Constraining isocurvature perturbations with the 21 cm emission from minihaloes

We investigate the effects of isocurvature perturbations on the 21 cm radiation from minihaloes (MHs) at high redshifts and examine constraints on the isocurvature amplitude and power spectrum using the next generation of radio telescopes such as the Square Kilometre Array. We find that there is a realistic prospect of observing the isocurvature imprints in the 21 cm emission from MHs, but only if the isocurvature spectral index is close to 3 (i.e. the spectrum is blue). When the isocurvature fraction increases beyond ∼10 per cent of the adiabatic component, we observe an unexpected decline in the 21 cm fluctuations from small-mass MHs, which can be explained by the incorporation small MHs into larger haloes. We perform a detailed Fisher-matrix analysis and conclude that the combination of future cosmic microwave background and 21 cm experiments (such as CMBPol and the Fast Fourier Transform Telescope) is ideal in constraining the isocurvature parameters, but will stop short of distinguishing between cold dark matter and baryon types of isocurvature perturbations, unless the isocurvature fraction is large and the spectrum is blue

Probing large scale filaments with HI and 3^3HeII

We explore the observability of the neutral hydrogen (HI) and the singly-ionized isotope helium-3 ($^3$HeII) in the intergalactic medium (IGM) from the Epoch of Reionization down to the local Universe. The hyperfine transition of $^3$HeII, which is not as well known as the HI transition, has energy splitting corresponding to 8 cm. It also has a larger spontaneous decay rate than that of neutral hydrogen, whereas its primordial abundance is much smaller. Although both species are mostly ionized in the IGM, the balance between ionization and recombination in moderately high density regions renders them abundant enough to be observed. We estimate the emission signal of both hyperfine transitions from large scale filamentary structures and discuss the prospects for observing them with current and future radio telescopes. We conclude that HI in filaments is possibly observable even with current telescopes after 100 hours of observation. On the other hand, $^3$HeII is only detectable with future telescopes, such as SKA, after the same amount of time.Comment: 21 pages, 13 figures, 2 tables, accepted to MNRA

Application of cross correlations between CMB and large scale structure to constraints on the primordial non-Gaussianity

The primordial non-Gaussianity of local type affects the clustering of dark matter halos, and the planned deep and wide photometric surveys are suitable for examining this class of non-Gaussianity. In our previous paper, we investigated the constraint from the cross correlation between CMB lensing potential and galaxy angular distribution on the primordial non-Gaussianity, without taking into account redshift slicing. To improve our previous analysis, in this paper, we add the galaxy lensing shear into our analysis and take into account redshift slicing to follow the redshift evolution of the clustering. By calculating 81 power spectra and using the Fisher matrix method, we find that the constraint on the primordial non-Gaussianity can be improved from {\Delta}fNL \sim 5.4 to 5.1 by including the galaxy-galaxy lensing shear cross correlations expected from the Hyper Suprime-Cam survey (HSC), in comparison with the constraint without any cross correlations. Moreover, the constraint can go down to {\Delta}fNL \sim 4.8 by including the galaxy-CMB lensing cross correlations from the ACTPol and Planck experiments.Comment: 17 pages, 9 figuers, 7 tables, published in Phys. Rev. D 201

Results of surgical treatment of thymomas with special reference to the involved organs

AbstractObjective: The purpose of this study is to clarify the significance of the particular involved organ as a prognostic factor and its relation to other previously reported factors. Methods: The prognoses of 194 consecutive patients with thymoma who had undergone complete or subtotal resection were reviewed retrospectively. Survival was evaluated as actuarial freedom from tumor death. Analysis of prognostic factors was performed by the Kaplan-Meier method with the log rank test and Cox's proportional hazards model. Results: The Masaoka staging system and involvement of the great vessels were the independent prognostic factors in the entire study group; age, sex, histologic subtype, completeness of resection, association of myasthenia gravis, or involvement of other organs were not factors. The 10-year and 20-year survivals were 99% and 90% in stage I, 94% and 90% in stage II, 88% and 56% in stage III, 30% and 15% in stage IVa, 0% and 0% in stage IVb, 93% and 83% in the absence of involvement of the great vessels, and 54% and 20% in the presence of it. Involvement of the great vessels was also the single independent prognostic factor in the patients with stage III disease although completeness of resection or involvement of other organs were not. The 10-year and 20-year survivals in patients with stage III disease were 97% and 75% in the absence of involvement of the great vessels, and 70% and 29% in the presence of it. Conclusion: Although the Masaoka staging system is a valuable prognostic factor, the category of stage III is heterogeneous and consists of 2 groups with distinct prognoses depending on involvement of the great vessels. (J Thorac Cardiovasc Surg 1999;117:605-13

Inhibition of interleukin-6 signaling attenuates aortitis, left ventricular hypertrophy and arthritis in interleukin-1 receptor antagonist deficient mice

The aim of the present study was to examine whether inhibition of Interleukin (IL)-6 signaling by MR16-1, an IL-6 receptor antibody, attenuates aortitis, cardiac hypertrophy, and arthritis in IL-1 receptor antagonist deficient (IL-1RA KO) mice. Four weeks old mice were intraperitoneally administered with either MR16-1 or non-immune IgG at dosages that were adjusted over time for 5 weeks. These mice were stratified into four groups: MR16-1 treatment groups, KO/MR low group (first 2.0 mg, following 0.5 mg/week, n=14) and KO/MR high group (first 4.0 mg, following 2.0 mg/week, n=19) in IL-1RA KO mice, and IgG treatment groups, KO/IgG group (first 2.0 mg, following 1.0 mg/week, n=22) in IL-1RA KO mice, and wild/IgG group (first 2.0 mg, following 1.0 mg/week, n=17) in wild mice. Aortitis, cardiac hypertrophy and arthropathy were histologically analyzed. Sixty-eight percent of the KO/IgG group developed aortitis (53% developed severe aortitis). In contrast, only 21% of the KO/MR high group developed mild aortitis, without severe aortitis (P<0.01, vs KO/IgG group). Infiltration of inflammatory cells, such as neutrophils, T cells, and macrophages, was frequently observed around aortic sinus of the KO/IgG group. Left ventricle and cardiomyocyte hypertrophy were observed in IL-1RA KO mice. Administration of high dosage of MR16-1 significantly suppressed cardiomyocyte hypertrophy. MR16-1 attenuated the incidence and severity of arthritis in IL-1RA KO mice in a dose-dependent manner. In conclusion, blockade of IL-6 signaling may exert a beneficial effect to attenuate severe aortitis, left ventricle hypertrophy, and arthritis

The Aggregation Inhibitor Peptide QBP1 as a Therapeutic Molecule for the Polyglutamine Neurodegenerative Diseases

Misfolding and abnormal aggregation of proteins in the brain are implicated in the pathogenesis of various neurodegenerative diseases including Alzheimer's, Parkinson's, and the polyglutamine (polyQ) diseases. In the polyQ diseases, an abnormally expanded polyQ stretch triggers misfolding and aggregation of the disease-causing proteins, eventually resulting in neurodegeneration. In this paper, we introduce our therapeutic strategy against the polyQ diseases using polyQ binding peptide 1 (QBP1), a peptide that we identified by phage display screening. We showed that QBP1 specifically binds to the expanded polyQ stretch and inhibits its misfolding and aggregation, resulting in suppression of neurodegeneration in cell culture and animal models of the polyQ diseases. We further demonstrated the potential of protein transduction domains (PTDs) for in vivo delivery of QBP1. We hope that in the near future, chemical analogues of aggregation inhibitor peptides including QBP1 will be developed against protein misfolding-associated neurodegenerative diseases