Robustness of Baryon Acoustic Oscillations Measurements with Photometric Redshift Uncertainties

We investigate the robustness of baryon acoustic oscillations (BAO) measurements with a photometric galaxy sample using mock galaxy catalogs with various sizes of photometric redshift (photo-$z$) uncertainties. We first investigate the robustness of BAO measurements, assuming we have a perfect knowledge of photo-$z$ uncertainties. We find that the BAO shift parameter $\alpha$ can be constrained in an unbiased manner for various sizes of photometric redshift uncertainties at $z=0.251$, $0.617$, and $1.03$ as long as the number density of galaxies is high. A sparse galaxy sample causes additional noise in the covariance matrix calculation and it can bias the constraint on $\alpha$. Next, we investigate the scenario where incorrect photometric redshift uncertainties are assumed in the fitting model and find that underestimating the photo-$z$ uncertainty leads to a degradation in the constraining power on $\alpha$. In addition, we investigate BAO measurements with a cross-correlation signal between a spec-$z$ sample and a photo-$z$ sample. We find BAO constraints are unbiased and slightly tighter than the auto-correlation signal of a photo-$z$ sample. We also quantify the constraining power on $\Omega_{\rm m0}$ assuming the LSST-like covariance and find that the 95\% confidence level is $\sigma(\Omega_{\rm m0})\sim0.03$-$0.05$ corresponding to the photo-$z$ uncertainties of 1\% to 3\% respectively. Finally, we examine whether the skewness in the photometric redshift can bias the constraint on $\alpha$ and confirm that the constraint on $\alpha$ is unbiased even if we use a fitting model assuming a Gaussian photo-$z$ uncertainty.Comment: 10 pages, 11 figures, 3 table

Galaxy-galaxy weak-lensing measurement from SDSS: II. host halo properties of galaxy groups

As the second paper of a series on studying galaxy-galaxy lensing signals using the Sloan Digital Sky Survey Data Release 7 (SDSS DR7), we present our measurement and modelling of the lensing signals around groups of galaxies. We divide the groups into four halo mass bins, and measure the signals around four different halo-center tracers: brightest central galaxy (BCG), luminosity-weighted center, number-weighted center and X-ray peak position. For X-ray and SDSS DR7 cross identified groups, we further split the groups into low and high X-ray emission subsamples, both of which are assigned with two halo-center tracers, BCGs and X-ray peak positions. The galaxy-galaxy lensing signals show that BCGs, among the four candidates, are the best halo-center tracers. We model the lensing signals using a combination of four contributions: off-centered NFW host halo profile, sub-halo contribution, stellar contribution, and projected 2-halo term. We sample the posterior of 5 parameters i.e., halo mass, concentration, off-centering distance, sub halo mass, and fraction of subhalos via a MCMC package using the galaxy-galaxy lensing signals. After taking into account the sampling effects (e.g. Eddington bias), we found the best fit halo masses obtained from lensing signals are quite consistent with those obtained in the group catalog based on an abundance matching method, except in the lowest mass bin. Subject headings: (cosmology:) gravitational lensing, galaxies: clusters: generalComment: 12 pages, 7 figures, submitted to Ap

Optical Cluster Cosmology with SDSS redMaPPer clusters and HSC-Y3 lensing measurements

We present cosmology results obtained from a blind joint analysis of the abundance, projected clustering, and weak lensing of galaxy clusters measured from the Sloan Digital Sky Survey (SDSS) redMaPPer cluster catalog and the Hyper-Suprime Cam (HSC) Year3 shape catalog. We present a full-forward model for the cluster observables, which includes empirical modeling for the anisotropic boosts on the lensing and clustering signals of optical clusters. We validate our analysis via mock cluster catalogs which include observational systematics, such as the projection effect and the effect of baryonic feedback, and find that our analysis can robustly constrain cosmological parameters in an unbiased manner without any informative priors on our model parameters. The joint analysis of our observables in the context of the flat $\Lambda$CDM model results in cosmological constraints for $S_8\equiv \sigma_8 \sqrt{\Omega_{\rm m} / 0.3}=0.816^{+0.041}_{-0.039}$. Our result is consistent with the $S_8$ inference from other cosmic microwave background- and large scale structure-based cosmology analyses, including the result from the \emph{Planck} 2018 primary CMB analysis.Comment: v1: 22 pages, 15 figures, Comments welcom

Hyper Suprime-Cam Year 3 Results: Cosmology from Cosmic Shear Two-point Correlation Functions

