Cosmological HII Bubble Growth During Reionization

We present general properties of ionized hydrogen (HII) bubbles and their growth based on a state-of-the-art large-scale (100 Mpc/h) cosmological radiative transfer simulation. The simulation resolves all halos with atomic cooling at the relevant redshifts and simultaneously performs radiative transfer and dynamical evolution of structure formation. Our major conclusions include: (1) for significant HII bubbles, the number distribution is peaked at a volume of $\sim 0.6 {\rm Mpc^{3}/h^{3}}$ at all redshifts. But, at $z\le 10$, one large, connected network of bubbles dominates the entire HII volume. (2) HII bubbles are highly non-spherical. (3) The HII regions are highly biased with respect to the underlying matter distribution with the bias decreasing with time. (4) The non-gaussianity of the HII region is small when the universe becomes 50% ionized. The non-gaussianity reaches its maximal near the end of the reionization epoch $z\sim 6$. But at all redshifts of interest there is a significant non-gaussianity in the HII field. (5) Population III galaxies may play a significant role in the reionization process. Small bubbles are initially largely produced by Pop III stars. At $z\ge 10$ even the largest HII bubbles have a balanced ionizing photon contribution from Pop II and Pop III stars, while at $z\le 8$ Pop II stars start to dominate the overall ionizing photon production for large bubbles, although Pop III stars continue to make a non-negligible contribution. (6) The relationship between halo number density and bubble size is complicated but a strong correlation is found between halo number density and bubble size for large bubbles.Comment: 10 pages, 14 figures; accepted version; higher resolution figures and supplementary material can be found at http://www.astro.princeton.edu/~msshin/reionization/web.ht

Protective effect of Acorus tatarinowii extract against alzheimer in 3xTg-AD mice

Purpose: To investigate the protective effect of Acorus tatarinowii extract (ATE) against Alzheimer's disease in 3xTg-AD mice. Method: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of the amyloid beta deposits and NeuN in the hippocampus were evaluated by immunohistochemical assay while brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ATE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in animals treated with 600 mg/kg ATE (24.8 ± 1.3 s) was significantly increased relative to ontreated 3xTg-AD mice (8.5 ± 1.0 s, p < 0.01). In addition, ATE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expression of BDNF (1.9 ± 0.4, p < 0.05) and TrkB (1.9 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: These results suggest that ATE treatment may be a useful strategy for managing memory impairment induced by several neurodegenerative diseases

The HINT1 tumor suppressor regulates both γ-H2AX and ATM in response to DNA damage

Hint1 is a haploinsufficient tumor suppressor gene and the underlying molecular mechanisms for its tumor suppressor function are unknown. In this study we demonstrate that HINT1 participates in ionizing radiation (IR)–induced DNA damage responses. In response to IR, HINT1 is recruited to IR-induced foci (IRIF) and associates with γ-H2AX and ATM. HINT1 deficiency does not affect the formation of γ-H2AX foci; however, it impairs the removal of γ-H2AX foci after DNA damage and this is associated with impaired acetylation of γ-H2AX. HINT1 deficiency also impairs acetylation of ATM and activation of ATM and its downstream effectors, and retards DNA repair, in response to IR. HINT1-deficient cells exhibit resistance to IR-induced apoptosis and several types of chromosomal abnormalities. Our findings suggest that the tumor suppressor function of HINT1 is caused by, at least in part, its normal role in enhancing cellular responses to DNA damage by regulating the functions of both γ-H2AX and ATM

Lower-Luminosity Galaxies could reionize the Universe: Very Steep Faint-End Slopes to the UV Luminosity Functions at z>=5-8 from the HUDF09 WFC3/IR Observations

