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Expression of Estrogen Receptors ? and ? in Early Steps of Human Breast Carcinogenesis: Hormonal Carcinogenesis V (2008), pp. 139-148.Associ ation of hormonal factors and preinvasive mammary lesions increase the risk of sporadic breast cancer (BC) incidence. Indeed, the mitogenic activity of estrogens and their role as a promoter of BC was confirmed by epidemiologica l, clinical, and experimental studies (1). Preinvasive mammary lesions frequently precede the development of invasive BC. They correspond to nonproliferati ve and proliferative benign breast disease without or with atypia and ductal carcinoma in-situ (DCIS) (2).Pascal Roger, Majida Esslimani-Sahl a, Christophe Delfour, Gwendal Lazennec, Henri Rochefort, Thierry Maudelonde

Source: Hormonal Carcinogenesis V (2008), pp. 139-148.
Identification of a functional variant of estrogen receptor beta in an African population: Carcinogenesis , Vol. 25, No. 11. (1 November 2004), pp. 2067-2073.In this study, we identified five novel polymorphisms in the estrogen receptor beta (ERbeta) gene in an African population. Interestingly, two of these variants are expected to change the amino acid sequence of the ERbeta protein. These changes correspond to an isoleucine to valine substitution at amino acid position 3 (I3V) and a valine to glycine substitution at position 320 (V320G), respectively. The functional consequences of these amino acid substitutions were determined in different in vitro assays. The I3V mutation displayed no differences with regard to transcriptiona l activity in a reporter assay, as compared with the wild-type receptor. The V320G mutation, however, showed significantly decreased maximal transcriptiona l activity in a reporter assay, although its binding affinity for 17beta-estradi ol was not affected. A pull-down assay indicated that the interaction of full-length TIF2 with hERbetaV320G was weaker than with hERbetawt. Moreover, surface plasmon resonance analysis revealed reduced interaction of the V320G ERbeta variant with the NR box I and II modules of TIF2. To our knowledge, this represents the first identification of a functional polymorphism in the ERbeta gene. This novel polymorphism provides a tool for human genetic studies of diseases in the African population. 10.1093/carcin /bgh215Chunyan Zhao, Li Xu, Michio Otsuki, Gudrun Toresson, Konrad Koehler, Qiang Pan-Hammarstro m, Lennart Hammarstrom, Stefan Nilsson, Jan-Ake Gustafsson, Karin Dahlman-Wright

Source: Carcinogenesis, Vol. 25, No. 11. (1 November 2004), pp. 2067-2073.
Direct Observation of a Preinactivated , Open State in BK Channels with beta2 Subunits: J. Gen. Physiol., Vol. 127, No. 2. (30 January 2006), pp. 119-131.Protei ns arising from the Slo family assemble into homotetramers to form functional large-conducta nce, Ca2+- and voltage-activa ted K+ channels, or BK channels. These channels are also found in association with accessory beta subunits, which modulate several aspects of channel gating and expression. Coexpression with either of two such subunits, beta2 or beta3b, confers time-dependent inactivation onto BK currents. mSlo1+beta3b channels display inactivation that is very rapid but incomplete. Previous studies involving macroscopic recordings from these channels have argued for the existence of a second, short-lived conducting state in rapid equilibrium with the nonconducting, inactivated conformation. This state has been termed "pre-inactivat ed," or O*. beta2-mediated inactivation, in contrast, occurs more slowly but is virtually complete at steady state. Here we demonstrate, using both macroscopic and single channel current recordings, that a preinactivated state is also a property of mSlo1+beta2 channels. Detection of this state is enhanced by a mutation (W4E) within the initial beta2 NH2-terminal segment critical for inactivation. This mutation increases the rate of recovery to the preinactivated open state, yielding macroscopic inactivation properties qualitatively more similar to those of beta3b. Furthermore, short-lived openings corresponding to entry into the preinactivated state can be observed directly with single-channel recording. By examining the initial openings after depolarization of a channel containing beta2-W4E, we show that channels can arrive directly at the preinactivated state without passing through the usual long-lived open conformation. This final result suggests that channel opening and inactivation are at least partly separable in this channel. Mechanisticall y, the preinactivated and inactivated conformations may correspond to binding of the beta subunit NH2 terminus in the vicinity of the cytoplasmic pore mouth, followed by definitive movement of the NH2 terminus into a position of occlusion within the ion-conducting pathway.Richar d Benzinger, Xiao-Ming Xia, Christopher Lingle