We perform a blinded cosmology analysis with cosmic shear two-point correlation functions (2PCFs) measured from more than 25 million galaxies in the Hyper Suprime-Cam three-year shear catalog in four tomographic redshift bins ranging from 0.3 to 1.5. After conservative masking and galaxy selection, the survey covers 416 deg$^2$ of the northern sky with an effective galaxy number density of 15 arcmin$^{-2}$ over the four redshift bins. The 2PCFs adopted for cosmology analysis are measured in the angular range: $7.1 < \theta/{\rm arcmin} < 56.6$ for $\xi_+$ and $31.2 <\theta/{\rm arcmin} < 248$ for $\xi_-$, with a total signal-to-noise ratio of 26.6. We apply a conservative, wide, flat prior on the photometric redshift errors on the last two tomographic bins, and the relative magnitudes of the cosmic shear amplitude across four redshift bins allow us to calibrate the photometric redshift errors. With this flat prior on redshift errors, we find $\Omega_{\rm m}=0.256_{-0.044}^{+0.056}$ and $S_8\equiv \sigma_8 \sqrt{\Omega_{\rm m}/0.3}=0.769_{-0.034}^{+0.031}$ (both 68\% CI) for a flat $\Lambda$ cold dark matter cosmology. We find, after unblinding, that our constraint on $S_8$ is consistent with the Fourier space cosmic shear and the 3$\times$2pt analyses on the same HSC dataset. We carefully study the potential systematics from astrophysical and systematic model uncertainties in our fiducial analysis using synthetic data, and report no biases (including projection bias in the posterior space) greater than $0.5\sigma$ in the estimation of $S_8$. Our analysis hints that the mean redshifts of the two highest tomographic bins are higher than initially estimated. In addition, a number of consistency tests are conducted to assess the robustness of our analysis. Comparing our result with Planck-2018 cosmic microwave background observations, we find a ~$2\sigma$ tension for the $\Lambda$CDM model.Comment: 38 pages, 32 figures, 4 tables (PRD in press.

The clustering of galaxies in the SDSS-III Baryon Oscillation Spectroscopic Survey: the low-redshift sample

We report on the small-scale (0.5 r h−1 Mpc) clustering of 78 895 massive (M* ~ 1011.3 M⊙) galaxies at 0.2 z 13 h−1 M⊙, a large-scale bias of ~2.0 and a satellite fraction of 12 ± 2 per cent. Thus, these galaxies occupy haloes with average masses in between those of the higher redshift BOSS CMASS sample and the original SDSS I/II luminous red galaxy sample

Mitochondrial Dysfunction Links Ceramide Activated HRK Expression and Cell Death

Cell death is an essential process in normal development and homeostasis. In eyes, corneal epithelial injury leads to the death of cells in underlying stroma, an event believed to initiate corneal wound healing. The molecular basis of wound induced corneal stromal cell death is not understood in detail. Studies of others have indicated that ceramide may play significant role in stromal cell death following LASIK surgery. We have undertaken the present study to investigate the mechanism of death induced by C6 ceramide in cultures of human corneal stromal (HCSF) fibroblasts.Cultures of HCSF were established from freshly excised corneas. Cell death was induced in low passage (p<4) cultures of HCSF by treating the cells with C6 ceramide or C6 dihydroceramide as a control. Cell death was assessed by Live/Dead cell staining with calcein AM and ethidium homodimer-1 as well as Annexin V staining, caspase activation and TUNEL staining Mitochondrial dysfunction was assessed by Mito Sox Red, JC-1 and cytochrome C release Gene expression was examined by qPCR and western blotting.Our data demonstrate ceramide caused mitochondrial dysfunction as evident from reduced MTT staining, cyto c release from mitochondria, enhanced generation of ROS, and loss in mitochondrial membrane potential (ΔΨm). Cell death was evident from Live -Dead Cell staining and the inability to reestablish cultures from detached cells. Ceramide induced the expression of the harikari gene(HRK) and up-regulated JNK phosphorylation. In ceramide treated cells HRK was translocated to mitochondria, where it was found to interact with mitochondrial protein p32. The data also demonstrated HRK, p32 and BAD interaction. Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.Our data document that ceramide is capable of inducing death of corneal stromal fibroblasts through the induction of HRK mediated mitochondria dysfunction

Hyper Suprime-Cam Year 3 results: cosmology from cosmic shear power spectra

We measure weak lensing cosmic shear power spectra from the 3-year galaxy shear catalog of the Hyper Suprime-Cam (HSC) Subaru Strategic Program imaging survey. The shear catalog covers 416  deg2 of the northern sky, with a mean i-band seeing of 0.59 arcsec and an effective galaxy number density of 15  arcmin−2 within our adopted redshift range. With an i-band magnitude limit of 24.5 mag, and four tomographic redshift bins spanning 0.3≤zph≤1.5 based on photometric redshifts, we obtain a high-significance measurement of the cosmic shear power spectra, with a signal-to-noise ratio of approximately 26.4 in the multipole range 300<ℓ<1800. The accuracy of our power spectrum measurement is tested against realistic mock shear catalogs, and we use these catalogs to get a reliable measurement of the covariance of the power spectrum measurements. We use a robust blinding procedure to avoid confirmation bias, and model various uncertainties and sources of bias in our analysis, including point spread function systematics, redshift distribution uncertainties, the intrinsic alignment of galaxies and the modeling of the matter power spectrum. For a flat ΛCDM model, we find S8≡σ8(Ωm/0.3)0.5=0.776+0.032−0.033, which is in excellent agreement with the constraints from the other HSC Year 3 cosmology analyses, as well as those from a number of other cosmic shear experiments. This result implies a ∼2σ-level tension with the Planck 2018 cosmology. We study the effect that various systematic errors and modeling choices could have on this value, and find that they can shift the best-fit value of S8 by no more than ∼0.5σ, indicating that our result is robust to such systematics

