pinecone/core-2020-05-10-deduplication huggingface dataset:
Holstein-Primakoff/Bogoliubov Transformations and the Multiboson System

As an aid to understanding the {\it displacement operator} definition of
squeezed states for arbitrary systems, we investigate the properties of systems
where there is a Holstein-Primakoff or Bogoliubov transformation. In these
cases the {\it ladder-operator or minimum-uncertainty} definitions of squeezed
states are equivalent to an extent displacement-operator definition. We
exemplify this in a setting where there are operators satisfying $[A,
A^{\dagger}] = 1$, but the $A$'s are not necessarily the Fock space $a$'s; the
multiboson system. It has been previously observed that the ground state of a
system often can be shown to to be a coherent state. We demonstrate why this
must be so. We close with a discussion of an alternative, effective definition
of displacement-operator squeezed states.Comment: Two sections added and new title. LaTeX, 18 pages. Accepted by
  Forschritte der Physi
Solitons, monopoles and duality: from sine-Gordon to Seiberg-Witten

An elementary introduction into the Seiberg-Witten theory is given. Many
efforts are made to get it as pedagogical as possible, within a reasonable
size. The selection of the relevant material is heavily oriented towards
graduate students. The basic ideas about solitons, monopoles, supersymmetry and
duality are reviewed from first principles, and they are illustrated on the
simplest examples. The exact Seiberg-Witten solution to the low-energy
effective action of the four-dimensional N=2 supersymmetric pure Yang-Mills
theory with the gauge group SU(2) is the main subject of the review. Other
gauge groups are also considered. Some related issues (like adding matter,
confinement, string dualities) are outlined.Comment: 72 pages, LaTeX, macros included, a few references adde
Physical States and Gauge Independence of the Energy-Momentum Tensor in
  Quantum Electrodynamics

Discussions are made on the relationship between physical states and gauge
independence in QED. As the first candidate take the LSZ-asymptotic states in a
covariant canonical formalism to investigate gauge independence of the
(Belinfante's) symmetric energy-momentum tensor. It is shown that expectation
values of the energy-momentum tensor in terms of those asymptotic states are
gauge independent to all orders. Second, consider gauge invariant operators of
electron or photon, such as the Dirac's electron or Steinmann's covariant
approach, expecting a gauge invariant result without any restriction. It is,
however, demonstrated that to single out gauge invariant quantities is merely
synonymous to a gauge fixing, resulting again in use of the asymptotic
condition when proving gauge independence. Nevertheless, it is commented that
these invariant approaches is helpful to understand the mechanism of the
LSZ-mapping and furthermore of quark confinement in QCD. As the final
candidate, it is shown that gauge transformations are freely performed under
the functional representation or the path integral expression on account of the
fact that the functional space is equivalent to a collection of infinitely many
inequivalent Fock spaces. The covariant LSZ formalism is shortly reviewed and
the basic facts on the energy-momentum tensor are also illustrated.Comment: 36 pages, 17 figures, LaTeX, uses epsf.tex for figure
Implications of a dilaton in gauge theory and cosmology

After a review of theoretical motivations to consider theories with direct
couplings of scalar fields to Ricci and gauge curvature terms, we consider the
dynamics and non-perturbative stabilization of a dilaton in three and in four
dimensions. In particular, we derive generalized Coulomb potentials in the
presence of a dilaton and discuss a low energy effective dilaton potential
induced by instanton effects and the S--dual coupling to axions. We conclude
with a discussion of cosmological implications of a light dilaton.Comment: 61 pages, LaTe
Heavy-Quark Production in the Target Fragmentation Region

