Multiple Gamma Function and Its Application to Computation of Series

The multiple gamma function $\Gamma_n$, defined by a recurrence-functional equation as a generalization of the Euler gamma function, was originally introduced by Kinkelin, Glaisher, and Barnes around 1900. Today, due to the pioneer work of Conrey, Katz and Sarnak, interest in the multiple gamma function has been revived. This paper discusses some theoretical aspects of the $\Gamma_n$ function and their applications to summation of series and infinite products.Comment: 20 pages, Latex, uses kluwer.cls, will appear in The Ramanujan Journa

Universality of finite-size corrections to the number of critical percolation clusters

Monte-Carlo simulations on a variety of 2d percolating systems at criticality suggest that the excess number of clusters in finite systems over the bulk value of nc is a universal quantity, dependent upon the system shape but independent of the lattice and percolation type. Values of nc are found to high accuracy, and for bond percolation confirm the theoretical predictions of Temperley and Lieb, and Baxter, Temperley, and Ashley, which we have evaluated explicitly in terms of simple algebraic numbers. Predictions for the fluctuations are also verified for the first time.Comment: 13 pages, 2 figs., Latex, submitted to Phys. Rev. Let

A Gauge-Gravity Relation in the One-loop Effective Action

We identify an unusual new gauge-gravity relation: the one-loop effective action for a massive spinor in 2n dimensional AdS space is expressed in terms of precisely the same function [a certain multiple gamma function] as the one-loop effective action for a massive charged scalar in 4n dimensions in a maximally symmetric background electromagnetic field [one for which the eigenvalues of F_{\mu\nu} are maximally degenerate, corresponding in 4 dimensions to a self-dual field, equivalently to a field of definite helicity], subject to the identification F^2 \Lambda, where \Lambda is the gravitational curvature. Since these effective actions generate the low energy limit of all one-loop multi-leg graviton or gauge amplitudes, this implies a nontrivial gauge-gravity relation at the non-perturbative level and at the amplitude level.Comment: 6 page

Choice of method of diagnosis hypogonadism in obesity and metabolic syndrome in men

Nowadays, obesity and metabolic syndrome are considered as symptoms of male hypogonadism, which underlines the need for hormonal screening in these patients. However, remain unsolved some questions of laboratory diagnostics testosterone deficiency. In particular, there are contradictions in the choice of research method of free testosterone. The objectives of our work was to conduct a comparative evaluation of methods for studying androgen status of young and middle-aged men with obesity and metabolic syndrome, and determining the relationship between hormonal indicators and metabolic profile, blood pressure, anthropometric characteristics of obesity. The study included 51 patients with symptoms of obesity and metabolic syndrome, aged from 20 to 50 years, the control group consisted of 19 equal-age men with normal body weight. A significant decrease in total testosterone in men with metabolic syndrome was revealed. The dependence of the concentration of total testosterone with age and content sex-steroid-binding globulin was found. The role of free testosterone in the formation of the metabolic syndrome was shown. It was found that free saliva testosterone significantly correlated with the level of calculated serum free testosterone. In patients with obesity and metabolic syndrome there are a statistically significant increase in saliva testosterone indicators compared to calculated serum free testosterone, while at normal body weight differences are absent. It is concluded that saliva testosterone is more sensitive and appropriate marker for obesity and metabolic syndrome

Matrix model eigenvalue integrals and twist fields in the su(2)-WZW model

We propose a formula for the eigenvalue integral of the hermitian one matrix model with infinite well potential in terms of dressed twist fields of the su(2) level one WZW model. The expression holds for arbitrary matrix size n, and provides a suggestive interpretation for the monodromy properties of the matrix model correlators at finite n, as well as in the 1/n-expansion.Comment: 27 pages, 4 figures; v2: typos corrected, reference added, version to be published in JHE

Naloxone's Pentapeptide Binding Site on Filamin A Blocks Mu Opioid Receptor–Gs Coupling and CREB Activation of Acute Morphine

Chronic morphine causes the mu opioid receptor (MOR) to switch its coupling from Gi/o to Gs, resulting in excitatory signaling via both Gαs and its Gβγ dimer. Ultra-low-dose naloxone (NLX) prevents this switch and attenuates opioid tolerance and dependence. This protective effect is mediated via a high-affinity interaction of NLX to a pentapeptide region in c-terminal filamin A (FLNA), a scaffolding protein interacting with MOR. In organotypic striatal slice cultures, we now show that acute morphine induces a dose-dependent Go-to-Gs coupling switch at 5 and 15 min that resolves by 1 hr. The acute Gs coupling induced by 100 µM morphine was completely prevented by co-treatment with 100 pM NLX, (+)NLX, or naltrexone (NTX), or their pentapeptide binding site (FLNA2561–2565), which we show can act as a decoy for MOR or bind to FLNA itself. All of these co-treatments presumably prevent the MOR–FLNA interaction. Since ultra-low-dose NTX also attenuates the addictive properties of opioids, we assessed striatal cAMP production and CREB phosphorylation at S133. Correlating with the Gs coupling, acute morphine induced elevated cAMP levels and a several-fold increase in pS133CREB that were also completely blocked by NLX, NTX or the FLNA pentapeptide. We propose that acute, robust stimulation of MOR causes an interaction with FLNA that allows an initially transient MOR–Gs coupling, which recovers with receptor recycling but persists when MOR stimulation is repeated or prolonged. The complete prevention of this acute, morphine-induced MOR–Gs coupling by 100 pM NLX/NTX or 10 µM pentapeptide segment of FLNA further elucidates both MOR signaling and the mechanism of action of ultra-low-dose NLX or NTX in attenuating opioid tolerance, dependence and addictive potential

