Cooper Pair Formation in U(1) Gauge Theory of High Temperature Superconductivity

We study the two-dimensional spin-charge separated Ginzburg-Landau theory containing U(1) gauge interactions as a semi-phenomenological model describing fluctuating condensates in high temperature superconductivity. Transforming the original GL action, we abstract the effective action of Cooper pair. Especially, we clarify how Cooper pair correlation evolves in the normal state from the point of view of spin-charge separation. Furthermore, we point out how Cooper pair couples to gauge field in a gauge-invariant way, stressing the insensitivity of Cooper pair to infrared gauge field fluctuation.Comment: 4 pages, 5 figures included, submitted to J. Phys. Soc. Jp

Phase Separation Based on U(1) Slave-boson Functional Integral Approach to the t-J Model

We investigate the phase diagram of phase separation for the hole-doped two dimensional system of antiferromagnetically correlated electrons based on the U(1) slave-boson functional integral approach to the t-J model. We show that the phase separation occurs for all values of J/t, that is, whether $0 < J/t < 1$ or $J/t \geq 1$ with J, the Heisenberg coupling constant and t, the hopping strength. This is consistent with other numerical studies of hole-doped two dimensional antiferromagnets. The phase separation in the physically interesting J region, $0 < J/t \lesssim 0.4$ is examined by introducing hole-hole (holon-holon) repulsive interaction. We find from this study that with high repulsive interaction between holes the phase separation boundary tends to remain robust in this low $J$ region, while in the high J region, J/t > 0.4, the phase separation boundary tends to disappear.Comment: 4 pages, 2 figures, submitted to Phys. Rev.

Stripes due to the next-nearest neighbor exchange in high-Tc cuprates

We propose a possible mechanism of the charge stripe order due to the next-nearest neighbor exchange interaction J' in the two-dimensional t-J model, based on the concept of the phase separation. We also calculate some hole correlation functions of the finite cluster of the model using the numerical diagonalization, to examine the realization of the mechanism. It is also found that the next-nearest neighbor hopping t' suppresses the stripe order induced by the present mechanism for t'0.Comment: 4 pages, Revtex, with 5 eps figures, to appear in Phys. Rev. B Rapid Communications (April 1, 2001

Non-Fermi liquid behavior and scaling of low frequency suppression in optical conductivity spectra of CaRuO3_3

Optical conductivity spectra $\sigma_1(\omega)$ of paramagnetic CaRuO$_3$ are investigated at various temperatures. At T=10 K, it shows a non-Fermi liquid behavior of $\sigma_1(\omega)\sim 1/{\omega}^{\frac 12}$, similar to the case of a ferromagnet SrRuO$_3$. As the temperature ($T$) is increased, on the other hand, $\sigma_1(\omega)$ in the low frequency region is progressively suppressed, deviating from the 1/{\omega}^{\frac 12%}-dependence. Interestingly, the suppression of $\sigma_1(\omega)$ is found to scale with $\omega /T$ at all temperatures. The origin of the $$ scaling behavior coupled with the non-Fermi liquid behavior is discussed.Comment: 4 pages, 3 figure

Boundary degrees of freedom in fractional quantum Hall effect: Excitations on common boundary of two samples

Using the Carlip's method we have derived the boundary action for the fermion Chern-Simons theory of quantum Hall effects on a planar region with a boundary. We have computed both the bulk and edge responses of currents to the external electric field. From this we obtain the well-known anomaly relation and the boundary Hall current without introducing any ad hoc assumptions such as the chirality condition. In addition, the edge current on the common boundary of two samples is found to be proportional to the difference between Chern-Simons coupling strengths.Comment: 20 pages, uses revte

Conventional and molecular cytogenetics of human non-medullary thyroid carcinoma: characterization of eight cell line models and review of the literature on clinical samples

