Direct observation of lattice symmetry breaking at the hidden-order transition in URu2Si2

Since the 1985 discovery of the phase transition at $T_{\rm HO}=17.5$ K in the heavy-fermion metal URu$_2$Si$_2$, neither symmetry change in the crystal structure nor magnetic ordering have been observed, which makes this "hidden order" enigmatic. Some high-field experiments have suggested electronic nematicity which breaks fourfold rotational symmetry, but direct evidence has been lacking for its ground state at zero magnetic field. Here we report on the observation of lattice symmetry breaking from the fourfold tetragonal to twofold orthorhombic structure by high-resolution synchrotron X-ray diffraction measurements at zero field, which pins down the space symmetry of the order. Small orthorhombic symmetry-breaking distortion sets in at $T_{\rm HO}$ with a jump, uncovering the weakly first-order nature of the hidden-order transition. This distortion is observed only in ultrapure sample, implying a highly unusual coupling nature between the electronic nematicity and underlying lattice.Comment: 17 pages, 3 figures. Submitted version. Revisions have been made through the review process. See the published version in Nature Communication

A Sharp Peak of the Zero-Temperature Penetration Depth at Optimal Composition in BaFe2(As1-xPx)2

In a superconductor, the ratio of the carrier density, $n$, to their effective mass, $m^*$, is a fundamental property directly reflecting the length scale of the superfluid flow, the London penetration depth, $\lambda_L$. In two dimensional systems, this ratio $n/m^*$ ($\sim 1/\lambda_L^2$) determines the effective Fermi temperature, $T_F$. We report a sharp peak in the $x$-dependence of $\lambda_L$ at zero temperature in clean samples of BaFe$_2$(As$_{1-x}$P$_x$)$_2$ at the optimum composition $x = 0.30$, where the superconducting transition temperature $T_c$ reaches a maximum of 30\,K. This structure may arise from quantum fluctuations associated with a quantum critical point (QCP). The ratio of $T_c/T_F$ at $x = 0.30$ is enhanced, implying a possible crossover towards the Bose-Einstein condensate limit driven by quantum criticality.Comment: Main text (5 pages, 4 figures) + Supplementary Materials (5 pages, 5 figures). Published on June 22, 201

Defective Membrane Remodeling in Neuromuscular Diseases: Insights from Animal Models

Proteins involved in membrane remodeling play an essential role in a plethora of cell functions including endocytosis and intracellular transport. Defects in several of them lead to human diseases. Myotubularins, amphiphysins, and dynamins are all proteins implicated in membrane trafficking and/or remodeling. Mutations in myotubularin, amphiphysin 2 (BIN1), and dynamin 2 lead to different forms of centronuclear myopathy, while mutations in myotubularin-related proteins cause Charcot-Marie-Tooth neuropathies. In addition to centronuclear myopathy, dynamin 2 is also mutated in a dominant form of Charcot-Marie-Tooth neuropathy. While several proteins from these different families are implicated in similar diseases, mutations in close homologues or in the same protein in the case of dynamin 2 lead to diseases affecting different tissues. This suggests (1) a common molecular pathway underlying these different neuromuscular diseases, and (2) tissue-specific regulation of these proteins. This review discusses the pathophysiology of the related neuromuscular diseases on the basis of animal models developed for proteins of the myotubularin, amphiphysin, and dynamin families. A better understanding of the common mechanisms between these neuromuscular disorders will lead to more specific health care and therapeutic approaches