秋成とともに同時代を生き、上方和学の展開を担った国学者の言説、学芸、伝記、学統等を総合的に解明することで、近世中後期における上方和学の実態を多角的に把握することを目指す。.

Late Tokugawa society and the crisis of community -- Before the Kojikiden : the divine age narrative in Tokugawa Japan -- Motoori Norinaga : discovering Japan -- Ueda Akinari : history and community -- Fujitani Mitsue : the poetics off community -- Tachibana Moribe : cosmology and community -- National literature, intellectual history, and the new Kokugaku -- Conclusion : imagined Japan(s).

In lieu of an abstract, here is a brief excerpt of the content:The Peculiarly Favored Condition of GeneticsJames J. Lee, PhD (bio) and Damien Morris, MSc (bio)Turkheimer and Greer (2024) (henceforth “T&G”) make some fair points about problems in the scientific profession, including the regrettable tendency to promise practical applications of research that then never materialize. However, T&G’s sustained critique of a body of work associated with one particular researcher to make these general points struck us as uncharitable. More pressingly, (...) we feel that the far-reaching conclusions that T&G attempt to draw from the results they review from the Spit for Science (S4S) cohort are unjustified and risk misleading readers that psychiatric and behavioral genetics is in a parlous state.T&G state that S4S “produced a clear answer to the question it was designed to address,” namely, that its results “unambiguously contradict the hypothesis that alcohol-related behaviors have a meaningful genetic basis.” But S4S cannot possibly have provided affirmative evidence for the null hypothesis, because as a single cohort it lacked the statistical power to do so. Elsewhere T&G acknowledge that the sample size of S4S does not suffice for many purposes; they cannot have it both ways. When GCTA has been applied to samples of greater size, it has unambiguously supported the hypothesis that alcohol-related behaviors have a meaningful genetic basis. The UK Biobank yielded estimates exceeding 0.10 for the contribution of single nucleotide polymorphisms (SNPs) with minor allele frequency of greater than 0.05 to the heritability of drinks per week, estimates more than ten times their standard errors (Liu et al., 2019).This heritability contributed by common variants is sometimes called “SNP heritability,” and T&G disparage it for the alleged “disadvantage of being substantially smaller” than “twin and family heritabilities.” Nowhere do T&G consider what the precise numbers actually mean—an approach that can be hazardous to your scientific health, as the late John Loehlin might have said. Let us, then, consider these numbers. Under a model of pure neutrality, SNP and pedigree narrow-sense heritabilities should be fairly close, essentially as a result of factors p(1 − p) canceling in the multiplication of the numbers of SNPs to be found at a given allele frequency by the average heritability contributed per SNP (Hill, 2010). If SNP and pedigree heritabilities are not close, then natural selection must have been acting on [End Page 441] the trait, preventing new mutations of large effect from becoming common and thereby concentrating heritability at allele frequencies lower than those typically studied in genome-wide association studies (GWAS). This deduction has been abundantly confirmed: the tendency of GWAS SNPs to reside in evolutionarily conserved regions (Finucane et al., 2015; Kim et al., 2019), the younger age of GWAS SNPs when compared to control SNPs of comparable frequencies (Gazal et al., 2017), the discovery of several rare variants with larger effects than those observed in typical GWAS (Barton et al., 2021; Chen et al., 2023; Marouli et al., 2017), the directly measured deleterious fitness effects of mutations in evolutionarily constrained genes (Gardner et al., 2022), and the substantial additional genetic variance accumulated when rare variants are included in GCTA-type studies, sometimes enough to close the gap between SNP and pedigree heritabilities (Evans et al., 2018; Jang et al., 2022; Pathan et al., 2024; Wainschtein et al., 2022).The genetic architecture of a typical quantitative trait consists of many sites across the genome that can mutate to affect it, numbering potentially in the millions (Agarwala et al., 2013; Zeng et al., 2021), of which those that are common SNPs have very small effects as a result of selection. This is the message, but T&G seem to find fault with the messenger, painting “tiny” effect sizes as an embarrassment to the field of behavioral genetics as a whole. We prefer to view the finding of high polygenicity as a revelation about nature, rather than as a debating point. What is this finding telling us? If one takes the action of stabilizing selection as the initial assumption (Uyeda et al., 2011), then the extreme polygenicity revealed by GWAS becomes part of the answer to the question regarding how traits can... (shrink)