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At least 127 records · Page 7Linked to original sources

Synchronization and coherence in thermodynamic coupled map lattices with intermediate-range coupling.

In spatially extended systems, intermediate-range interactions arise naturally in some physical contexts. To study them, we investigate a model of coupled map lattices (CML's) with intermediate-range coupling, and derive analytic conditions for its synchronization. We find that in these CML's, if the range of coupling is fixed, the law of large numbers applies for the mean field. The total normalized power in nonzero components of the power spectrum of the mean field goes to zero in the thermodynamic limit. We also show that in the same limit the relevant parameter for synchronization and coherence is the fraction of sites coupled, and not their number.

Journal Article↗

Synchronization and control of coupled ginzburg-landau equations using local coupling

In this paper we discuss the properties of a recently introduced coupling scheme for spatially extended systems based on local spatially averaged coupling signals [see Z. Tasev et al., Int. J. Bifurcation Chaos Appl. Sci. Eng. (to be published); and L. Junge et al., Int. J. Bifurcation Chaos Appl. Sci. Eng. 9, 2265 (1999)]. Using the Ginzburg-Landau model, we performed an extensive numerical examination of this coupling scheme, i.e., a complete scan through the relevant coupling parameters. Furthermore, we demonstrate suppression and control of spatiotemporal chaos, e.g., stabilizing the homogeneous steady state and spatially localized control. As an application all model parameters of the Ginzburg-Landau equation are estimated given only the local information of the system.

Journal Article↗

Functional coupling between glycolysis and excitation-contraction coupling underlies alternans in cat heart cells.

Electromechanical alternans was characterized in single cat atrial and ventricular myocytes by simultaneous measurements of action potentials, membrane current, cell shortening and changes in intracellular Ca2+ concentration ([Ca2+]i). Using laser scanning confocal fluorescence microscopy, alternans of electrically evoked [Ca2+]i transients revealed marked differences between atrial and ventricular myocytes. In ventricular myocytes, electrically evoked [Ca2+]i transients during alternans were spatially homogeneous. In atrial cells Ca2+ release started at subsarcolemmal peripheral regions and subsequently spread toward the centre of the myocyte. In contrast to ventricular myocytes, in atrial cells propagation of Ca2+ release from the sarcoplasmic reticulum (SR) during the small-amplitude [Ca2+]i transient was incomplete, leading to failures of excitation-contraction (EC) coupling in central regions of the cell. The mechanism underlying alternans was explored by evaluating the trigger signal for SR Ca2+ release (voltage-gated L-type Ca2+ current, ICa,L) and SR Ca2+ load during alternans. Voltage-clamp experiments revealed that peak ICa,L was not affected during alternans when measured simultaneously with changes of cell shortening. The SR Ca2+ content, evaluated by application of caffeine pulses, was identical following the small-amplitude and the large-amplitude [Ca2+]i transient. These results suggest that the primary mechanism responsible for cardiac alternans does not reside in the trigger signal for Ca2+ release and SR Ca2+ load. beta-Adrenergic stimulation with isoproterenol (isoprenaline) reversed electromechanical alternans, suggesting that under conditions of positive cardiac inotropy and enhanced efficiency of EC coupling alternans is less likely to occur. The occurrence of electromechanical alternans could be elicited by impairment of glycolysis. Inhibition of glycolytic flux by application of pyruvate, iodoacetate or beta-hydroxybutyrate induced electromechanical and [Ca2+]i transient alternans in both atrial and ventricular myocytes. The data support the conclusion that in cardiac myocytes alternans is the result of periodic alterations in the gain of EC coupling, i. e. the efficacy of a given trigger signal to release Ca2+ from the SR. It is suggested that the efficiency of EC coupling is locally controlled in the microenvironment of the SR Ca2+ release sites by mechanisms utilizing ATP, produced by glycolytic enzymes closely associated with the release channel.

Action Potentials↗

Enhanced activation of Akt and extracellular-regulated kinase pathways by simultaneous occupancy of Gq-coupled 5-HT2A receptors and Gs-coupled 5-HT7A receptors in PC12 cells.

