Strack F, Martin LL, Stepper S. “Inhibiting and facilitating conditions of the human smile: a nonobtrusive test of the facial feedback hypothesis. ” J. Pers. Soc. Psychol. 54, 768–777 (1988)
Registered Replication Report: Strack, Martin, & Stepper (1988). (2016) The original Strack et al. (1988) study reported a rating difference of 0.82 units on a 10-point Likert scale. Our meta-analysis revealed a rating difference of 0.03 units with a 95% confidence interval ranging from −0.11 to 0.16. Strackらの再現を試みた実験だが、再現性が認められないという結果に。
笑っている声
人間は声だけ聴いたときでも、その人が笑っているときの声なのかどうかを聴覚のみで判断できます。
Human social interaction relies, for the most part, on the ability to extract and decode facial and vocal expressions, from which we can infer each other’s social traits and emotional states (Willis and Todorov, 2006). Among such expressions, the smile—the bilateral stretching of the lips by the zygomaticus major muscles—is remarkable for being produced and recognised early in development (Oostenbroek et al., 2016) and across cultures (Ekman et al., 1969). Smiling is not only perceived visually, but can also be heard in spoken voice (or smiled speech, Tartter, 1980; Basso and Oullier, 2010).https://pubs.aip.org/asa/jasa/article/143/1/EL19/616107/Uncovering-mental-representations-of-smiled-speech
表情フィードバック仮説に関するChatGPTによる説明
The Facial Feedback Hypothesis is a psychological theory that suggests that facial expressions can influence and modulate emotions. In other words, the act of making a certain facial expression can trigger or intensify the corresponding emotion. This hypothesis posits that our facial muscles not only reflect our emotional states but also play an active role in shaping them. 顔の筋肉は感情の状態を反映するだけでなく、逆に、顔の筋肉の状態が感情の状態に影響を与える。
Key points about the Facial Feedback Hypothesis include:
Emotions and Facial Expressions: According to the theory, our brains continuously monitor the facial expressions we make. When we contract the muscles associated with a particular emotion, our brain interprets these signals and generates or amplifies the corresponding emotional experience.
James-Lange Theory Connection: The Facial Feedback Hypothesis is related to the James-Lange theory of emotions. The James-Lange theory suggests that emotions arise as a result of physiological changes in the body. The Facial Feedback Hypothesis extends this idea to include facial muscles as one of the physiological pathways through which emotions are generated.
Experimental Evidence: Research studies have provided some support for the Facial Feedback Hypothesis. For example, studies have shown that when people are asked to mimic facial expressions associated with specific emotions (e.g., smiling or frowning), they often report feeling the corresponding emotion more intensely.
Limitations: While there is evidence to support the idea that facial expressions can influence emotions, the Facial Feedback Hypothesis is not without its critics. Some studies have failed to replicate the effects predicted by the hypothesis, and the relationship between facial expressions and emotions is likely more complex than initially proposed.
Real-World Implications: The Facial Feedback Hypothesis has real-world implications, particularly in fields like psychology, therapy, and human-computer interaction. It suggests that intentionally changing one’s facial expressions (e.g., smiling when feeling down) might have a positive impact on one’s emotional state.
It’s important to note that while the Facial Feedback Hypothesis provides an interesting perspective on the relationship between facial expressions and emotions, it is not the only theory in the field of emotion research. Emotions are complex and influenced by a combination of factors, including cognitive processes, physiological responses, and social and cultural influences.
Foetus 18 Weeks: the greatest photograph of the 20th century? Charlotte Jansen Mon 18 Nov 2019 06.00 GMT The Gurdian Nilsson was only able to photograph one living foetus, though, using an endoscopic camera that travelled into a womb. This picture was included in Life and is distinct from the others – being taken inside the uterus means it can’t capture the foetus in its entirety. All the other images were either miscarried or terminated pregnancies.
Picturing Abortion Opposition in Sweden: Lennart Nilsson’s Early Photographs of Embryos and Fetuses Advance Access published 13 March 2017 Social History of Medicine Vol. 31, No. 2 pp. 278–307
Polygenic Inheritance thefactfactor.com Galton (1883) predicted that in human population characters such as height, skin colour and intelligence show continuous variations in expression and not only two contrasting expressions.
Cross-species identification of Mendel’s I locus Armstead et al., Science . 2007 Jan 5;315(5808):73. doi: 10.1126/science.1132912. A key gene involved in plant senescence, mutations of which partially disable chlorophyll catabolism and confer stay-green leaf and cotyledon phenotypes, has been identified in Pisum sativum, Arabidopsis thaliana, and Festuca pratensis by using classical and molecular genetics and comparative genomics. ‥ Genetic mapping in pea demonstrated cosegregation with the yellow/green cotyledon polymorphism (I/i) first reported by Gregor Mendel in 1866.