Source: J. Gen. Physiol., Vol. 127, No. 2. (30 January 2006), pp. 119-131.
Insider Trading and the Exploitation of Inside Information: Some Empirical Evidence: The Journal of Business, Vol. 58, No. 1. (1985), pp. 69-87.Insider trading was found by previous research to yield excess return. This excess return was attributed to exploitation of inside information, leading to the inference that insiders possess and use superior information for their trading. This study examines the extent to which the abnormal return gained by insiders is realized by price changes arising from the disclosure of the trade itself or from subsequent disclosure of specific news about the company to which the insiders might be privy. The results from our sample indicate that a major part of the observed abnormal performance of insiders is likely to be due to price changes arising from the information revealed through the trades themselves. The findings also suggest that there is a low incidence of insider trading in anticipation of an impending new disclosure.Dan Givoly, Dan Palmon

Source: The Journal of Business, Vol. 58, No. 1. (1985), pp. 69-87.
Long-range temporal correlations in alpha and beta oscillations: effect of arousal level and test-retest reliability: Clinical Neurophysiolog y, Vol. 115, No. 8. (August 2004), pp. 1896-1908.Obje ctive: The aim of the present study was to evaluate test-retest reliability and condition sensitivity of long-range temporal correlations in the amplitude dynamics of electroencepha lographic alpha and beta oscillations.M ethods: Twelve normal subjects were measured two times with a test-retest interval of several days. Open- and closed-eyes conditions were used, representing different levels of arousal. The amplitude of the alpha and beta oscillations was extracted with bandpass filtering and the Hilbert transform. The long-range temporal correlations were quantified with detrended fluctuation analysis.Resul ts: The amplitude dynamics of the alpha and beta oscillations demonstrated power-law long-range temporal correlations lasting for tens of seconds. These correlations were degraded in the open- compared to the closed-eyes condition. Test-retest statistics demonstrated that the long-range temporal correlations had significant reliability, which was greatest in the closed-eyes condition.Conc lusions: The presence of long-range temporal correlations indicates that the amplitude of neuronal oscillations at a given time is dependent on the amplitude at times as remote in the past as tens of seconds. The reliability of long-range temporal correlations suggests that the mechanisms generating the amplitude fluctuations are not perturbed over several days. The systematic changes in the scaling exponents at different levels of arousal indicate that these changes occur on many time scales (5-80 s) as a result of modifications in the intrinsic dynamics of the neuronal oscillations.S ignificance: This study demonstrates that the dynamics of spontaneous neuronal oscillations possess long-range temporal correlations with properties suitable for functional and clinical studies.Vadim Nikulin, Tom Brismar

Source: Clinical Neurophysiology, Vol. 115, No. 8. (August 2004), pp. 1896-1908.
Mechanoelectri cal feedback: role of beta-adrenergi c receptor activation in mediating load-dependent shortening of ventricular action potential and refractoriness .: Circulation, Vol. 104, No. 4. (24 July 2001), pp. 486-490.BACKGR OUND: Augmented preload increases myocardial excitability by shortening action potential duration (APD). The mechanism governing this phenomenon is unknown. Because myocardial stretch increases intracellular cAMP, we hypothesized that load-dependent changes in myocardial excitability are mediated by beta-adrenergi c stimulation of a cAMP-sensitive K(+) current. METHODS AND RESULTS: The effects of propranolol on load-induced changes in electrical excitability were studied in 7 isolated ejecting canine hearts. LV monophasic APD at 50% and 90% repolarization (MAPD(50) and MAPD(90)) and refractoriness were determined at low (9+/-3 mL) and high (39+/-4 mL) load before and after beta-adrenergi c blockade. During control, the MAPD(50) decreased from 193+/-26 to 184+/-26 ms with increased load, as did the MAPD(90) (238+/-28 to 233+/-28 ms), P

Source: Circulation, Vol. 104, No. 4. (24 July 2001), pp. 486-490.
Modulation of the Ca(2+)-induced Ca(2+) release cascade by beta-adrenergi c stimulation in rat ventricular myocytes.: J Physiol, Vol. 533, No. Pt 3. (15 June 2001), pp. 837-848.1. To define the sub-cellular mechanisms of modulation of cardiac excitation-con traction (E-C) coupling by the beta-adrenergi c pathway, we carried out confocal Ca(2+) imaging in conjunction with recordings of inward Ca(2+) current in fluo-3-loaded patch-clamped rat ventricular myocytes. 2. Isoproterenol (isoprenaline; ISO) increased the amplitude of the inward Ca(2+) current and the globally measured intracellular Ca(2+) transients. The gain of calcium-induce d calcium release (CICR) was increased at all membrane potentials but especially at positive membrane potentials (> +30 mV). ISO dramatically broadened the bell-shaped voltage dependence of intracellular Ca(2+) transients by shifting the descending portion of the curve to very high membrane potentials. 3. The number of local release events (solitary sparks and conglomerates of overlapping sparks) induced by depolarizing steps to +30 mV was increased significantly by ISO. This potentiation of events was due to increased trigger calcium current (I(Ca)) as well the enhanced ability of I(Ca) to induce release. The amplitude and duration of solitary sparks were increased in the presence of ISO. In addition, ISO dramatically increased the proportion and the size ('mass') of clustered events. 4. Exclusion of Na(+) from the intra- and extracellular solutions prevented ISO from enhancing the ability of I(Ca) to trigger sparks. 5. We conclude that beta-adrenergi c stimulation enhances the gain of the CICR cascade by increasing the fidelity of dihydropyridin e receptor (DHPR)--ryanod ine receptor (RyR) coupling and by promoting cross-activati on of RyRs in neighbouring release sites. Reverse Na(+)--Ca(2+) exchange (NCX) appears to play a role in the beta-adrenergi c enhancement of CICR by effectively contributing to the Ca(2+) trigger.S Viatchenko-Kar pinski, S Györke

