SOLVING THE BETHE--SALPETER EQUATION IN MINKOWSKI SPACE: SCALAR THEORIES

The Bethe-Salpeter (BS) equation for scalar-scalar bound states in scalar theories without derivative coupling is formulated and solved in Minkowski space. This is achieved using the perturbation theory integral representation (PTIR), which allows these amplitudes to be expressed as integrals over weight functions and known singularity structures and hence allows us to convert the BS equation into an integral equation involving weight functions. We obtain numerical solutions using this formalism for a number of scattering kernels to illustrate the generality of the approach. It applies even when the na\"{\i}ve Wick rotation is invalid. As a check we verify, for example, that this method applied to the special case of the massive ladder exchange kernel reproduces the same results as are obtained by Wick rotation.Comment: 8 pages, regular latex, no figures. Entire manuscript available as a ps file at http://www.physics.adelaide.edu.au/theory/home.html Also available via anonymous ftp at ftp://adelphi.adelaide.edu.au/pub/theory/ADP-95-28.T182.p

Solving the Bethe-Salpeter equation for bound states of scalar theories in Minkowski space

We apply the perturbation theory integral representation (PTIR) to solve for the bound state Bethe-Salpeter (BS) vertex for an arbitrary scattering kernel, without the need for any Wick rotation. The results derived are applicable to any scalar field theory (without derivative coupling). It is shown that solving directly for the BS vertex, rather than the BS amplitude, has several major advantages, notably its relative simplicity and superior numerical accuracy. In order to illustrate the generality of the approach we obtain numerical solutions using this formalism for a number of scattering kernels, including cases where the Wick rotation is not possible.Comment: 28 pages of LaTeX, uses psfig.sty with 5 figures. Also available via WWW at http://www.physics.adelaide.edu.au/theory/papers/ADP-97-10.T248-abs.html or via anonymous ftp at ftp://bragg.physics.adelaide.edu.au/pub/theory/ADP-97-10.T248.ps A number of (crucial) typographical errors in Appendix C corrected. To be published in Phys. Rev. D, October 199

Solving the Bethe-Salpeter Equation for Scalar Theories in Minkowski Space

The Bethe-Salpeter (BS) equation for scalar-scalar bound states in scalar theories without derivative coupling is formulated and solved in Minkowski space. This is achieved using the perturbation theory integral representation (PTIR), which allows these amplitudes to be expressed as integrals over weight functions and known singularity structures and hence allows us to convert the BS equation into an integral equation involving weight functions. We obtain numerical solutions using this formalism for a number of scattering kernels to illustrate the generality of the approach. It applies even when the na\"{\i}ve Wick rotation is invalid. As a check we verify, for example, that this method applied to the special case of the massive ladder exchange kernel reproduces the same results as are obtained by Wick rotation.Comment: 23 pages with 3 uuencoded, compressed Postscript figures. Entire manuscript available as a ps file at http://www.physics.adelaide.edu.au/theory/home.html . Also available at ftp://adelphi.adelaide.edu.au/pub/theory/ADP-94-24.T164.p

Identification of 45 New Neutron-Rich Isotopes Produced by In-Flight Fission of a 238U Beam at 345 MeV/nucleon

A search for new isotopes using in-flight fission of a 345 MeV/nucleon 238U beam has been carried out at the RI Beam Factory at the RIKEN Nishina Center. Fission fragments were analyzed and identified by using the superconducting in-flight separator BigRIPS. We observed 45 new neutron-rich isotopes: 71Mn, 73,74Fe, 76Co, 79Ni, 81,82Cu, 84,85Zn, 87Ga, 90Ge, 95Se, 98Br, 101Kr, 103Rb, 106,107Sr, 108,109Y, 111,112Zr, 114,115Nb, 115,116,117Mo, 119,120Tc, 121,122,123,124Ru, 123,124,125,126Rh, 127,128Pd, 133Cd, 138Sn, 140Sb, 143Te, 145I, 148Xe, and 152Ba

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection

DOCK2 is involved in the host genetics and biology of severe COVID-19

「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target