The most commonly prescribed antidepressants, the serotonin (5-HT) selective reuptake inhibitors, increase 5-HT without targeting specific receptors. Yet, little is known about the interaction of multiple receptor subtypes expressed by individual neurons. Specifically, the effect of increases in cAMP induced by Gs-coupled 5-HT receptor subtypes on the signaling pathways modulated by other receptor subtypes has not been studied. We have, therefore, examined the activation of the extracellular-regulated kinase (ERK) and Akt pathways by Gs-coupled 5-HT7A receptors and Gq-coupled 5-HT2A receptors, which are co-expressed in discrete brain regions. Agonists for both receptors were found to activate ERK and Akt in transfected PC12 cells. 5-HT2A receptor-mediated activation of the two pathways was found to be Ca2+-dependent. In contrast, 5-HT7A receptor-mediated activation of Akt required increases in both [cAMP] and intracellular [Ca2+], while activation of ERK was inhibited by Ca2+. The activation of ERK and Akt stimulated by simultaneous treatment of cells with 5-HT2A and 5-HT7A receptor agonists was found to be at least additive. Cell-permeable cAMP analogs mimicked 5-HT7A receptor agonists in enhancing 5-HT2A receptor-mediated activation of ERK and Akt. A role was identified for the cAMP-guanine exchange factor, Epac, in this augmentation of ERK, but not Akt, activation. Our finding of enhanced activation of neuroprotective Akt and ERK pathways by simultaneous occupancy of 5-HT2A and 5-HT7A receptors may also be relevant to the interaction of other neuronally expressed Gq- and Gs-coupled receptors.

Amphetamines↗

The Adult Attachment Interview and observed couple interaction: implications for an intergenerational perspective on couple therapy.

One of the assumptions of intergenerational family therapy is that how a person thinks and talks about family-of-origin experiences has important implications for current family relationships. The Adult Attachment Interview (AAI) is a measure of attachment security based on how coherently the person can discuss attachment experiences in childhood. This study examined the relationship between attachment security, as measured by the AAI, and couple interaction, as measured by the Georgia Marriage Q-Sort (GMQ), in a sample of 28 couples in therapy for relationship problems. During a conflict resolution discussion, those individuals who were less coherent in discussing their family of origin expressed more negative affect, less respect, less openness, more avoidance, and less willingness to negotiate when interacting with their partner. No evidence of intra-couple effects or "buffering" was found. The findings support a key assumption of intergenerational approaches to family therapy and suggest that applying attachment theory is a promising direction for refining and developing new interventions for couples.

Adult↗

Activation of nematode G protein GOA-1 by the human muscarinic acetylcholine receptor M2 subtype. Functional coupling of G-protein-coupled receptor and G protein originated from evolutionarily distant animals.

Signal transduction mediated by heterotrimeric G proteins regulates a wide variety of physiological functions. We are interested in the manipulation of G-protein-mediating signal transduction using G-protein-coupled receptors, which are derived from evolutionarily distant organisms and recognize unique ligands. As a model, we tested the functionally coupling GOA-1, G alpha(i/o) ortholog in the nematode Caenorhabditis elegans, with the human muscarinic acetylcholine receptor M2 subtype (M2), which is one of the mammalian G alpha(i/o)-coupled receptors. GOA-1 and M2 were prepared as a fusion protein using a baculovirus expression system. The affinity of the fusion protein for GDP was decreased by addition of a muscarinic agonist, carbamylcholine and the guanosine 5'-[3-O-thio]triphosphate ([35S]GTPgammaS) binding was increased with an increase in the carbamylcholine concentrations in a dose-dependent manner. These effects evoked by carbamylcholine were completely abolished by a full antagonist, atropine. In addition, the affinity for carbamylcholine decreased under the presence of GTP as reported for M2-G alpha(i/o) coupling. These results indicate that the M2 activates GOA-1 as well as G alpha(i/o).

Amino Acid Sequence↗

Dependence of electrical coupling on mechanical coupling in cardiac myocytes: insights gained from cardiomyopathies caused by defects in cell-cell connections.