The HUDF09 data are the deepest near-IR observations ever, reaching to 29.5 mag. Luminosity functions (LF) from these new HUDF09 data for 132 z\sim7 and z\sim8 galaxies are combined with new LFs for z\sim5-6 galaxies and the earlier z\sim4 LF to reach to very faint limits (<0.05 L*(z=3)). The faint-end slopes alpha are steep: -1.79+/-0.12 (z\sim5), -1.73+/-0.20 (z\sim6), -2.01+/-0.21 (z\sim7), and -1.91+/-0.32 (z\sim8). Slopes alpha\lesssim-2 lead to formally divergent UV fluxes, though galaxies are not expected to form below \sim-10 AB mag. These results have important implications for reionization. The weighted mean slope at z\sim6-8 is -1.87+/-0.13. For such steep slopes, and a faint-end limit of -10 AB mag, galaxies provide a very large UV ionizing photon flux. While current results show that galaxies can reionize the universe by z\sim6, matching the Thomson optical depths is more challenging. Extrapolating the current LF evolution to z>8, taking alpha to be -1.87+/-0.13 (the mean value at z\sim6-8), and adopting typical parameters, we derive Thomson optical depths of 0.061_{-0.006}^{+0.009}. However, this result will change if the faint-end slope alpha is not constant with redshift. We test this hypothesis and find a weak, though uncertain, trend to steeper slopes at earlier times (dalpha/dz\sim-0.05+/-0.04), that would increase the Thomson optical depths to 0.079_{-0.017}^{+0.063}, consistent with recent WMAP estimates (tau=0.088+/-0.015). It may thus not be necessary to resort to extreme assumptions about the escape fraction or clumping factor. Nevertheless, the uncertainties remain large. Deeper WFC3/IR+ACS observations can further constrain the ionizing flux from galaxies.Comment: 6 pages, 4 figures, 1 table, accepted for publication in Astrophysical Journal Letters, updated to match the version in pres

A new topological aspect of the arbitrary dimensional topological defects

We present a new generalized topological current in terms of the order parameter field $\vec \phi$ to describe the arbitrary dimensional topological defects. By virtue of the $$-mapping method, we show that the topological defects are generated from the zero points of the order parameter field $\vec \phi$, and the topological charges of these topological defects are topological quantized in terms of the Hopf indices and Brouwer degrees of $\phi$-mapping under the condition that the Jacobian $$. When $J(\frac \phi v)=0$, it is shown that there exist the crucial case of branch process. Based on the implicit function theorem and the Taylor expansion, we detail the bifurcation of generalized topological current and find different directions of the bifurcation. The arbitrary dimensional topological defects are found splitting or merging at the degenerate point of field function $\vec \phi$ but the total charge of the topological defects is still unchanged.Comment: 24 pages, 10 figures, Revte

Mendelian randomization analysis identified tumor necrosis factor as being associated with severe COVID-19

Background: Observational studies have shown that anti-tumor necrosis factor (TNF) therapy may be beneficial for patients with coronavirus disease 2019 (COVID-19). Nevertheless, because of the methodological restrictions of traditional observational studies, it is a challenge to make causal inferences. This study involved a two-sample Mendelian randomization analysis to investigate the causal link between nine TNFs and COVID-19 severity using publicly released genome-wide association study summary statistics.Methods: Summary statistics for nine TNFs (21,758 cases) were obtained from a large-scale genome-wide association study. Correlation data between single-nucleotide polymorphisms and severe COVID-19 (18,152 cases vs. 1,145,546 controls) were collected from the COVID-19 host genetics initiative. The causal estimate was calculated by inverse variance-weighted (IVW), MR–Egger, and weighted median methods. Sensitivity tests were conducted to assess the validity of the causal relationship.Results: Genetically predicted TNF receptor superfamily member 6 (FAS) positively correlated with the severity of COVID-19 (IVW, odds ratio = 1.10, 95% confidence interval = 1.01–1.19, p = 0.026), whereas TNF receptor superfamily member 5 (CD40) was protective against severe COVID-19 (IVW, odds ratio = 0.92, 95% confidence interval = 0.87–0.97, p = 0.002).Conclusion: Genetic evidence from this study supports that the increased expression of FAS is associated with the risk of severe COVID-19 and that CD40 may have a potential protective effect against COVID-19

Pulmonary blastoma treatment response to anti-PD-1 therapy: a rare case report and literature review

Pulmonary blastoma (PB) is a rare and invasive malignancy of the lungs with a poor prognosis. Although the mainstay treatment of PB is surgery, and radiotherapy and chemotherapy have been reported, no standard therapy exists for patients inoperable in advanced stages. Moreover, little is known about driver mutation status and immunotherapy efficacy. This paper presents a male patient diagnosed with classic biphasic PB using CT-guided lung biopsy pathology and immunohistochemistry. The patient’s symptoms included cough, chest pain, shortness of breath, hemoptysis, and hypodynamia. The primary focus of this paper is to discuss the impact of anti-PD-1 immunotherapy on PB. The patient experienced progression-free survival (PFS) of over 27 months following sintilimab second-line anti-PD-1 therapy. The patient has currently survived for nearly 40 months with a satisfactory quality of life