High-Affinity Naloxone Binding to Filamin A Prevents Mu Opioid Receptor–Gs Coupling Underlying Opioid Tolerance and Dependence

Ultra-low-dose opioid antagonists enhance opioid analgesia and reduce analgesic tolerance and dependence by preventing a G protein coupling switch (Gi/o to Gs) by the mu opioid receptor (MOR), although the binding site of such ultra-low-dose opioid antagonists was previously unknown. Here we show that with approximately 200-fold higher affinity than for the mu opioid receptor, naloxone binds a pentapeptide segment of the scaffolding protein filamin A, known to interact with the mu opioid receptor, to disrupt its chronic opioid-induced Gs coupling. Naloxone binding to filamin A is demonstrated by the absence of [3H]-and FITC-naloxone binding in the melanoma M2 cell line that does not contain filamin or MOR, contrasting with strong [3H]naloxone binding to its filamin A-transfected subclone A7 or to immunopurified filamin A. Naloxone binding to A7 cells was displaced by naltrexone but not by morphine, indicating a target distinct from opioid receptors and perhaps unique to naloxone and its analogs. The intracellular location of this binding site was confirmed by FITC-NLX binding in intact A7 cells. Overlapping peptide fragments from c-terminal filamin A revealed filamin A2561-2565 as the binding site, and an alanine scan of this pentapeptide revealed an essential mid-point lysine. Finally, in organotypic striatal slice cultures, peptide fragments containing filamin A2561-2565 abolished the prevention by 10 pM naloxone of both the chronic morphine-induced mu opioid receptor–Gs coupling and the downstream cAMP excitatory signal. These results establish filamin A as the target for ultra-low-dose opioid antagonists previously shown to enhance opioid analgesia and to prevent opioid tolerance and dependence

Dexmedetomidine is neuroprotective in an in vitro model for traumatic brain injury

<p>Abstract</p> <p>Background</p> <p>The α₂-adrenoreceptor agonist dexmedetomidine is known to provide neuroprotection under ischemic conditions. In this study we investigated whether dexmedetomidine has a protective effect in an <it>in vitro </it>model for traumatic brain injury.</p> <p>Methods</p> <p>Organotypic hippocampal slice cultures were subjected to a focal mechanical trauma and then exposed to varying concentrations of dexmedetomidine. After 72 h cell injury was assessed using propidium iodide. In addition, the effects of delayed dexmedetomidine application, of hypothermia and canonical signalling pathway inhibitors were examined.</p> <p>Results</p> <p>Dexmedetomidine showed a protective effect on traumatically injured hippocampal cells with a maximum effect at a dosage of 1 μM. This effect was partially reversed by the simultaneous administration of the ERK inhibitor PD98059.</p> <p>Conclusion</p> <p>In this TBI model dexmedetomidine had a significant neuroprotective effect. Our results indicate that activation of ERK might be involved in mediating this effect.</p

Структура и функции ароматазы и ее нестероидные ингибиторы

The analysis of the structure and function of aromatase (SYP19) - enzyme from the family of cytochrome P-450 that catalyzes the aromatization of six-membered ring A of the steroidal skeleton, namely transformation of androgens into estrogens peripheral and tumor tissues in the body, has been performed, and data in its non-steroidal inhibitors have been summarized.Проведен анализ структуры и функции ароматазы (СYP19) - фермента семейства цитохромов Р-450, кодируемого расположенным на коротком плече 15-й хромосомы (локус 15q21) геном CYP19A1, катализирующего ароматизацию шестичленного цикла А стероидного скелета и обуславливающего метаболизм стероидных гормонов, а именно трансформацию андрогенов в эстрогены периферическими и опухолевыми тканями организма. Обобщены данные по ее нестероидным ингибиторам. Обсуждены особенности первичной и пространственной структуры СYP19, обуславливающие взаимодействие с мембраной клетки и субстратом, обеспечивающие транспорт последнего между липидным бислоем мембраны и активным центром фермента. Показано, что наиболее эффективными ингибиторами СYP19 в настоящее время являются соединения, содержащие в составе молекулы азольные и азиновые гетероциклические фрагменты