Kyushu University Academic Staff Educational and Research Activities Database
List of Reports
Chikara Meno Last modified date:2022.06.13

Professor / Bioregulation / Department of Basic Medicine / Faculty of Medical Sciences

1. H Hamada, C Meno, Y Saijoh, H Adachi, K Yashiro, R Sakuma, H Shiratori, Role of asymmetric signals in left-right patterning in the mouse, AMERICAN JOURNAL OF MEDICAL GENETICS, Vol.101, No.4, pp.324-327, 2001.07, Left-right asymmetric signaling molecules in mammals include three transforming growth factor beta (TGF beta)-related factors, Nodal, Lefty1 and Lefty2. They are all expressed on the left half of developing mouse embryos. Nodal acts as a left-side determinant by transducing signals through Smad and FAST and by inducing Pitx2 expression on the left side. Lefty proteins are antagonists that inhibit Nodal signaling. There are positive and negative transcriptional regulatory loops between nodal and lefty2 genes. Thus, Nodal activates its own gene and lefty2, Lefty2 protein produced then inhibits Nodal signaling and terminates expression of both genes. This feedback mechanism can restrict the range and duration of Nodal signaling in developing embryos, (C) 2001 Wiley-Liss, Inc..
2. Hiroshi Hamada, Chikara Meno, Daisuke Watanabe, Yukio Saijoh, Establishment of vertebrate left-right asymmetry., Nature reviews. Genetics, Vol.3, No.2, pp.103-13, 2002.02, The generation of morphological, such as left-right, asymmetry during development is an integral part of the establishment of a body plan. Until recently, the molecular basis of left-right asymmetry was a mystery, but studies indicate that Nodal and the Lefty proteins, transforming growth factor-beta-related molecules, have a central role in generating asymmetric signals. Although the initial mechanism of symmetry breaking remains unknown, developmental biologists are beginning to analyse the pathway that leads to left-right asymmetry establishment and maintenance..
3. Robert H Anderson, Nigel A Brown, Chikara Meno, Diane E Spicer, The importance of being isomeric., Clinical anatomy (New York, N.Y.), 10.1002/ca.22517, Vol.28, No.4, pp.477-86, 2015.05, In the normal individual, the parietal components of the body are mirror-imaged and appropriately described as isomeric. The thoraco-abdominal organs, in contrast, are lateralized. However, in "visceral heterotaxy," the thoraco-abdominal organs also show some degree of isomerism, best seen in the arrangement of the bronchial tree. Whether isomerism can be found within the heart remains controversial. One of two recent publications in this journal emphasized the crucial features of bronchial isomerism; the other, in contrast, confused the situation of isomerism within the heart. In this review, we show how the topic of cardiac isomerism is clarified by concentrating on the anatomical features of the cardiac components and determining how best they can be described. Appropriate manipulation of developing mice produces unequivocal evidence of isomerism of the atrial appendages, but with no evidence of ventricular isomerism. In hearts from patients with so-called "heterotaxy," only the atrial appendages, distinguished on the basis of the pectinate muscles lining their walls, are uniformly isomeric, permitting the syndrome to be differentiated into the subsets of left as opposed to right atrial appendage isomerism. Thus, controversies are defused by simply describing the isomerism of the atrial appendages rather than "atrial isomerism," recognizing the frequency of abnormal venoatrial connections in these settings. Any suggestion of ambiguity is removed by the equally simple expedient of describing all the variable cardiac features, describing the arrangements of the thoracic and abdominal organs separately should there be discordances..