Transient mTOR Inhibition Facilitates Continuous Growth of Liver Tumors by Modulating the Maintenance of CD133+ Cell Populations

The mammalian target of the rapamycin (mTOR) pathway, which drives cell proliferation, is frequently hyperactivated in a variety of malignancies. Therefore, the inhibition of the mTOR pathway has been considered as an appropriate approach for cancer therapy. In this study, we examined the roles of mTOR in the maintenance and differentiation of cancer stem-like cells (CSCs), the conversion of conventional cancer cells to CSCs and continuous tumor growth in vivo. In H-Ras-transformed mouse liver tumor cells, we found that pharmacological inhibition of mTOR with rapamycin greatly increased not only the CD133+ populations both in vitro and in vivo but also the expression of stem cell-like genes. Enhancing mTOR activity by over-expressing Rheb significantly decreased CD133 expression, whereas knockdown of the mTOR yielded an opposite effect. In addition, mTOR inhibition severely blocked the differentiation of CD133+ to CD133- liver tumor cells. Strikingly, single-cell culture experiments revealed that CD133- liver tumor cells were capable of converting to CD133+ cells and the inhibition of mTOR signaling substantially promoted this conversion. In serial implantation of tumor xenografts in nude BALB/c mice, the residual tumor cells that were exposed to rapamycin in vivo displayed higher CD133 expression and had increased secondary tumorigenicity compared with the control group. Moreover, rapamycin treatment also enhanced the level of stem cell-associated genes and CD133 expression in certain human liver tumor cell lines, such as Huh7, PLC/PRC/7 and Hep3B. The mTOR pathway is significantly involved in the generation and the differentiation of tumorigenic liver CSCs. These results may be valuable for the design of more rational strategies to control clinical malignant HCC using mTOR inhibitors

High expression of MKP1/DUSP1 counteracts glioma stem cell activity and mediates HDAC inhibitor response

Abstract The elucidation of mechanisms involved in resistance to therapies is essential to improve the survival of patients with malignant gliomas. A major feature possessed by glioma cells that may aid their ability to survive therapy and reconstitute tumors is the capacity for self-renewal. We show here that glioma stem cells (GSCs) express low levels of MKP1, a dual-specificity phosphatase, which acts as a negative inhibitor of JNK, ERK1/2, and p38 MAPK, while induction of high levels of MKP1 expression are associated with differentiation of GSC. Notably, we find that high levels of MKP1 correlate with a subset of glioblastoma patients with better prognosis and overall increased survival. Gain of expression studies demonstrated that elevated MKP1 impairs self-renewal and induces differentiation of GSCs while reducing tumorigenesis in vivo. Moreover, we identified that MKP1 is epigenetically regulated and that it mediates the anti-tumor activity of histone deacetylase inhibitors (HDACIs) alone or in combination with temozolomide. In summary, this study identifies MKP1 as a key modulator of the interplay between GSC self-renewal and differentiation and provides evidence that the activation of MKP1, through epigenetic regulation, might be a novel therapeutic strategy to overcome therapy resistance in glioblastoma

FoxO and Stress Responses in the Cnidarian Hydra vulgaris

Background: In the face of changing environmental conditions, the mechanisms underlying stress responses in diverse organisms are of increasing interest. In vertebrates, Drosophila, and Caenorhabditis elegans, FoxO transcription factors mediate cellular responses to stress, including oxidative stress and dietary restriction. Although FoxO genes have been identified in early-arising animal lineages including sponges and cnidarians, little is known about their roles in these organisms. Methods/Principal Findings: We have examined the regulation of FoxO activity in members of the well-studied cnidarian genus Hydra. We find that Hydra FoxO is expressed at high levels in cells of the interstitial lineage, a cell lineage that includes multipotent stem cells that give rise to neurons, stinging cells, secretory cells and gametes. Using transgenic Hydra that express a FoxO-GFP fusion protein in cells of the interstitial lineage, we have determined that heat shock causes localization of the fusion protein to the nucleus. Our results also provide evidence that, as in bilaterian animals, Hydra FoxO activity is regulated by both Akt and JNK kinases. Conclusions: These findings imply that basic mechanisms of FoxO regulation arose before the evolution of bilaterians an