There is a long-standing debate about whether spin-charge separation is the root cause of the peculiar normal-state properties and high superconducting transition temperatures of the high-Tc materials. In the proposed state of matter, the elementary excitations are not electron-like, as in conventional metals, but rather the electron 'fractionalizes' to give excitations that are chargeless spin-1/2 fermions (spinons) and charge +e bosons (chargons). Although spin-charge separation has been well established in one dimension, the theoretical situation for two dimensions is controversial and experimental evidence for it in the high-Tc materials is indirect. A model with sharp experimental tests for a particular type of separation in two dimensions has recently been proposed. Here we report the results of those experimental tests, placing a conservative upper limit of 190 K on the energy of the proposed topological defects known as visons. There is still debate about the extent to which this experiment can settle the issue of spin-charge separation in the high-Tc copper oxides, because some forms of the separation are able to avoid the need for visons. But at least one class of theories that all predict a vortex-memory effect now are unlikely models for the copper oxides.

Many studies have suggested that disialogangliosides, GD2 and GD3, are involved in the development of various tumor types. However, the functional relationships between ganglioside expression and cancer development or aggressiveness are not fully described. GD3 is upregulated in approximately half of all invasive ductal breast carcinoma cases, and enhanced expression of GD3 synthase (GD3S, alpha-N-acetylneuraminide alpha-2,8-sialyltransferase) in estrogen receptor-negative breast tumors, was shown to correlate with reduced overall patient survival. We previously found that GD2 and GD3, together with their common upstream glycosyltransferases, GD3S and GD2/GM2 synthase, maintain a stem cell phenotype in breast cancer stem cells (CSCs). In the current study, we demonstrate that GD3S alone can sustain CSC properties and also promote malignant cancer properties. Using MALDI-MS and flow cytometry, we found that breast cancer cell lines, of various subtypes with or without ectopic GD3S-expression, exhibited distinct GD2/GD3 expression profiles. Furthermore, we found that GD3 was associated with EGFR and activated EGFR signaling in both breast CSCs and breast cancer cell lines. In addition, GD3S knockdown enhanced cytotoxicity of the EGFR-inhibitor gefitinib in resistant MDA-MB468 cells, both in vitro and in vivo. Based on this evidence, we propose that GD3S contributes to gefitinib-resistance in EGFR-positive breast cancer cells and may be an effective therapeutic target in drug-resistant breast cancers.

Magnetic flux in superconductors is usually quantized in units of h/2e. Here we report scanning SQUID and scanning Hall probe studies of single fluxoids in high purity YBa2Cu3O6.35 crystals (T(c) less, similar 13 K), extending flux quantization studies to a region of the cuprate phase diagram where the superfluid density is sufficiently low that novel behavior has been predicted. Some scenarios in which superconductivity results from spin-charge separation predict h/e fluxoids in materials with low superfluid density. Our observations of only h/2e fluxoids set limits on these theories.

G protein‐coupled estrogen receptor‐1 (GPER), a member of the G protein‐coupled receptor (GPCR) superfamily, mediates estrogen‐induced proliferation of normal and malignant breast epithelial cells. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here we showed greater expression of GPER in BCSCs than non‐BCSCs of three patient‐derived xenografts of ER−/PR+ breast cancers. GPER silencing reduced stemness features of BCSCs as reflected by reduced mammosphere forming capacity in vitro, and tumor growth in vivo with decreased BCSC populations. Comparative phosphoproteomics revealed greater GPER‐mediated PKA/BAD signaling in BCSCs. Activation of GPER by its ligands, including tamoxifen (TMX), induced phosphorylation of PKA and BAD‐Ser118 to sustain BCSC characteristics. Transfection with a dominant‐negative mutant BAD (Ser118Ala) led to reduced cell survival. Taken together, GPER and its downstream signaling play a key role in maintaining the stemness of BCSCs, suggesting that GPER is a potential therapeutic target for eradicating BCSCs.