The Genetic Foundations of Attitude Formation: The Case of Left-Right Political Orientations

Kandler C, Bell E, Shikishima C, Yamagata S, Riemann R. The Genetic Foundations of Attitude Formation: The Case of Left-Right Political Orientations. In: R. A. S, S. M. K, eds. Emerging Trends in the Social and Behavioral Sciences: Interdisciplinary Directions. In Press.Since the pioneering work of Eaves and Eysenck (1974) appeared in Nature some 40 years ago,psychologists, sociologists, political scientists, and behavioral geneticists have investigated the effects of nature and nurture on the formation of social attitudes. It has consistently been found that manifestations of social attitudes (i.e., preferences, values, and beliefs pertaining to things like politics, religion, the treatment of ingroups and outgroups, etc.) are genetically influenced. More recently, researchers have focused their efforts on the psycho-physiological pathways between gene activity and attitudes. In particular, a broad body of research examines how personality traits may be a link between genetic factors and political orientations. The latter are typically treated as either a single left-right dimension or divided into two core aspects: resistance to change/authoritarian conservatism and acceptance of inequality/social dominance orientation. In this article, we provide an overview of this research, present some findings from our recent international behavioral genetic study on the topic, and identify key issues for future research. We suggest that future studies treat attitude formation as a complex process in which genetic factors and the psycho-physiological phenomena that stem from them are affected by the surrounding social environment and culture. Such research will require: (1) international study designs capturing individual and cultural levels of variation; and: (2) interdisciplinary collaboration among scientists and researchers in various fields of study such as genetics, psychology, sociology, political science, neuroscience, and human biology

Psychosocial twin cohort studies in Japan: the Keio Twin Research Center (KoTReC)

The Keio Twin Research Center (KoTReC) was established in 2009 at Keio University to combine two longitudinal cohort projects — the Keio Twin Study (KTS) for adolescence and adulthood and the Tokyo Twin Cohort Project (ToTCoP) for infancy and childhood. KoTReC also conducted a two-time panel study of self-control and psychopathology in twin adolescence in 2012 and 2013 and three independent anonymous cross-sectional twin surveys (ToTcross) before 2012 — the ToTCross, the Junior and Senior High School Survey and the High School Survey. This article introduces the recent research designs of KoTReC and its publications

Preliminary report of "Arctic Airborne Measurement Program 2002" (AAMP02)

The Arctic Airborne Measurement Program 2002(AAMP 02) campaign was carried out in March 2002 as one of the sub programs of the project Variations of atmospheric constituents and their climate impact in the Arctic". The main goal of the project was to investigate the transport, transformation and radiative effect of trace gases and aerosols, and their role in the global climate. An instrumented jet plane, Gulfstream II(G-II), was flown from Nagoya, Japan via Barrow, Alaska to Longyearbyen(78°N , 15°E ), Svalbard, crossing the Arctic Ocean in the lower stratospher. Three local flights were made over the Greenland Sea around Svalbard and two profile flights near Barrow. The plane was equipped with CO_2 and ozone analyzers, gas and aerosol sampling systems, aerosol particle counter, nephelometer, absorption photometer, PMS particle probes, sunphotometer, dew point hygrometer and dropsonde system. During the campaign, intensitive surface operations were also conducted at Ny-Ålesund(79°N , 12°E ), Svalbard. Vertical profiles of several trace gases gave information about transport, a new observation by sunphotometer derived an aerosol optical depth in the stratosphere, and another new observation by dropsonde gave information on the polar vortex

Long-term maintenance of the mucosal healing induced by azacitidine therapy in a patient with intestinal Behçet's-like disease accompanied with myelodysplastic syndrome involving trisomy 8

ArticleImmunological medicine. 42(3): 135-141 (2019)journal articl

Canonical versus non-canonical transsynaptic signaling of neuroligin 3 tunes development of sociality in mice

社会性の発達を調節する新たな機構を発見. 京都大学プレスリリース. 2021-03-26.Neuroligin 3 (NLGN3) and neurexins (NRXNs) constitute a canonical transsynaptic cell-adhesion pair, which has been implicated in autism. In autism spectrum disorder (ASD) development of sociality can be impaired. However, the molecular mechanism underlying NLGN3-mediated social development is unclear. Here, we identify non-canonical interactions between NLGN3 and protein tyrosine phosphatase δ (PTPδ) splice variants, competing with NRXN binding. NLGN3-PTPδ complex structure revealed a splicing-dependent interaction mode and competition mechanism between PTPδ and NRXNs. Mice carrying a NLGN3 mutation that selectively impairs NLGN3-NRXN interaction show increased sociability, whereas mice where the NLGN3-PTPδ interaction is impaired exhibit impaired social behavior and enhanced motor learning, with imbalance in excitatory/inhibitory synaptic protein expressions, as reported in the Nlgn3 R451C autism model. At neuronal level, the autism-related Nlgn3 R451C mutation causes selective impairment in the non-canonical pathway. Our findings suggest that canonical and non-canonical NLGN3 pathways compete and regulate the development of sociality

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