Genomic region associated with pod color variation in pea (Pisum sativum) Shirasawa et al., G3 Genes|Genomes|Genetics, Volume 11, Issue 5, May 2021. DNA sequences at this genomic location and transcriptome profiles of green and yellow pod lines were analyzed, and genes encoding 3′ exoribonucleases were selected as potential candidates controlling pod color.
Genetics and Analysis of Quantitative Traits 1998/1/19 Michael Lynch, Bruce Walsh
Introduction to Quantitative Genetics 1989/5/1 D.S. Falconer
量的遺伝学のYOUTUBE講義動画
Bruce Walsh
Introduction to Quantitative Genetics by Bruce Walsh International Centre for Theoretical Sciences チャンネル登録者数 5.7万人
講義ノート Introduction to Quantitative Genetics by Bruce Walsh Letcure notes などのキーワードでグーグル検索すると、この講義動画に沿った内容の講義ハンドアウトがネットで引っかかります。YOUTUBEには同じシリーズの他の動画もあります。
Lynn Jorde
Introduction to Population Genetics – Lynn Jorde (2016) National Human Genome Research Institute チャンネル登録者数 4.14万人
Using Falconer’s formula (Falconer et al., 1996) heritability can be calculated as twice the difference between monozygotic and dizygotic twin correlation (rmz and rdz, respectively), as shown in Equation 1.
Analysis of Heritability Using Genome-wide Data Jacob B. Hall and William S. Bush（Author manuscript）Curr Protoc Hum Genet. 2016 Oct 11; 91: 1.30.1–1.30.10. doi: 10.1002/cphg.25
GCTA: A Tool for Genome-wide Complex Trait Analysis. The American Journal of Human Genetics Volume 88, Issue 1, 7 January 2011, Pages 76-82 (Open access) There has not been any consensus on the explanation of the “missing heritability.” Possible explanations include a large number of common variants with small effects, rare variants with large effects, and DNA structural variation.
For quantitative traits, heritability can be estimated as 2(rMZ − rDZ) where rMZ refers to the co-twin phenotypic correlation for MZ twins and rDZ refers to the correlation for DZ twins.
Thirty years of investigations into the genetic causes of colorectal cancer have identified 14 genes that, when mutated, are associated with an increased risk of the disease. Now, a Saudi-US research collaboration has found two more genes, greatly improving the ability of clinicians to identify at-risk individuals, while indicating potential therapeutic options for chemo-therapy-resistant patients. ‥ The results showed two heritable genetic mutations in the genes ATM and PALB2 that were morecommon in cancer patients, suggesting a causal link. （Revealing the missing heritability of colorectal cancer Diagnosis of colorectal cancer may improve following the discovery of two gene mutations. References: AlDubayan, S. et al.The American Journal of Human Genetics102, 401-414 (2018).）
The missing heritability of familial colorectal cancer Mutagenesis. 2020 Jul; 35(3): 221–231. doi: 10.1093/mutage/gez027 PMCID: PMC7352099
Scientists Uncover Nearly All Genetic Variants Linked to Height Largest genome-wide association study achieves ‘the impossible’ By ALLESSANDRA DiCORATO | Broad Institute October 14, 2022 Now, by studying the DNA of 5.4 million people, a team led by those same geneticists has done what they thought years ago would be impossible. In the largest study of its kind to date, members of the GIANT consortium — including researchers at the Broad Institute of MIT and Harvard, Harvard Medical School, and Boston Children’s Hospital — have identified more than 12,000 genetic variants that influence height. These variants explain 10 percent to 40 percent of all variation in height, depending on a person’s ancestry. They cluster around parts of the genome involved in skeletal growth.
背丈の「失われた遺伝率」が見つかる 2万人分のゲノム解析から、稀な遺伝子バリアントによって形質が受け継がれる仕組みの一端が見えてきた。 Genetic study homes in on height’s heritability mystery Nature (2019-04-23) | DOI: 10.1038/d41586-019-01157-y Linda Geddes （2022 Assessing the contribution of rare variants to complex trait heritability from whole-genome sequence dataがバイオアーカイブに発表されたときの紹介）
How much of human height is genetic and how much is due to nutrition? Molecular biologist Chao-Qiang Lai of the Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University answers December 11, 2006 For example, say a man 175 cm tall marries a woman 165 cm tall, and both are from a Chinese population with a population mean of 170 cm for men and 160 cm for women. We can predict the height of their children, assuming the heritability is 65 percent for men and 60 percent for women in this population. For a son, the expected height difference from the population mean is: 0.65 x [(175 – 170) + (165 – 160)] / 2, which equals 3.25 cm; for a daughter, the difference is 0.6 x [(175 – 170) + (165 – 160)] / 2, which equals 3 cm. Thus, the expected height of a son is 170 + 3.2, or 173.2 cm, and of a daughter 160 + 3, or 163 cm. On the other hand, environmental effects can add 1.75 cm to a son’s height: 0.35 x [(175 – 170) + (165 – 160)] / 2, and 2 cm to a daughter’s: 0.4 x [(175 – 170) + (165 – 160)] / 2.