Fixed-target experiments permit the study of hadron production in the target fragmentation region. It is expected that the tagging of specific particles in the target fragments can be employed to introduce a bias in the hard scattering process towards a specific flavour content. The case of hadrons containing a heavy quark is particularly attractive because of the clear experimental signatures and the applicability of perturbative QCD. The standard approach to one-particle inclusive processes based on fragmentation functions is valid in the current fragmentation region and for large transverse momenta $p_T$ in the target fragmentation region, but it fails for particle production at small $p_T$ in the target fragmentation region. A collinear singularity, which cannot be absorbed in the standard way into the phenomenological distribution functions, prohibits the application of this procedure. This situation is remedied by the introduction of a new set of distribution functions, the target fragmentation functions. They describe particle production in the target fragmentation region, and can be viewed as correlated distribution functions in the momentum fractions of the observed particle and of the parton initiating the hard scattering process. It is shown in a next-to-leading-order calculation for the case of deeply inelastic lepton-nucleon scattering that the additional singularity can be consistently absorbed into the renormalized target fragmentation functions on the one-loop level. The formalism is derived in detail and is applied to the production of heavy quarks. The renormalization group equation of the target fragmentation functions for the perturbative contribution is solved numerically, and the results of a case study for deeply inelastic lepton-nucleon scattering at DESY (H1 and ZEUS at HERA), at CERN (NA47) and at Fermilab (E665) are discussed. We also comment briefly on the case of an intrinsic heavy-quark content of the proton
Identification of Extracellular d-Catenin Accumulation for Prostate Cancer Detection

BACKGROUND—Prostate cancer is the second leading cause of cancer death in men, and early
detection is essential to reduce mortality and increase survival. δ-Catenin is a unique β-catenin
superfamily protein primarily expressed in the brain but is upregulated in human prostatic
adenocarcinomas. Despite its close correlation with the disease, it is unclear whether δ-catenin
presents the potential in prostate cancer screening because it is an intracellular protein. In this study,
we investigated the hypothesis of δ-catenin accumulation in the urine of prostate cancer patients and
its potential pathways of excretion into extracellular milieu.
METHODS—Prostate cancer cell cultures, human tissue biopsies, and voided urines were
characterized to determine extracellular δ-catenin accumulation and co-isolation with exosomes/
prostasomes.
RESULTS—We identified δ-catenin in culture media and in the stroma of human prostate cancer
tissues. In PC-3 cells in culture, δ-catenin was partially co-localized and co-isolated with raftassociated
membrane protein caveolin-1 and glycosylphosphatidylinositol-anchored protein CD59,
suggesting its potential excretion into extracellular milieu through exosome/prostasome associated
pathways. Interference with endocytic pathway using wortmannin did not block prostasome
excretion, but δ-catenin overexpression promoted the extracellular accumulation of caveolin-1. δ-
Catenin, caveolin-1, and CD59 were all detected in cell-free human voided urine prostasomes. δ-
Catenin immunoreactivity was significantly increased in the urine of prostate cancer patients
(p<0.0005).
CONCLUSIONS—This study demonstrated, for the first time, the extracellular accumulation of
δ-catenin in urine supporting its potential utility for non-invasive prostate cancer detection. Originally published The Prostate, Vol. 69, No. 4, March 1 200
Invasive and Metastatic Properties of Advanced Prostate Cancer

Prostate cancer is initially androgen-dependent (AD) and therefore androgen deprivation therapy (ADT) is generally used to treat advanced prostate cancer. However, the long-term treatment effects are insufficient and over time an androgen-independent (AI) tumor relapses, which is generally highly aggressive and metastatic. Treatment regimens in the AI stage are only palliative and median patient survival is less than a year. Therefore, new treatment concepts are urgently needed. The purpose of this thesis was to investigate molecular and cellular characteristics of advanced prostate cancer. The specific focus was on characteristics related to invasivity and metastatic ability in the AI stage. An experimental model system comprising of an AD and an AI prostate cancer cell line was used for in vitro studies in cell culture and in vivo studies in immunodeficient mice. In addition, samples from prostate cancer patients were included in the studies and evaluated by immunohistochemical analyses. Studies performed using the experimental model showed that transition into androgen-independency was associated with several prometastatic alterations, including increased migration and tumor cell invasivity into blood vessels. Further, the AI tumors displayed elevated levels of N-cadherin, matrix metalloproteinase 9 (MMP-9) and membrane type-1(MT1)-MMP and decreased expression of the tumor suppressor E-cadherin compared to the AD tumors. Further studies demonstrated that intraprostatic AI tumors were suppressed when grown in intact mice compared to castrated mice, probably by androgen-regulated factors secreted from the prostatic stromal cells. In addition, the proinvasive factor N-cadherin was increased by androgen deprivation in experimental AI tumors and in samples from human prostate cancer. Similarly, N-cadherin was increased in specimens from AI prostate tumors compared to early non-treated tumors and was associated with Gleason score and metastasis. Finally, the results show that the lymphangiogenic factor vascular endothelial growth factor C (VEGF-C) and its receptor VEGFR-3 were elevated in primary tumors from patients with regional lymph node metastases compared to patients without lymph node metastases. In summary, this thesis shows that androgen deprivation and the subsequent development of AI tumors are associated with several prometastatic alterations in the prostate cancer cells. The results also suggest that AI tumors do not thrive in the prostatic environment and supports previous observations of frequent progression of AI prostate cancer as metastases in patients. Moreover, the results indicate a possible role for VEGF-C and N-cadherin in promoting dissemination of tumor cells to distant sites. Thus, N-cadherin and VEGF-C might be potential therapeutic targets for future anti-metastatic treatment for advanced prostate cancer
Early onset prostate cancer has a significant genetic component

