Direct observation of Tomonaga-Luttinger-liquid state in carbon nanotubes at low temperatures

The electronic transport properties of conventional three-dimensional metals are successfully described by Fermi-liquid theory. But when the dimensionality of such a system is reduced to one, the Fermi-liquid state becomes unstable to Coulomb interactions, and the conduction electrons should instead behave according to Tomonaga-Luttinger-liquid (TLL) theory. Such a state reveals itself through interaction-dependent anomalous exponents in the correlation functions, density of states and momentum distribution of the electrons. Metallic single-walled carbon nanotubes (SWNTs) are considered to be ideal one-dimensional systems for realizing TLL states. Indeed, the results of transport measurements on metal-SWNT and SWNT-SWNT junctions have been attributed to the effects of tunnelling into or between TLLs, although there remains some ambiguity in these interpretations. Direct observations of the electronic states in SWNTs are therefore needed to resolve these uncertainties. Here we report angle-integrated photoemission measurements of SWNTs. Our results reveal an oscillation in the pi-electron density of states owing to one-dimensional van Hove singularities, confirming the one-dimensional nature of the valence band. The spectral function and intensities at the Fermi level both exhibit power-law behaviour (with almost identical exponents) in good agreement with theoretical predictions for the TLL state in SWNTs.     

Between two worlds: Yamanouchi Shigeo and eugenics in early twentieth-century Japan

This paper explores the eugenic through of Yamanouchi Shigeo (1876-1973), who was trained in plant cytology under the tutelage of botanist and eugenicist John Coulter (1851-1928) in the USA, and later become one of the early and important popularizers of eugenic ideas in Japan. His career demonstrates a direct link between Japanese and US eugenics. Despite his academic training and research at various internationally renowned institutions, numerous publications, and longevity, his life has received little scholarly attention. By the early twentieth century, most biologists in Japan, as in the USA, began accepting Mendelian evolutionary theory and rejecting the Lamarckian notion of inheritance of acquire characteristics. However, Yamanouchi Shigeo's eugenic view represents a paradox: he was a mendelian cytologist sympathetic to Lamarckism. Was his 'nurture'-oriented eugenic view unscientific? is that why he was largely ignored in the history of botany in Japan? This study attempts to answer these questions and to analyse the origins and distinct features of Yamanouchi's eugenic ideas by situating Yamanouchi's eugenic through historically and culturally. After examining his scientific papers, popular writings, and documents of various organizations to which he belonged, I argue that Yamanouchi's 'softer' (or less biologically deterministic) perspective may have reflected the Japanese desire to catch up with the dominant 'race' by using eugenics without accepting permanent inferior status.     

A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities

Rheumatoid arthritis is a common autoimmune disease with a complex genetic etiology. Here we identify a SNP in the promoter region of FCRL3, a member of the Fc receptor-like family, that is associated with susceptibility to rheumatoid arthritis (odds ratio = 2.15, P = 0.00000085). This polymorphism alters the binding affinity of nuclear factor-kappaB and regulates FCRL3 expression. We observed high FCRL3 expression on B cells and augmented autoantibody production in individuals with the disease-susceptible genotype. We also found associations between the SNP and susceptibility to autoimmune thyroid disease and systemic lupus erythematosus. FCRL3 may therefore have a pivotal role in autoimmunity.     

CD38 is critical for social behaviour by regulating oxytocin secretion

CD38, a transmembrane glycoprotein with ADP-ribosyl cyclase activity, catalyses the formation of Ca2+ signalling molecules, but its role in the neuroendocrine system is unknown. Here we show that adult CD38 knockout (CD38-/-) female and male mice show marked defects in maternal nurturing and social behaviour, respectively, with higher locomotor activity. Consistently, the plasma level of oxytocin (OT), but not vasopressin, was strongly decreased in CD38-/- mice. Replacement of OT by subcutaneous injection or lentiviral-vector-mediated delivery of human CD38 in the hypothalamus rescued social memory and maternal care in CD38-/- mice. Depolarization-induced OT secretion and Ca2+ elevation in oxytocinergic neurohypophysial axon terminals were disrupted in CD38-/- mice; this was mimicked by CD38 metabolite antagonists in CD38+/+ mice. These results reveal that CD38 has a key role in neuropeptide release, thereby critically regulating maternal and social behaviours, and may be an element in neurodevelopmental disorders.     

A genome-wide association study identifies two new susceptibility loci for lung adenocarcinoma in the Japanese population

Lung adenocarcinoma is the most common histological type of lung cancer, and its incidence is increasing worldwide. To identify genetic factors influencing risk of lung adenocarcinoma, we conducted a genome-wide association study and two validation studies in the Japanese population comprising a total of 6,029 individuals with lung adenocarcinoma (cases) and 13,535 controls. We confirmed two previously reported risk loci, 5p15.33 (rs2853677, P(combined) = 2.8 × 10(-40), odds ratio (OR) = 1.41) and 3q28 (rs10937405, P(combined) = 6.9 × 10(-17), OR = 1.25), and identified two new susceptibility loci, 17q24.3 (rs7216064, P(combined) = 7.4 × 10(-11), OR = 1.20) and 6p21.3 (rs3817963, P(combined) = 2.7 × 10(-10), OR = 1.18). These data provide further evidence supporting a role for genetic susceptibility in the development of lung adenocarcinoma.     

Between Two Worlds: Yamanouchi Shigeo and Eugenics in Early Twentieth‐Century Japan

The 1935 conflict on the nature of relativistic degeneracy that pitted Subrahmanyan Chandrasekhar against Arthur Stanley Eddington is part of astronomical lore. In recountings of the events surrounding the dispute, the complaint is frequently aired that Chandrasekhar, who faced the pre-eminent astrophysicist of his time, did not enjoy the support of the astronomical community, which opted to side instead with Eddington. We reconsider these statements in the light of the published record and argue that the reception of Chandrasekhar's ideas was, if anything, rather favourable and that any perceived lack of support may have been due in great part to the inability to distinguish, on an observational basis, between the predictions of the competing theories. We further argue that the observational situation improved little over the subsequent thirty years, but that this did not prevent Chandrasekhar's version of relativistic degeneracy, and associated theory of electron-degenerate stars, from gaining a central position within the realm of stellar structure and evolution. We briefly compare this status to that enjoyed by general relativity before 1960.     

Mutations in SLC6A19, encoding B0AT1, cause Hartnup disorder

Hartnup disorder, an autosomal recessive defect named after an English family described in 1956 (ref. 1), results from impaired transport of neutral amino acids across epithelial cells in renal proximal tubules and intestinal mucosa. Symptoms include transient manifestations of pellagra (rashes), cerebellar ataxia and psychosis. Using homozygosity mapping in the original family in whom Hartnup disorder was discovered, we confirmed that the critical region for one causative gene was located on chromosome 5p15 (ref. 3). This region is homologous to the area of mouse chromosome 13 that encodes the sodium-dependent amino acid transporter B(0)AT1 (ref. 4). We isolated the human homolog of B(0)AT1, called SLC6A19, and determined its size and molecular organization. We then identified mutations in SLC6A19 in members of the original family in whom Hartnup disorder was discovered and of three Japanese families. The protein product of SLC6A19, the Hartnup transporter, is expressed primarily in intestine and renal proximal tubule and functions as a neutral amino acid transporter.