Defining the role of common variation in the genomic and biological architecture of adult human height. (PubMed full text) Nat Genet . 2014 Nov;46(11):1173-86. doi: 10.1038/ng.3097. Epub 2014 Oct 5. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid.
Genetics of human height Brian P. McEvoy, Peter M. Visscher Economics & Human Biology Volume 7, Issue 3, December 2009, Pages 294-306 無料要旨
First common height gene identified 2007 For the first time, scientists have identified one of the many genes which commonly influence our height. The work, which was partly funded by the EU, is published online by the journal Nature Genetics. The scientists studied the DNA of 5,000 people, looking for tiny differences in the genetic code which appeared more often in tall people than shorter people. This revealed that people with a certain version of a gene called HGMA2 were likely to be taller than people with a different version of the gene. The results were confirmed by a follow-up study of over 19,000 people. ‥ Little is known about the precise role of HGMA2, but the scientists believe that it could influence height by causing increased cell production. （HGMA2 ウィキペディア）
日本人の身長に関する研究
日本人における身長のポリジェニックスコアの地理的多様性 一色 真理子 東京大学理学系研究科 ヒトゲノム多様性研究室 アルバートアインシュタイン医科大学 遺伝学科 Geographic variation in the polygenic score of height in Japan. Mariko Isshiki, Yusuke Watanabe, Jun Ohashi J Hum Genet. 2021;66:1053-1060. 20220628 日本人類遺伝学会 論文紹介
Akiyama, M., Ishigaki, K., Sakaue, S., Momozawa, Y., Horikoshi, M. Hirata, M., Matsuda, K., Ikegawa, S., Takahashi, A., Kanai, M. et al. Characterizing rare and low-frequency height-associated variants in the Japanese population. Nature Communications10, 4393 (2019). doi: 10.1038/s41467-019-12276-5
Some rare gene variants have dramatic effects on height (for example, variants in the FGFR3gene cause achondroplasia, a rare condition characterized by short stature). For most individuals, though, height is controlled largely by a combination of genetic variants that each have more modest effects on height, plus a smaller contribution from environmental factors (such as nutrition). More than 700 such gene variants have been discovered and many more are expected to be identified. Some of these variants are in genes that directly or indirectly affect cartilage in growth plates, which are areas in the long bones of the legs and arms where new bone is produced, lengthening the bones as children grow. The function of many other height-associated genes remains unknown. https://medlineplus.gov/genetics/understanding/traits/height/
Your pituitary gland normally releases HGH in short bursts (pulses) throughout the day. The release of HGH is mainly controlled by two hormones your hypothalamus releases: growth hormone-releasing hormone (GHRH), which stimulates hGH release, and somatostatin, which prevents (inhibits) HGH release. Several other endocrine hormones also regulate HGH, including insulin-like growth factor 1 (IGF-1). IGF-1 is a major suppressor of GH production, whereas thyroxine, glucocorticoids and ghrelin stimulate HGH release. （https://my.clevelandclinic.org/health/articles/23309-human-growth-hormone-hgh）
For many years, growth hormone (GH) has been known to be the primary hormone responsible for body growth. The tallest man on record (http://www.guinnessworldrecords.com/world-records/tallest-man-ever/), Robert Wadlow, had an untreated pituitary tumor that secreted abnormally high levels of GH [7]. He grew throughout life, achieving a height of 8 ft., 11 in. at the time of his death. Even today, the tallest people on record tend to achieve their great heights due to untreated pituitary tumors. The reverse is also true. Individuals who, for whatever reason, do not make normal levels of GH as children or have defective GH receptors, are short statured [14]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7644140/
Specification of unique Pit-1 activity in the hGH locus control region Brian M. Shewchuk, Stephen A. Liebhaber, and Nancy E. CookeAuthors Info & Affiliations August 20, 2002 99 (18) 11784-11789 https://doi.org/10.1073/pnas.182418199 The hGH gene cluster spans 48 kb on chromosome 17q22-24 (for details see Fig. 1; ref. 9). This cluster contains the pituitary-expressed hGH-N and four genes expressed in the placenta: Chorionic somatomammotropin-like (hCS-L), hCS-A, hGH-variant (hGH-V), and hCS-B (Fig. 1).
P10912 · GHR_HUMANReceptor for pituitary gland growth hormone involved in regulating postnatal body growth. On ligand binding, couples to the JAK2/STAT5 pathway (By similarity).
The Growth Hormone Receptor: Mechanism of Receptor Activation, Cell Signaling, and Physiological Aspects Front Endocrinol (Lausanne). 2018; 9: 35. Published online 2018 Feb 13. doi: 10.3389/fendo.2018.00035 PMCID: PMC5816795
During puberty, hormones are essential for regulating body growth. These include thyroid hormones, human growth hormones, and sex hormones such as testosterone and estrogen. https://medicover-genetics.com/the-genetics-of-height/
