New constraints on cosmological modified gravity theories from anisotropic three-point correlation functions of BOSS DR12 galaxies

We report a new test of modified gravity theories using the large-scale structure of the Universe. This paper is the first attempt to (1) apply a joint analysis of the anisotropic components of galaxy two- and three-point correlation functions (2 and 3PCFs) to actual galaxy data and (2) constrain the nonlinear effects of degenerate higher-order scalar-tensor (DHOST) theories on cosmological scales. Applying this analysis to the Baryon Oscillation Spectroscopic Survey (BOSS) data release 12, we obtain the lower bounds of $-1.655 < \xi_{\rm t}$ and $-0.504 < \xi_{\rm s}$ at the $95\%$ confidence level on the parameters characterising the time evolution of the tidal and shift terms of the second-order velocity field. These constraints are consistent with GR predictions of $\xi_{\rm t}=15/1144$ and $\xi_{\rm s}=0$. Moreover, they represent a $35$-fold and $20$-fold improvement, respectively, over the joint analysis with only the isotropic 3PCF. We ensure the validity of our results by investigating various quantities, including theoretical models of the 3PCF, window function corrections, cumulative ${\rm S/N}$, Fisher matrices, and statistical scattering effects of mock simulation data. We also find statistically significant discrepancies between the BOSS data and the Patchy mocks for the 3PCF measurement. Finally, we package all of our 3PCF analysis codes under the name \textsc{HITOMI} and make them publicly available so that readers can reproduce all the results of this paper and easily apply them to ongoing future galaxy surveys.Comment: 60 pages, 21 figures, 22 tables; a set of codes for data analysis is publicly available at https://github.com/naonori/hitomi.gi

First test of the consistency relation for the large-scale structure using the anisotropic three-point correlation function of BOSS DR12 galaxies (An explanatory video is available at https://youtu.be/Zi36ooLPhss.)

We present, for the first time, an observational test of the consistency relation for the large-scale structure (LSS) of the Universe through a joint analysis of the anisotropic two- and three-point correlation functions (2PCF and 3PCF) of galaxies. We parameterise the breakdown of the LSS consistency relation in the squeezed limit by $E_{\rm s}$, which represents the ratio of the coefficients of the shift terms in the second-order density and velocity fluctuations. $E_{\rm s}\neq1$ is a sufficient condition under which the LSS consistency relation is violated. A novel aspect of this work is that we constrain $E_{\rm s}$ by obtaining information about the nonlinear velocity field from the quadrupole component of the 3PCF without taking the squeezed limit. Using the galaxy catalogues in the Baryon Oscillation Spectroscopic Survey (BOSS) Data Release 12, we obtain $E_{\rm s} = -0.92_{-3.26}^{+3.13}$, indicating that there is no violation of the LSS consistency relation in our analysis within the statistical errors. Our parameterisation is general enough that our constraint can be applied to a wide range of theories, such as multicomponent fluids, modified gravity theories, and their associated galaxy bias effects. Our analysis opens a new observational window to test the fundamental physics using the anisotropic higher-order correlation functions of galaxy clustering.Comment: 17 pages, 6 figures. Explanatory videos are available in several languages: https://youtu.be/Zi36ooLPhss (English), https://youtu.be/d2ZamcDt6hs (French), https://youtu.be/iSm5yPWmZ9c (Spanish), https://youtu.be/Go7ox-ciHIc (German), https://youtu.be/6Ith7cE723o (Chinese), and https://youtu.be/rH9-C3eKoYc (English with my voice

Bubble burst as jamming phase transition

Recently research on bubble and its burst attract much interest of researchers in various field such as economics and physics. Economists have been regarding bubble as a disorder in prices. However, this research strategy has overlooked an importance of the volume of transactions. In this paper, we have proposed a bubble burst model by focusing the transactions incorporating a traffic model that represents spontaneous traffic jam. We find that the phenomenon of bubble burst shares many similar properties with traffic jam formation by comparing data taken from US housing market. Our result suggests that the transaction could be a driving force of bursting phenomenon.Comment: 9 pages,12 figure

Primordial magnetic fields from second-order cosmological perturbations: Tight coupling approximation

We explore the possibility of generating large-scale magnetic fields from second-order cosmological perturbations during the pre-recombination era. The key process for this is Thomson scattering between the photons and the charged particles within the cosmic plasma. To tame the multi-component interacting fluid system, we employ the tight coupling approximation. It is shown that the source term for the magnetic field is given by the vorticity, which signals the intrinsically second-order quantities, and the product of the first order perturbations. The vorticity itself is sourced by the product of the first-order quantities in the vorticity evolution equation. The magnetic fields generated by this process are estimated to be $\sim 10^{-29}$Gauss on the horizon scale at the recombination epoch. Although our rough estimate suggests that the current generation mechanism can work even on smaller scales, more careful investigation is needed to make clear whether it indeed works in a wide range of spatial scales.Comment: 10pages, minor corrections, accepted for publication in Class. Quant. Gra

The process of displacing the single-stranded DNA-binding protein from single-stranded DNA by RecO and RecR proteins

