A Selberg integral for the Lie algebra A_n

A new q-binomial theorem for Macdonald polynomials is employed to prove an A_n analogue of the celebrated Selberg integral. This confirms the g=A_n case of a conjecture by Mukhin and Varchenko concerning the existence of a Selberg integral for every simple Lie algebra g.Comment: 32 page

Search for the Decays B^0 -> D^{(*)+} D^{(*)-}

Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one candidate signal event, with an expected background of 0.022 +/- 0.011 events. This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) = (5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0 -> D^{*+} D^{*-}) D^{*\pm} D^\mp and B^0 -> D^+ D^-, no significant excess of signal above the expected background level is seen, and we calculate the 90% CL upper limits on the branching fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+ D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter

ΛΛˉ\Lambda\bar{\Lambda} Production in Two-Photon Interactions at CLEO

Using the CLEO detector at the Cornell $e^+e^-$ storage ring, CESR, we study the two-photon production of $\Lambda \bar{\Lambda}$, making the first observation of $\gamma \gamma \to \Lambda \bar{\Lambda}$. We present the cross-section for $\gamma \gamma \to \Lambda \bar{\Lambda}$ as a function of the $\gamma \gamma$ center of mass energy and compare it to that predicted by the quark-diquark model.Comment: 10 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN

Thermodynamical limit of general gl(N) spin chains II: Excited states and energies

We consider the thermodynamical limit of a gl(N) spin chain with arbitrary representation at each site of the chain. We consider excitations (with holes and new strings) above the vacuum and compute their corrections in 1/L to the densities and the energy.Comment: 29 pages misprints in the example of sect 5.1 amended and a mistake in theorem 5.4 correcte

Nicotine Promotes Tumor Growth and Metastasis in Mouse Models of Lung Cancer

Nicotine is the major addictive component of tobacco smoke. Although nicotine is generally thought to have limited ability to initiate cancer, it can induce cell proliferation and angiogenesis in a variety of systems. These properties might enable nicotine to facilitate the growth of tumors already initiated. Here we show that nicotine significantly promotes the progression and metastasis of tumors in mouse models of lung cancer. This effect was observed when nicotine was administered through intraperitoneal injections, or through over-the-counter transdermal patches.In the present study, Line1 mouse adenocarcinoma cells were implanted subcutaneously into syngenic BALB/c mice. Nicotine administration either by intraperitoneal (i.p.) injection or transdermal patches caused a remarkable increase in the size of implanted Line1 tumors. Once the tumors were surgically removed, nicotine treated mice had a markedly higher tumor recurrence (59.7%) as compared to the vehicle treated mice (19.5%). Nicotine also increased metastasis of dorsally implanted Line1 tumors to the lungs by 9 folds. These studies on transplanted tumors were extended to a mouse model where the tumors were induced by the tobacco carcinogen, NNK. Lung tumors were initiated in A/J mice by i.p. injection of NNK; administration of 1 mg/kg nicotine three times a week led to an increase in the size and the number of tumors formed in the lungs. In addition, nicotine significantly reduced the expression of epithelial markers, E-Cadherin and beta-Catenin as well as the tight junction protein ZO-1; these tumors also showed an increased expression of the alpha(7) nAChR subunit. We believe that exposure to nicotine either by tobacco smoke or nicotine supplements might facilitate increased tumor growth and metastasis.Our earlier results indicated that nicotine could induce invasion and epithelial-mesenchymal transition (EMT) in cultured lung, breast and pancreatic cancer cells. This study demonstrates for the first time that administration of nicotine either by i.p. injection or through over-the-counter dermal patches can promote tumor growth and metastasis in immunocompetent mice. These results suggest that while nicotine has only limited capacity to initiate tumor formation, it can facilitate the progression and metastasis of tumors pre-initiated by tobacco carcinogens

An overlooked connection: serotonergic mediation of estrogen-related physiology and pathology

BACKGROUND: In humans, serotonin has typically been investigated as a neurotransmitter. However, serotonin also functions as a hormone across animal phyla, including those lacking an organized central nervous system. This hormonal action allows serotonin to have physiological consequences in systems outside the central nervous system. Fluctuations in estrogen levels over the lifespan and during ovarian cycles cause predictable changes in serotonin systems in female mammals. DISCUSSION: We hypothesize that some of the physiological effects attributed to estrogen may be a consequence of estrogen-related changes in serotonin efficacy and receptor distribution. Here, we integrate data from endocrinology, molecular biology, neuroscience, and epidemiology to propose that serotonin may mediate the effects of estrogen. In the central nervous system, estrogen influences pain transmission, headache, dizziness, nausea, and depression, all of which are known to be a consequence of serotonergic signaling. Outside of the central nervous system, estrogen produces changes in bone density, vascular function, and immune cell self-recognition and activation that are consistent with serotonin's effects. For breast cancer risk, our hypothesis predicts heretofore unexplained observations of the opposing effects of obesity pre- and post-menopause and the increase following treatment with hormone replacement therapy using medroxyprogesterone. SUMMARY: Serotonergic mediation of estrogen has important clinical implications and warrants further evaluation

Ecoacoustics and multispecies semiosis: naming, semantics, semiotic characteristics, and competencies

Biosemiotics to date has focused on the exchange of signals between organisms, in line with bioacoustics; consideration of the wider acoustic environment as a semiotic medium is under-developed. The nascent discipline of ecoacoustics, that investigates the role of environmental sound in ecological processes and dynamics, fills this gap. In this paper we introduce key ecoacoustic terminology and concepts in order to highlight the value of ecoacoustics as a discipline in which to conceptualise and study intra- and interspecies semiosis. We stress the inherently subjective nature of all sensory scapes (vivo-, land-, vibro- and soundscapes) and propose that they should always bear an organismic attribution. Key terms to describe the sources (geophony, biophony, anthropophony, technophony) and scales (sonotopes, soundtopes, sonotones) of soundscapes are described. We introduce epithets for soundscapes to point to the degree to which the global environment is implicated in semiosis (latent, sensed and interpreted soundscapes); terms for describing key ecological structures and processes (acoustic community, acoustic habitat, ecoacoustic events) and examples of ecoacoustic events (choruses and noise) are described. The acoustic eco-field is recognized as the semiotic model that enables soniferous species to intercept core resources like food, safety and roosting places. We note that whilst ecoacoustics to date has focused on the critical task of the development of metrics for application in conservation and biodiversity assessment, these can be enriched by advancing conceptual and theoretical foundations. Finally, the mutual value of integrating ecoacoustic and biosemiotics perspectives is considered