calculation of the spectrum. We find that the amplitude of the stochastic GW spectrum is slightly lower than the one for the Gaussian case, but it can still be detectable with the LISA sensitivity. We also find that the non-Gaussian contribution can appear on the high-frequency side through their complicated momentum configurations. Although this feature emerges under the LISA sensitivity, it might be possible to obtain information about the non-Gaussianity from GW observation with a deeper sensitivity such as the DECIGO mission.Comment: 33 pages, 19 figure

The repeating dislodgement of an ASO device

Transcatheter closure with an Amplatzer Septal Occluder (ASO) has become the standard treatment for secundum atrial septal defect (ASD). However, this procedure is associated with complications, such as device dislodgement. A 52-year-old woman was admitted with exertional dyspnea. Transesophageal echocardiography showed an ASD involving a 29 mm defect. Calculated Qp/Qs was 5.6 and all the rims were > 5 mm, with the exception of the posterior rim, which was 3 mm. Transcatheter ASD closure with an ASO was performed under general anesthesia. During emergence from anesthesia, tachycardia developed and the ASO device became dislodged. Hemodynamic changes associated with the end of anesthetic administration were believed to have led to device dislodgement. In a second transcatheter ASD closure, a low dose of propofol and remifentanil was maintained during emergence from anesthesia to reduce hemodynamic changes. However, device dislodgement occurred with nonsustained ventricular tachycardia. Finally, surgical ASD closure was performed. The large defect size, high Qp/Qs, and rim deficiency may have predisposed to device dislodgement after transcatheter ASD closure with ASO. The risk of device dislodgement should be considered in advance of surgery and, in high-risk cases, the patient's cardiovascular status should be closely monitored

Uncoupling protein 3 attenuates generation of reactive oxygen species by interacting with thioredoxin 2 in the mitochondrial intermembrane space

Katsuya Hirasaka1*, Edward M Mills2, Shohei Kohno1, Tomoki Abe1, Chika Ikeda1, Tasuku Maeda1, Shigetada Kondo1, Ayako Maita1, Yuushi Okumura1 and Takeshi Nikawa1 Author Affiliations 1 Department of Nutritional Physiology, Institute of Health Biosciences, University of Tokushima, Tokushima, 770-8503, Japan 2 Division of Pharmacology/Toxicology, University of Texas at Austin, Austin, TX 78712, USAPoster presentation Uncoupling protein 3 (UCP3) is primarily expressed in the inner membrane of skeletal muscle mitochondria. It has been proposed that UCP3 reduces production of reactive oxygen species (ROS) and oxidative damage. However, the mechanisms by which UCP3 attenuates ROS production are not well understood. Here we report that UCP3 interacts with the non-processed form of thioredoxin 2 (Trx2), a redox protein that is localized in mitochondria, but not processed Trx2, which is involved in cellular responses to ROS. The hydrophilic sequences within the N-terminal tail of UCP3, which faces the intermembrane space, are necessary for binding to Trx2. In addition, Trx2 directly associated with UCP3 through a mitochondrial targeting signaling sequence, was processed in the intermembrane space, and thereby allowing redox reactions. A bimolecular fluorescence complementation analysis demonstrated that the interaction of these proteins occurs in the mitochondrial intermembrane space. Furthermore, increased UCP3 expression significantly attenuated ROS production in isolated mitochondrial without effects on membrane potential, however this effect is lost by Trx2 knock down. These results suggest that UCP3 binds to Trx2 in the mitochondrial intermembrane space and attenuates ROS production.Pharmac