Cardiac myocytes are electrically coupled by large gap junctions to ensure safe conduction. Membrane regions containing gap junction channels are rigid and susceptible to fragmentation in response to shear stress. Thus, gap junctions in cardiac myocytes are located in close proximity to points of cell-cell adhesion within the intercalated disk. These adhesion junctions mechanically stabilize the sarcolemmas of adjacent cells to allow formation and maintenance of large arrays of intercellular channels. It has been proposed that the extent to which cardiac myocytes are coupled mechanically at cell-cell adhesion junctions is an important determinant of the extent to which cells can become electrically coupled at gap junctions. This hypothesis has been tested by analyzing gap junctions in human cardiomyopathies caused by mutations in plakoglobin and desmoplakin, intracellular proteins that link adhesion molecules at cell-cell junctions to the cardiac myocyte cytoskeleton. Marked remodeling of cardiac gap junctions, despite the presence of normal intracellular levels of connexin43, was observed. This suggests that defects in cell-cell adhesion, or the presence of discontinuities between adhesion junctions and the cytoskeleton, destabilize gap junctions and diminish electrical coupling. This could contribute to the high incidence of ventricular arrhythmias and sudden death known to occur in these cardiomyopathies.

Cardiomyopathies↗

[Coupling of bovine gamma globulin to carbonochloridate-activated cellulose beads, CNBr-activated Sepharose CL-4B and NaIO4-oxidized Sepharose 6B and use of the coupled products for immunoaffinity chromatography].

For coupling 25 mg of bovine IgG (BGG) were given to 5 ml volumes of packed bead cellulose activated by 5-norbornene-2.3-dicarboximido carbonochloridate and CNBr-activated Sepharose CL-4B, respectively. Thus, BGG-immunosorbents were obtained with 4.6 to 4.9 mg BGG/ml matrix. 5 ml volumes of packed NaIO4-oxidized Sepharose 6B coupled 27% from 25 mg of BGG, only. In this case, immunosorbents with 1.35 mg BGG/ml matrix were produced. All BGG-immunosorbents were chemically relatively stable. The use of these immunosorbents for affinity chromatography results in the isolation of one milligram of pure rabbit anti-BGG antibodies by means of about 4.6 mg of BGG coupled to the cellulose or the Sepharose-CL-4B matrices. On the other side, only 3.4 mg of BGG coupled to the NaIO4-activated Sepharose 6B were necessary in order to isolate one milligram of antibodies in an immunoelectrophoretically pure state.

Animals↗

Molecular mechanisms of G protein-coupled receptor signaling: role of G protein-coupled receptor kinases and arrestins in receptor desensitization and resensitization.

Dynamic regulation of G protein-coupled receptor signaling demands a coordinated balance between mechanisms leading to the generation, turning off and re-establishment of agonist-mediated signals. G protein-coupled receptor kinases (GRKs) and arrestin proteins not only mediate agonist-dependent G protein-coupled receptor desensitization, but also initiate the internalization (sequestration) of activated receptors, a process leading to receptor resensitization. Studies on the specificity of beta-arrestin functions reveal a multiplicity of G protein-coupled receptor endocytic pathways and suggest that beta-arrestins might serve as adaptors specifically targeting receptors for dynamin-dependent clathrin-mediated endocytosis. Moreover, inactivation of the GRK2 gene in mice has lead to the discovery of an unexpected role of GRK2 in cardiac development, further emphasizing the pleiotropic function of GRKs and arrestins.

Animals↗

Analysing home-ownership of couples: the effect of selecting couples at the time of the survey.

"The analysis of events encountered by couple and family households may suffer from sample selection bias when data are restricted to couples existing at the moment of interview. The paper discusses the effect of sample selection bias on event history analyses of buying a home [in the Netherlands] by comparing analyses performed on a sample of existing couples with analyses of a more complete sample including past as well as current partner relationships. The results show that, although home-buying in relationships that have ended differs clearly from behaviour in existing relationships, sample selection bias is not alarmingly large." (SUMMARY IN FRE)

Bias↗

Movement of 'gating charge' is coupled to ligand binding in a G-protein-coupled receptor.

