Realization of SU(2)*SU(6) Fermi System

We report the realization of a novel degenerate Fermi mixture with an SU(2)*SU(6) symmetry in a cold atomic gas. We successfully cool the mixture of the two fermionic isotopes of ytterbium 171Yb with the nuclear spin I=1/2 and 173Yb with I=5/2 below the Fermi temperature T_ F as 0.46T_F for 171Yb and 0.54T_F for 173Yb. The same scattering lengths for different spin components make this mixture featured with the novel SU(2)*SU(6) symmetry. The nuclear spin components are separately imaged by exploiting an optical Stern-Gerlach effect. In addition, the mixture is loaded into a 3D optical lattice to implement the SU(2)*SU(6) Hubbard model. This mixture will open the door to the study of novel quantum phases such as a spinor Bardeen-Cooper-Schrieffer-like fermionic superfluid.Comment: 4 pages, 5 figures V2: revised reference

Vestigial-like 2 contributes to normal muscle fiber type distribution in mice

Honda, M., Hidaka, K., Fukada, Si. et al. Vestigial-like 2 contributes to normal muscle fiber type distribution in mice. Sci Rep 7, 7168 (2017). https://doi.org/10.1038/s41598-017-07149-

TRIAC disrupts cerebral thyroid hormone action via negative feedback and heterogenous distribution among organs

Summary: As 3,3′,5-triiodothyroacetic acid (TRIAC), a metabolite of thyroid hormones (THs), was previously detected in sewage effluent, we aimed to investigate exogenous TRIAC’s potential for endocrine disruption. We administered either TRIAC or 3,3′,5-triiodo-L-thyronine (LT3) to euthyroid mice and 6-propyl-2-thiouracil-induced hypothyroid mice. In hypothyroid mice, TRIAC administration suppressed the hypothalamus-pituitary-thyroid (HPT) axis and upregulated TH-responsive genes in the pituitary gland, the liver, and the heart. We observed that, unlike LT3, TRIAC administration did not upregulate cerebral TH-responsive genes. Measurement of TRIAC contents suggested that TRIAC was not efficiently trafficked into the cerebrum. By analyzing euthyroid mice, we found that cerebral TRIAC content did not increase despite TRIAC administration at higher concentrations, whereas serum levels and cerebral contents of THs were substantially decreased. Disruption by TRIAC is due to the additive effects of circulating endogenous THs being depleted via a negative feedback loop involving the HPT axis and heterogeneous distribution of TRIAC among different organs