High-temperature superconductivity in copper oxides occurs when the materials are chemically tuned to have a carrier concentration intermediate between their metallic state at high doping and their insulating state at zero doping. The underlying evolution of the electron system in the absence of superconductivity is still unclear, and a question of central importance is whether it involves any intermediate phase with broken symmetry. The Fermi surface of the electronic states in the underdoped 'YBCO' materials YBa2Cu3O(y) and YBa2Cu4O8 was recently shown to include small pockets, in contrast with the large cylinder that characterizes the overdoped regime, pointing to a topological change in the Fermi surface. Here we report the observation of a negative Hall resistance in the magnetic-field-induced normal state of YBa2Cu3O(y) and YBa2Cu4O8, which reveals that these pockets are electron-like rather than hole-like. We propose that these electron pockets most probably arise from a reconstruction of the Fermi surface caused by the onset of a density-wave phase, as is thought to occur in the electron-doped copper oxides near the onset of antiferromagnetic order. Comparison with materials of the La2CuO4 family that exhibit spin/charge density-wave order suggests that a Fermi surface reconstruction also occurs in those materials, pointing to a generic property of high-transition-temperature (T(c)) superconductors.
In the quest to increase the critical temperature T c of cuprate superconductors, it is essential to identify the factors that limit the strength of superconductivity. The upper critical field H c2 is a fundamental measure of that strength, yet there is no agreement on its magnitude and doping dependence in cuprate superconductors. Here we show that the thermal conductivity can be used to directly detect H c2 in the cuprates YBa 2 Cu 3 O y , YBa 2 Cu 4 O 8 and Tl 2 Ba 2 CuO 6 þ d , allowing us to map out H c2 across the doping phase diagram. It exhibits two peaks, each located at a critical point where the Fermi surface of YBa 2 Cu 3 O y is known to undergo a transformation. Below the higher critical point, the condensation energy, obtained directly from H c2 , suffers a sudden 20-fold collapse. This reveals that phase competitionassociated with Fermi-surface reconstruction and charge-density-wave order-is a key limiting factor in the superconductivity of cuprates.
We report the observation of Shubnikov-de Haas oscillations in the underdoped cuprate superconductor YBa2Cu4O8 (Y124). For fields aligned along the c axis, the frequency of the oscillations is 660+/-30 T, which corresponds to approximately 2.4% of the total area of the first Brillouin zone. The effective mass of the quasiparticles on this orbit is measured to be 2.7+/-0.3 times the free electron mass. Both the frequency and mass are comparable to those recently observed for ortho-II YBa2Cu3O6.5 (Y123-II). We show that although small Fermi surface pockets may be expected from band-structure calculations in Y123-II, no such pockets are predicted for Y124. Our results therefore imply that these small pockets are a generic feature of the copper oxide plane in underdoped cuprates.
Abstract(À)-Epigallocatechin gallate (EGCG), a major biologically active constituent of green tea, inhibits activation of the epidermal growth factor (EGF) receptor (EGFR) and downstream signaling pathways in several types of human cancer cells, but the precise mechanism is not known. Because several plasma membrane-associated receptor tyrosine kinases (RTK) including EGFR are localized in detergent-insoluble ordered membrane domains, so-called ''lipid rafts,'' we examined whether the inhibitory effect of EGCG on activation of the EGFR is associated with changes in membrane lipid order in HT29 colon cancer cells. First, we did cold Triton X-100 solubility assays. Phosphorylated (activated) EGFR was found only in the Triton X-100-insoluble (lipid raft) fraction, whereas total cellular EGFR was present in the Triton X-100-soluble fraction. Pretreatment with EGCG inhibited the binding of Alexa Fluor 488-labeled EGF to the cells and also inhibited EGF-induced dimerization of the EGFR. To examine possible effects of EGCG on membrane lipid organization, we labeled the cells with the fluorescent lipid analogue 1, 1 ¶-dihexadecyl-3,3,3 ¶,3 ¶-tetramethylindocarbocyanine perchlorate, which preferentially incorporates into ordered membrane domains in cells and found that subsequent treatment with EGCG caused a marked reduction in the Triton X-100-resistant membrane fraction. Polyphenon E, a mixture of green tea catechins, had a similar effect but (À)-epicatechin (EC), the biologically inactive compound, did not significantly alter the Triton X-100 solubility properties of the membrane. Furthermore, we found that EGCG but not EC caused dramatic changes in the function of bilayer-incorporated gramicidin channels. Taken together, these findings suggest that EGCG inhibits the binding of EGF to the EGFR and the subsequent dimerization and activation of the EGFR by altering membrane organization. These effects may also explain the ability of EGCG to inhibit activation of other membrane-associated RTKs, and they may play a critical role in the anticancer effects of this and related compounds. [Cancer Res 2007; 67(13):6493-501]
Obesity and diabetes mellitus are risk factors for colon cancer. The activation of the insulin-like growth factor (IGF)/IGF-IR axis plays a critical role in this carcinogenesis. (−)-Epigallocatechin gallate (EGCG), the major constituent of green tea, seems to have both antiobesity and antidiabetic effects. This study examined the effects of EGCG on the development of azoxymethane-induced colonic premalignant lesions in C57BL/KsJ-db/db (db/db) mice, which are obese and develop diabetes mellitus. Male db/db mice were given four weekly s.c. injections of azoxymethane (15 mg/kg body weight) and then they received drinking water containing 0.01% or 0.1% EGCG for 7 weeks. At sacrifice, drinking water with EGCG caused a significant decrease in the number of total aberrant crypt foci, large aberrant crypt foci, and β-catenin accumulated crypts in these mice, all of which are premalignant lesions of the colon. The colonic mucosa of db/db mice expressed high levels of the IGF-IR, phosphorylated form of IGF-IR (p-IGF-IR), p-GSK-3β, β-catenin, cyclooxygenase-2, and cyclin D1 proteins, and EGCG in drinking water caused a marked decrease in the expression of these proteins. Treating these mice with EGCG also caused an increase in the serum level of IGFBP-3 while conversely decreasing the serum levels of IGF-I, insulin, triglyceride, cholesterol, and leptin. EGCG overcomes the activation of the IGF/IGF-IR axis, thereby inhibiting the development of colonic premalignant lesions in an obesity-related colon cancer model, which was also associated with hyperlipidemia, hyperinsulinemia, and hyperleptinemia. EGCG may be, therefore, useful in the chemoprevention or treatment of obesity-related colorectal cancer.
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