The regions of single-stranded (ss) DNA that result from DNA damage are immediately coated by the ssDNA-binding protein (SSB). RecF pathway proteins facilitate the displacement of SSB from ssDNA, allowing the RecA protein to form protein filaments on the ssDNA region, which facilitates the process of recombinational DNA repair. In this study, we examined the mechanism of SSB displacement from ssDNA using purified Thermus thermophilus RecF pathway proteins. To date, RecO and RecR are thought to act as the RecOR complex. However, our results indicate that RecO and RecR have distinct functions. We found that RecR binds both RecF and RecO, and that RecO binds RecR, SSB and ssDNA. The electron microscopic studies indicated that SSB is displaced from ssDNA by RecO. In addition, pull-down assays indicated that the displaced SSB still remains indirectly attached to ssDNA through its interaction with RecO in the RecO-ssDNA complex. In the presence of both SSB and RecO, the ssDNA-dependent ATPase activity of RecA was inhibited, but was restored by the addition of RecR. Interestingly, the interaction of RecR with RecO affected the ssDNA-binding properties of RecO. These results suggest a model of SSB displacement from the ssDNA by RecF pathway proteins

Degradation of Mutant Protein Aggregates within the Endoplasmic Reticulum of Vasopressin Neurons

Misfolded or unfolded proteins in the ER are said to be degraded only after translocation or isolation from the ER. Here, we describe a mechanism by which mutant proteins are degraded within the ER. Aggregates of mutant arginine vasopressin (AVP) precursor were confined to ER-associated compartments (ERACs) connected to the ER in AVP neurons of a mouse model of familial neurohypophysial diabetes insipidus. The ERACs were enclosed by membranes, an ER chaperone and marker protein of phagophores and autophagosomes were expressed around the aggregates, and lysosomes fused with the ERACs. Moreover, lysosome-related molecules were present within the ERACs, and aggregate degradation within the ERACs was dependent on autophagic-lysosomal activity. Thus, we demonstrate that protein aggregates can be degraded by autophagic-lysosomal machinery within specialized compartments of the ER

RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS

Repulsive guidance molecule A (RGMa) was originally identified as a neuronal growth cone–collapsing factor. Previous reports have demonstrated the multifunctional roles of RGMa mediated by neogenin1. However, the pathogenic involvement of RGMa in amyotrophic lateral sclerosis (ALS) remains unclear. Here, we demonstrated that RGMa concentration was elevated in the cerebrospinal fluid of both patients with ALS and transgenic mice overexpressing the mutant human superoxide dismutase1 (mSOD1 mice). Treatment with humanized anti-RGMa monoclonal antibody ameliorated the clinical symptoms in mSOD1 mice. Histochemical analysis revealed that the anti-RGMa antibody significantly decreased mutant SOD1 protein accumulation in the motor neurons of mSOD1 mice via inhibition of actin depolymerization. In vitro analysis revealed that the anti-RGMa antibody inhibited the cellular uptake of the mutant SOD1 protein, presumably by reinforcing the neuronal actin barrier. Collectively, these data suggest that RGMa leads to the collapse of the neuronal actin barrier and promotes aberrant protein deposition, resulting in exacerbation of the ALS pathology.Shimizu Mikito, Shiraishi Naoyuki, Tada Satoru, et al. RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS. Science Advances 9, 686 (2023); https://doi.org/10.1126/sciadv.adg3193

Adalimumab Dose-Escalation Therapy Is Effective in Refractory Crohn’s Disease Patients with Loss of Response to Adalimumab, Especially in Cases without Previous Infliximab Treatment

Background/Aims: Adalimumab dose escalation is one of the most important options in refractory Crohn’s disease patients with loss of response to adalimumab. The goal of this study was to evaluate the effectiveness of adalimumab dose escalation in Crohn’s disease patients with loss of response to adalimumab, since there are few reports of adalimumab dose escalation, especially in East Asia. Methods: The clinical response to adalimumab dose escalation in Crohn’s disease patients with loss of response to adalimumab was evaluated retrospectively, using the Crohn’s disease activity index score, serum C-reactive protein levels, and endoscopic analyses. Results: Of the 203 Crohn’s disease patients treated with anti-tumor necrosis factor, 14 refractory Crohn’s disease patients with loss of response to adalimumab received adalimumab dose-escalation therapy. The C-reactive protein level was significantly reduced from the start to weeks 12 and 52 of adalimumab dose escalation in the whole group, although there were no significant reductions of Crohn’s disease activity index scores. Both Crohn’s disease activity index scores and C-reactive protein levels were significantly reduced from the start to weeks 12 and 52 of adalimumab dose escalation in patients without previous infliximab treatment, although C-reactive protein levels were positive in all cases with previous infliximab exposure at weeks 12 and 52. Endoscopic mucosal healing was achieved with adalimumab dose escalation in 2 cases without previous infliximab treatment. Conclusions: Adalimumab dose-escalation therapy is effective in refractory Crohn’s disease patients with loss of response to adalimumab, especially in cases without previous infliximab treatment