U(1) Gauge Theory as Quantum Hydrodynamics

It is shown that gauge theories are most naturally studied via a polar decomposition of the field variable. Gauge transformations may be viewed as those that leave the density invariant but change the phase variable by additive amounts. The path integral approach is used to compute the partition function. When gauge fields are included, the constraint brought about by gauge invariance simply means an appropriate linear combination of the gradients of the phase variable and the gauge field is invariant. No gauge fixing is needed in this approach that is closest to the spirit of the gauge principle. We derive an exact formula for the condensate fraction and in case it is zero, an exact formula for the anomalous exponent. We also derive a formula for the vortex strength which involves computing radiation corrections.Comment: 15 pages, Plain LaTeX, final published versio

Algebraic Comparison of Partial Lists in Bioinformatics

The outcome of a functional genomics pipeline is usually a partial list of genomic features, ranked by their relevance in modelling biological phenotype in terms of a classification or regression model. Due to resampling protocols or just within a meta-analysis comparison, instead of one list it is often the case that sets of alternative feature lists (possibly of different lengths) are obtained. Here we introduce a method, based on the algebraic theory of symmetric groups, for studying the variability between lists ("list stability") in the case of lists of unequal length. We provide algorithms evaluating stability for lists embedded in the full feature set or just limited to the features occurring in the partial lists. The method is demonstrated first on synthetic data in a gene filtering task and then for finding gene profiles on a recent prostate cancer dataset

Single-Particle Green Functions in Exactly Solvable Models of Bose and Fermi Liquids

Based on a class of exactly solvable models of interacting bose and fermi liquids, we compute the single-particle propagators of these systems exactly for all wavelengths and energies and in any number of spatial dimensions. The field operators are expressed in terms of bose fields that correspond to displacements of the condensate in the bose case and displacements of the fermi sea in the fermi case. Unlike some of the previous attempts, the present attempt reduces the answer for the spectral function in any dimension in both fermi and bose systems to quadratures. It is shown that when only the lowest order sea-displacement terms are included, the random phase approximation in its many guises is recovered in the fermi case, and Bogoliubov's theory in the bose case. The momentum distribution is evaluated using two different approaches, exact diagonalisation and the equation of motion approach. The novelty being of course, the exact computation of single-particle properties including short wavelength behaviour.Comment: Latest version to be published in Phys. Rev. B. enlarged to around 40 page

The Role of Nonequilibrium Dynamical Screening in Carrier Thermalization

We investigate the role played by nonequilibrium dynamical screening in the thermalization of carriers in a simplified two-component two-band model of a semiconductor. The main feature of our approach is the theoretically sound treatment of collisions. We abandon Fermi's Golden rule in favor of a nonequilibrium field theoretic formalism as the former is applicable only in the long-time regime. We also introduce the concept of nonequilibrium dynamical screening. The dephasing of excitonic quantum beats as a result of carrier-carrier scattering is brought out. At low densities it is found that the dephasing times due to carrier-carrier scattering is in picoseconds and not femtoseconds, in agreement with experiments. The polarization dephasing rates are computed as a function of the excited carrier density and it is found that the dephasing rate for carrier-carrier scattering is proportional to the carrier density at ultralow densities. The scaling relation is sublinear at higher densities, which enables a comparison with experiment.Comment: Revised version with additional refs. 12 pages, figs. available upon request; Submitted to Phys. Rev.

Hsa-miRNA-765 as a key mediator for inhibiting growth, migration and invasion in fulvestrant-treated prostate cancer

