Origin of the Suppression of Magnetic Order in MnSi under Hydrostatic Pressure.

We experimentally study the evolution of the magnetic moment m and exchange interaction J as a function of hydrostatic pressure in the zero-field helimagnetic phase of the strongly correlated electron system MnSi. The suppression of magnetic order at ≈1.5  GPa is shown to arise from the J collapse and not from a quantum fluctuations induced reduction of m.

Unveiling nodeless unconventional superconductivity proximate to honeycomb-vacancy ordering in the Ir-Sb binary system.

Vacancies in solid-state physics are underexplored in materials with strong electron-electron correlations. Recent research on the Ir-Sb binary system revealed an extended buckled-honeycomb vacancy (BHV) order. Superconductivity arises by suppressing BHV ordering through high-pressure growth with excess Ir atoms or Rh substitution, yet the superconducting pairing nature remains unknown.

Depth-dependent study of time-reversal symmetry-breaking in the kagome superconductor AVSb.

The breaking of time-reversal symmetry (TRS) in the normal state of kagome superconductors AVSb stands out as a significant feature, but its tunability is unexplored. Using low-energy muon spin rotation and local field numerical analysis, we study TRS breaking as a function of depth in single crystals of RbVSb (with charge order) and Cs(VTa)Sb (without charge order). In the bulk of RbVSb (>33 nm from the surface), we observed an increase in the internal magnetic field width in the charge-ordered state.

Microscopic probing of the superconducting and normal state properties of TaVSi by muon spin rotation.

The two-dimensional kagome lattice is an experimental playground for novel physical phenomena, from frustrated magnetism and topological matter to chiral charge order and unconventional superconductivity. A newly identified kagome superconductor, TaVSi has recently gained attention for possessing a record high critical temperature,  = 7.5 K for kagome metals at ambient pressure.

Role of Inflammation and the NF-κB Signaling Pathway in Hirschsprung's Disease.

Hirschsprung's disease (HSCR, incidence 1/5000 live births) is caused by the failure of neural crest-derived precursors to migrate, survive, proliferate, or differentiate during the embryonic development of the Enteric Nervous System (ENS), which could be disrupted by many factors, including inflammatory processes. The NF-κB family controls several biological processes, including inflammation, neurogenesis, and cell migration. With the aim of studying the potential role of NF-κB in HSCR, we have analyzed the expression of the NF-κB main subunits and other NF-κB-related genes by RT-qPCR in HSCR tissue samples (sub-divided into ganglionic and aganglionic segments).