Source: J Physiol, Vol. 533, No. Pt 3. (15 June 2001), pp. 837-848.
Modeling the actions of beta-adrenergi c signaling on excitation--co ntraction coupling processes.: Ann N Y Acad Sci, Vol. 1015 (May 2004), pp. 16-27.Activati on of the beta-adrenergi c (beta-AR) signaling pathway enhances cardiac function through protein kinase A (PKA)-mediated phosphorylatio n of target proteins involved in the process of excitation-con traction (EC) coupling. Experimental studies of the effects of beta-AR stimulation on EC coupling have yielded complex results, including increased, decreased, or unchanged EC coupling gain. In this study, we extend a previously developed model of the canine ventricular myocyte describing local control of sarcoplasmic reticulum (SR) calcium (Ca(2+)) release to include the effects of beta-AR stimulation. Incorporation of phosphorylatio n-dependent effects on model membrane currents and Ca(2+)-cycling proteins yields changes of action potential (AP) and Ca(2+) transients in agreement with those measured experimentally in response to the nonspecific beta-AR agonist isoproterenol (ISO). The model reproduces experimentally observed alterations in EC coupling gain in response to beta-AR agonists and predicts the specific roles of L-type Ca(2+) channel (LCC) and SR Ca(2+) release channel phosphorylatio n in altering the amplitude and shape of the EC coupling gain function. The model also indicates that factors that promote mode 2 gating of LCCs, such as beta-AR stimulation or activation of the Ca(2+)/calmodu lin-dependent protein kinase II (CaMKII), may increase the probability of occurrence of early after-depolari zations (EADs), due to the random, long-duration opening of LCC gating in mode 2.JL Greenstein, AJ Tanskanen, RL Winslow

Source: Ann N Y Acad Sci, Vol. 1015 (May 2004), pp. 16-27.
Using models of the myocyte for functional interpretation of cardiac proteomic data: The Journal of Physiology, Vol. 563, No. 1. (February 2005), pp. 73-81.Raimond Winslow, Sonia Cortassa, Joseph Greenstein

Source: The Journal of Physiology, Vol. 563, No. 1. (February 2005), pp. 73-81.
Mechanistic systems models of cell signaling networks: a case study of myocyte adrenergic regulation.: Prog Biophys Mol Biol, Vol. 85, No. 2-3. (l 2004), pp. 261-278.Signal transduction networks coordinate a wide variety of cellular functions, including gene expression, metabolism, and cell fate processes. Understanding biological networks quantitatively is a major challenge to post-genomic biology, and mechanistic systems models will be crucial for this task. Here, we review approaches towards developing mechanistic systems models of established cell signaling networks. The ability of mechanistic system models to generate testable biological hypotheses and experimental strategies is discussed. As a case study of model development and analysis, we examined the functional roles of phospholamban, the L-type calcium channel, the ryanodine receptor, and troponin I phosphorylatio n upon beta-adrenergi c stimulation in the rat ventricular myocyte. Model analysis revealed that while protein kinase A-mediated phosphorylatio n of the ryanodine receptor greatly increases its calcium sensitivity, calcium autoregulation may adapt quickly by negating potential increases in contractility. Systematic combinations of in silico perturbations supported the conclusion that phospholamban phosphoregulat ion is the primary mechanism for increased sarcoplasmic reticulum load and calcium relaxation rate during beta-adrenergi c stimulation, while both phospholamban and the L-type calcium channel contribute to increased systolic calcium. Combined with detailed experimental studies, mechanistic systems models will be valuable for developing a quantitative understanding of cell signaling networks.JJ Saucerman, AD McCulloch

Source: Prog Biophys Mol Biol, Vol. 85, No. 2-3. (l 2004), pp. 261-278.

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