Fulvestrant (ICI-182,780) has recently been shown to effectively suppress prostate cancer cell growth in vitro and in vivo. But it is unclear whether microRNAs play a role in regulating oncogene expression in fulvestrant-treated prostate cancer. Here, this study reports hsa-miR-765 as the first fulvestrant-driven, ERβ-regulated miRNA exhibiting significant tumor suppressor activities like fulvestrant, against prostate cancer cell growth via blockage of cell-cycle progression at the G2/M transition, and cell migration and invasion possibly via reduction of filopodia/intense stress-fiber formation. Fulvestrant was shown to upregulate hsa-miR-765 expression through recruitment of ERβ to the 5′-regulatory-region of hsa-miR-765. HMGA1, an oncogenic protein in prostate cancer, was identified as a downstream target of hsa-miR-765 and fulvestrant in cell-based experiments and a clinical study. Both the antiestrogen and the hsa-miR-765 mimic suppressed HMGA1 protein expression. In a neo-adjuvant study, levels of hsa-miR-765 were increased and HMGA1 expression was almost completely lost in prostate cancer specimens from patients treated with a single dose (250 mg) of fulvestrant 28 days before prostatectomy. These findings reveal a novel fulvestrant signaling cascade involving ERβ-mediated transcriptional upregulation of hsa-miR-765 that suppresses HMGA1 protein expression as part of the mechanism underlying the tumor suppressor action of fulvestrant in prostate cancer. © 2014 Leung et al

TMPRSS2-ERG -specific transcriptional modulation is associated with prostate cancer biomarkers and TGF-β signaling

<p>Abstract</p> <p>Background</p> <p><it>TMPRSS2-ERG </it>gene fusions occur in about 50% of all prostate cancer cases and represent promising markers for molecular subtyping. Although <it>TMPRSS2-ERG </it>fusion seems to be a critical event in prostate cancer, the precise functional role in cancer development and progression is still unclear.</p> <p>Methods</p> <p>We studied large-scale gene expression profiles in 47 prostate tumor tissue samples and in 48 normal prostate tissue samples taken from the non-suspect area of clinical low-risk tumors using Affymetrix GeneChip Exon 1.0 ST microarrays.</p> <p>Results</p> <p>Comparison of gene expression levels among <it>TMPRSS2-ERG </it>fusion-positive and negative tumors as well as benign samples demonstrated a distinct transcriptional program induced by the gene fusion event. Well-known biomarkers for prostate cancer detection like <it>CRISP3 </it>were found to be associated with the gene fusion status. WNT and TGF-β/BMP signaling pathways were significantly associated with genes upregulated in <it>TMPRSS2-ERG </it>fusion-positive tumors.</p> <p>Conclusions</p> <p>The <it>TMPRSS2-ERG </it>gene fusion results in the modulation of transcriptional patterns and cellular pathways with potential consequences for prostate cancer progression. Well-known biomarkers for prostate cancer detection were found to be associated with the gene fusion. Our results suggest that the fusion status should be considered in retrospective and future studies to assess biomarkers for prostate cancer detection, progression and targeted therapy.</p

Gene expression profiles of prostate cancer reveal involvement of multiple molecular pathways in the metastatic process

BACKGROUND: Prostate cancer is characterized by heterogeneity in the clinical course that often does not correlate with morphologic features of the tumor. Metastasis reflects the most adverse outcome of prostate cancer, and to date there are no reliable morphologic features or serum biomarkers that can reliably predict which patients are at higher risk of developing metastatic disease. Understanding the differences in the biology of metastatic and organ confined primary tumors is essential for developing new prognostic markers and therapeutic targets. METHODS: Using Affymetrix oligonucleotide arrays, we analyzed gene expression profiles of 24 androgen-ablation resistant metastatic samples obtained from 4 patients and a previously published dataset of 64 primary prostate tumor samples. Differential gene expression was analyzed after removing potentially uninformative stromal genes, addressing the differences in cellular content between primary and metastatic tumors. RESULTS: The metastatic samples are highly heterogenous in expression; however, differential expression analysis shows that 415 genes are upregulated and 364 genes are downregulated at least 2 fold in every patient with metastasis. The expression profile of metastatic samples reveals changes in expression of a unique set of genes representing both the androgen ablation related pathways and other metastasis related gene networks such as cell adhesion, bone remodelling and cell cycle. The differentially expressed genes include metabolic enzymes, transcription factors such as Forkhead Box M1 (FoxM1) and cell adhesion molecules such as Osteopontin (SPP1). CONCLUSION: We hypothesize that these genes have a role in the biology of metastatic disease and that they represent potential therapeutic targets for prostate cancer