<p>Abstract</p> <p>Background</p> <p>Cell lines are often poorly characterized from a genetic point of view, reducing their usefulness as tumor models. Our purpose was to assess the genetic background of eight commonly used human thyroid carcinoma models and to compare the findings with those reported for primary tumors of the gland.</p> <p>Methods</p> <p>We used chromosome banding analysis and comparative genomic hybridization to profile eight non-medullary thyroid carcinoma cell lines of papillary (TPC-1, FB2, K1 and B-CPAP), follicular (XTC-1) or anaplastic origin (8505C, C643 and HTH74). To assess the representativeness of the findings, we additionally performed a thorough review of cytogenetic (n = 125) and DNA copy number information (n = 270) available in the literature on clinical samples of thyroid carcinoma.</p> <p>Results</p> <p>The detailed characterization of chromosomal markers specific for each cell line revealed two cases of mistaken identities: FB2 was shown to derive from TPC-1 cells, whereas K1 cells have their origin in cell line GLAG-66. All cellular models displayed genomic aberrations of varying complexity, and recurrent gains at 5p, 5q, 8q, and 20q (6/7 cell lines) and losses at 8p, 13q, 18q, and Xp (4/7 cell lines) were seen. Importantly, the genomic profiles were compatible with those of the respective primary tumors, as seen in the meta-analysis of the existing literature data.</p> <p>Conclusion</p> <p>We provide the genomic background of seven independent thyroid carcinoma models representative of the clinical tumors of the corresponding histotypes, and highlight regions of recurrent aberrations that may guide future studies aimed at identifying target genes. Our findings further support the importance of routinely performing cytogenetic studies on cell lines, to detect cross-contamination mishaps such as those identified here.</p

Is PTEN loss associated with clinical outcome measures in human prostate cancer?

Inactivating PTEN mutations are commonly found in prostate cancer, resulting in an increased activation of Akt. In this study, we investigate the role of PTEN deletion and protein expression in the development of hormone-refractory prostate cancer using matched hormone-sensitive and hormone-refractory tumours. Fluorescent in situ hybridisation and immunohistochemistry was carried out to investigate PTEN gene deletion and PTEN protein expression in the transition from hormone-sensitive to hormone-refractory prostate cancer utilising 68 matched hormone sensitive and hormone-refractory tumour pairs (one before and one after hormone relapse). Heterogeneous PTEN gene deletion was observed in 23% of hormone sensitive tumours. This increased significantly to 52% in hormone-refractory tumours (P=0.044). PTEN protein expression was observed in the membrane, cytoplasm and the nucleus. In hormone sensitive tumours, low levels of cytoplasmic PTEN was independently associated with shorter time to relapse compared to high levels of PTEN (P=0.028, hazard ratio 0.51 (95%CI 0.27–0.93). Loss of PTEN expression in the nucleus of hormone sensitive tumours was independently associated with disease-specific survival (P=0.031, hazard ratio 0.52, 95%CI 0.29–0.95). The results from this study demonstrate a role for both cytoplasmic and nuclear PTEN in progression of prostate cancer to the hormone-refractory state

Investigation of the role of SDHB inactivation in sporadic phaeochromocytoma and neuroblastoma

Germline mutations in the succinate dehydrogenase (SDH) (mitochondrial respiratory chain complex II) subunit B gene, SDHB, cause susceptibility to head and neck paraganglioma and phaeochromocytoma. Previously, we did not identify somatic SDHB mutations in sporadic phaeochromocytoma, but SDHB maps to 1p36, a region of frequent loss of heterozygosity (LOH) in neuroblastoma as well. Hence, to evaluate SDHB as a candidate neuroblastoma tumour suppressor gene (TSG) we performed mutation analysis in 46 primary neuroblastomas by direct sequencing, but did not identify germline or somatic SDHB mutations. As TSGs such as RASSF1A are frequently inactivated by promoter region hypermethylation, we designed a methylation-sensitive PCR-based assay to detect SDHB promoter region methylation. In 21% of primary neuroblastomas and 32% of phaeochromocytomas (32%) methylated (and unmethylated) alleles were detected. Although promoter region methylation was also detected in two neuroblastoma cell lines, this was not associated with silencing of SDHB expression, and treatment with a demethylating agent (5-azacytidine) did not increase SDH activity. These findings suggest that although germline SDHB mutations are an important cause of phaeochromocytoma susceptibility, somatic inactivation of SDHB does not have a major role in sporadic neural crest tumours and SDHB is not the target of 1p36 allele loss in neuroblastoma and phaeochromocytoma

Consensus Statement on next-generation-sequencing-based diagnostic testing of hereditary phaeochromocytomas and paragangliomas

Genome Instability and Cance