BACKGROUND  Prostate cancer (PCa) affects more than 190,000 men each year with ∼10% of men diagnosed at ≤55 years, that is, early onset (EO) PCa. Based on historical findings for other cancers, EO PCa likely reflects a stronger underlying genetic etiology.    METHODS  We evaluated the association between EO PCa and previously identified single nucleotide polymorphisms (SNPs) in 754 Caucasian cases from the Michigan Prostate Cancer Genetics Project (mean 49.8 years at diagnosis), 2,713 Caucasian controls from Illumina's iControlDB database and 1,163 PCa cases diagnosed at >55 years from the Cancer Genetic Markers of Susceptibility Study (CGEMS).    RESULTS  Significant associations existed for 13 of 14 SNPs (rs9364554 on 6q25, rs10486567 on 7p15, rs6465657 on 7q21, rs6983267 on 8q24, rs1447295 on 8q24, rs1571801 on 9q33, rs10993994 on 10q11, rs4962416 on 10q26, rs7931342 on 11q13, rs4430796 on 17q12, rs1859962 on 17q24.3, rs2735839 on 19q13, and rs5945619 on Xp11.22, but not rs2660753 on 3p12). EO PCa cases had a significantly greater cumulative number of risk alleles (mean 12.4) than iControlDB controls (mean 11.2;  P  = 2.1 × 10 −33 ) or CGEMS cases (mean 11.9;  P  = 1.7 × 10 −5 ). Notably, EO PCa cases had a higher frequency of the risk allele than CGEMS cases at 11 of 13 associated SNPs, with significant differences for five SNPs. EO PCa cases diagnosed at <50 (mean 12.8) also had significantly more risk alleles than those diagnosed at 50–55 years (mean 12.1;  P  = 0.0003).    CONCLUSIONS  These results demonstrate the potential for identifying PCa‐associated genetic variants by focusing on the subgroup of men diagnosed with EO disease. Prostate 72:147–156, 2012. © 2011 Wiley Periodicals, Inc
The role of Pax2 in mouse prostate development

BACKGROUND  Loss‐of‐function of Pax2 results in severe defects of the male reproductive system, and Pax2 expression is detected in mouse prostate lobes and human prostatic cancers. However, the role for Pax2 in prostate development remains poorly understood.    METHODS  The expression of Pax2 was examined by in situ hybridization at various developmental stages. Urogenital sinuses were dissected out at E18.5 from mouse Pax2 mutants and controls, cultured in vitro or grafted under the renal capsule of CD1 nude mice. The expression of prostate developmental regulatory factors was analyzed by semi‐quantitative real‐time PCR or immuohistochemistry.    RESULTS  Pax2 is expressed in the epithelial cells of prostate buds. Loss‐of‐function of Pax2 does not affect the initiation of prostatic buds, but in vitro culture assays show that the prostates of Pax2 mutants are hypomorphic and branching is severely disrupted compared to controls. RT‐PCR data from Pax2 mutant prostates demonstrate increased expression levels of dorsolateral prostate marker MSMB and ventral prostate marker SBP and dramatically reduced expression levels of anterior prostate marker TGM4.    CONCLUSIONS  Pax2 is essential for mouse prostate development and regulates prostatic ductal growth, branching, and lobe‐specific identity. These findings are important for understanding the molecular regulatory mechanisms in prostate development. Prostate 72:217–224, 2012. © 2011 Wiley Periodicals, Inc
Chromosomes 4 and 8 implicated in a genome wide SNP linkage scan of 762 prostate cancer families collected by the ICPCG

BACKGROUND  In spite of intensive efforts, understanding of the genetic aspects of familial prostate cancer (PC) remains largely incomplete. In a previous microsatellite‐based linkage scan of 1,233 PC families, we identified suggestive evidence for linkage (i.e., LOD ≥ 1.86) at 5q12, 15q11, 17q21, 22q12, and two loci on 8p, with additional regions implicated in subsets of families defined by age at diagnosis, disease aggressiveness, or number of affected members.    METHODS  In an attempt to replicate these findings and increase linkage resolution, we used the Illumina 6000 SNP linkage panel to perform a genome‐wide linkage scan of an independent set of 762 multiplex PC families, collected by 11 International Consortium for Prostate Cancer Genetics (ICPCG) groups.    RESULTS  Of the regions identified previously, modest evidence of replication was observed only on the short arm of chromosome 8, where HLOD scores of 1.63 and 3.60 were observed in the complete set of families and families with young average age at diagnosis, respectively. The most significant linkage signals found in the complete set of families were observed across a broad, 37 cM interval on 4q13–25, with LOD scores ranging from 2.02 to 2.62, increasing to 4.50 in families with older average age at diagnosis. In families with multiple cases presenting with more aggressive disease, LOD scores over 3.0 were observed at 8q24 in the vicinity of previously identified common PC risk variants, as well as  MYC , an important gene in PC biology.    CONCLUSIONS  These results will be useful in prioritizing future susceptibility gene discovery efforts in this common cancer. Prostate 72:410–426, 2012. © 2011 Wiley Periodicals, Inc
Role of dutasteride in pre‐clinical ETS fusion‐positive prostate cancer models

BACKGROUND  Androgens play a crucial role in prostate cancer, hence the androgenic pathway has become an important target of therapeutic intervention. Previously we discovered that gene fusions between the 5′‐untranslated region of androgen regulated gene  TMPRSS2  and the  ETS  transcription factor family members were present in a majority of the prostate cancer cases. The resulting aberrant overexpression of ETS genes drives tumor progression.    METHODS  Here, we evaluated the expression levels of 5α‐reductase isoenzymes in prostate cancer cell lines and tissues. We tested the effect of dutasteride, a 5α‐reductase inhibitor, in  TMPRSS2–ERG  fusion‐positive VCaP cell proliferation and cell invasion. We also evaluated the effect of dutasteride on the  TMPRSS2–ERG  fusion gene expression. Finally, we tested dutasteride alone or in combination with an anti‐androgen in VCaP cell xenografts tumor model.    RESULTS  Our data showed that 5α‐reductase SRD5A1 and SRD5A3 isoenzymes that are responsible for the conversion of testosterone to DHT, are highly expressed in metastatic prostate cancer compared to benign and localized prostate cancer. Dutasteride treatment attenuated VCaP cell proliferation and invasion. VCaP cells pre‐treated with dutasteride showed a reduction in ERG and PSA expression. In vivo studies demonstrated that dutasteride in combination with the anti‐androgen bicalutamide significantly decreased tumor burden in VCaP cell xenograft model.    CONCLUSIONS  Our findings suggest that dutasteride can inhibit ERG fusion‐positive cell growth and in combination with anti‐androgen, significantly reduce the tumor burden. Our study suggests that anti‐androgens used in combination with dutasteride could synergistically augment the therapeutic efficacy in the treatment of ETS‐positive prostate cancer. Prostate 72:1542–1549, 2012. © 2012 Wiley Periodicals, Inc
Focus on ß-blocker use and ß2-adrenergic receptor level

List of papers. The papers are removed from the thesis due to publisher restrictions.<br><br>

Paper I: Grytli HH, Fagerland MW, Fosså SD, Taskén KA, Håheim LL. Use of ß-blockers is associated with prostate cancer-specific survival in prostate cancer patients on androgen deprivation therapy. Prostate. 2013 Feb 15;73(3):250-60. <a href="http://dx.doi.org/10.1002/pros.22564">doi:10.1002/pros.22564</a><br><br>

Paper II: Grytli HH, Fagerland MW, Fosså SD, Taskén KA. Association between use of ß-blockers and prostate cancer- specific survival; a cohort study of 3561 prostate cancer patients with high risk or metastatic disease. Eur Urol. 2013 Jan 14. pii: S0302-2838(13)00010-9. [Epub ahead of print] <a href="http://dx.doi.org/10.1016/j.eururo.2013.01.007">doi:10.1016/j.eururo.2013.01.007</a><br><br>

Paper III: Grytli HH, Ramberg H, Wang W, Braadland PR, Øgren O, Eide T, Krobert KA, Berge V, Paus E, Bjartell A, Levy FO, Svindland A, Taskén KA. The level of ß2-adrenergic receptor in prostate cancer tissue is associated with development of castration resistant prostate cancer: a pilot study. Submitted
CCL11 (eotaxin‐1): A new diagnostic serum marker for prostate cancer

BACKGROUND  The recent recommendation of the U.S. Preventive Services Task Force against PSA‐based screening for prostate cancer was based, in part, on the lack of demonstrated diagnostic utility of serum PSA values in the low, but detectable range to successfully predict prostate cancer. Though controversial, this recommendation reinforced the critical need to develop, validate, and determine the utility of other serum and/or urine transcript and protein markers as diagnostic markers for PCa. The studies described here were intended to determine whether inflammatory cytokines might augment serum PSA as a diagnostic marker for prostate cancer.    METHODS  Multiplex ELISA assays were performed to quantify CCL1, CCL2, CCL5, CCL8, CCL11, CCL17, CXCL1, CXCL5, CXCL8, CXCL10, CXCL12, and IL‐6 protein levels in the serum of 272 men demonstrating serum PSA values of <10 ng/ml and undergoing a 12 core diagnostic needle biopsy for detection of prostate cancer. Logistic regression was used to identify the associations between specific chemokines and prostate cancer status adjusted for prostate volume, and baseline PSA.    RESULTS  Serum levels for CCL1 (I‐309) were significantly elevated among all men with enlarged prostates ( P  < 0.04). Serum levels for CCL11 (Eotaxin‐1) were significantly elevated among men with prostate cancer regardless of prostate size ( P  < 0.01). The remaining 10 cytokines examined in this study did not exhibit significant correlations with either prostate volume or cancer status.    CONCLUSIONS  Serum CCL11 values may provide a useful diagnostic tool to help distinguish between prostatic enlargement and prostate cancer among men demonstrating low, but detectable, serum PSA values. Prostate 73: 573–581, 2013. © 2012 Wiley Periodicals, Inc
Monocarboxylate transporter 2 (MCT2) as putative biomarker in prostate cancer

INTRODUCTION:
Monocarboxylate transporter 2 (MCT2) is a transmembrane protein involved in the transport of monocarboxylates such as pyruvate and lactate. In a previous study we described overexpression of MCT2 in prostate carcinoma raising the hypothesis of using MCT2 as a possible biomarker in prostate cancer. With the present study we aimed to compare the pattern of expression of MCT2 and alpha-methylacyl-CoA racemase (AMACR), in prostate carcinoma, PIN lesions, non-neoplastic prostate tissue, and normal prostate and compare their sensitivity and specificity. Also, we wanted to evaluate the value of using MCT2 in combination with AMACR and the negative markers 34βE12 or p63 to detect prostate cancer.
METHODS:
A total of 349 cases, including prostate carcinoma, non-neoplastic prostate tissue and PIN lesions, from radical prostatectomies were examined by immunohistochemistry for AMACR, MCT2, p63, and 34βE12, using tissue microarrays (TMAs). Normal prostate from radical cystoprostatectomy was also studied.
RESULTS:
Our study revealed that MCT2, similarly to AMACR, was consistently expressed in prostate cancer regardless of the Gleason score. In combination with AMACR and p63 or 34βE12, MCT2 helped to improve the diagnosis of prostate carcinoma. Also, overexpression of MCT2 as well as AMACR in PIN lesions may indicate the involvement of these two proteins in prostate cancer initiation.
CONCLUSIONS:
We provided evidence for the presence of MCT2 in prostate cancer, selectively labeling malignant glands. Importantly, assessment of MCT2 together with AMACR, along with the negative markers, highly increases the accuracy in prostate cancer diagnosis.This work was supported by the FCT grant ref.PTDC/SAUMET/113415/2009 under the scope of ‘Programa Operacional Tematico Factores de Competitividade’’ (COMPETE) of ‘‘Quadro Comunitario de Apoio III’’ and co-financed by ‘‘Fundo Comunitario
Europeu’’ FEDER.
N.P.G. received fellowship from the Portuguese Foundation for Science and Technology (FCT), ref.  FRH/BD/61027/2009