Activation by agonist binding of G-protein-coupled receptors (GPCRs) controls most signal transduction processes. Although these receptors span the cell membrane, they are not considered to be voltage sensitive. Recently it was shown that both the activity of GPCRs and their affinity towards agonists are regulated by membrane potential. However, it remains unclear whether GPCRs intrinsically respond to changes in membrane potential. Here we show that two prototypical GPCRs, the m2 and m1 muscarinic receptors (m2R and m1R), display charge-movement-associated currents analogous to 'gating currents' of voltage-gated channels. The gating charge-voltage relationship of m2R correlates well with the voltage dependence of the affinity of the receptor for acetylcholine. The loop that couples m2R and m1R to their G protein has a crucial function in coupling voltage sensing to agonist-binding affinity. Our data strongly indicate that GPCRs serve as sensors for both transmembrane potential and external chemical signals.

Acetylcholine↗

Attachment injuries in couple relationships: a new perspective on impasses in couples therapy.

This article identifies and operationalizes the newly defined construct of attachment injury. An attachment injury occurs when one partner violates the expectation that the other will offer comfort and caring in times of danger or distress. This incident becomes a clinically recurring theme and creates an impasse that blocks relationship repair in couples therapy. An attachment injury is characterized by an abandonment or by a betrayal of trust during a critical moment of need. The injurious incident defines the relationship as insecure and maintains relationship distress because it is continually used as a standard for the dependability of the offending partner. The concept of an attachment injury is defined here in the context of emotionally focused therapy, an empirically validated, short-term approach to modifying distress in couples. The broad theoretical underpinnings of this concept may be found in attachment theory as applied to adult romantic relationships. Through the delineation of attachment injury events and the ongoing development of a detailed model of resolution, couples therapists will be better able to identify, describe, and effectively treat such injuries and address the therapeutic impasses that are associated with them.

Adult↗

Impact of marital and psychological distress on therapeutic alliance in couples undergoing couple therapy.

In this study, we describe the psychometric properties of the Couple Therapy Alliance Scale--revised (CTAS-r) and investigates the impact of marital and psychiatric distress on alliance. Seventy-nine couples in therapy completed a French version of the Dyadic Adjustment Scale and of the Psychiatric Symptoms Index at session one, and a French version of the CTAS-r at session three. Results indicate that the French version of the CTAS-r has adequate psychometric properties, although the subscales of the instrument are highly intercorrelated. Furthermore, marital adjustment predicts alliance scores, whereas psychiatric symptoms do not. Finally, male marital adjustment and female psychiatric symptoms are lower in couples where spouses have divergent perceptions of the alliance. Future research directions are discussed.

Adaptation, Psychological↗

Selective regulation of G protein-coupled receptor-mediated signaling by G protein-coupled receptor kinase 2 in FRTL-5 cells: analysis of thyrotropin, alpha(1B)-adrenergic, and A(1) adenosine receptor-mediated responses.

G protein-coupled receptor kinases (GRKs) play a key role in the process of receptor homologous desensitization. In the present study, we address the question of whether a variety of receptors coupled to different G protein subtypes and naturally expressed on the same cell are selectively regulated by GRK2. The signaling stimulated by thyrotropin (TSH), alpha(1B)-adrenergic, and A(1) adenosine receptors was studied in FRTL-5 cells permanently transfected to overexpress GRK2 and GRK2-K220R, a kinase dead GRK dominant negative mutant. In FRTL-5 overexpressing GRK2, TSH-induced cyclic AMP response was attenuated, indicating that TSH receptor is desensitized by this kinase. Consistently, FRTL-5 cells overexpressing GRK2-K220R show increased TSH-induced cyclic AMP response, demonstrating that this receptor is under tonic control by GRK. Unlike TSH receptor, alpha(1B)-adrenergic receptor response was unaffected in FRTL-5 overexpressing GRK2 and GRK2-K220R. When A(1) adenosine receptors were stimulated, G(ialpha)-mediated cyclic AMP inhibition was totally unaffected by overexpression of either GRK2 or GRK2-K220R. By contrast, G(betagamma)-mediated response (activation of mitogen-activated protein kinases) was efficiently desensitized by GRK2 but was unaffected by GRK2-K220R overexpression. The present study documents that overexpression of GRK2 results in a selective regulation of different G protein-coupled receptors expressed on the same cell and that this kinase can regulate preferentially only one of the different pathways activated by the same receptor. The preferential regulation of the A(1) adenosine receptor-stimulated mitogen-activated protein kinases by GRK2 indicates that this kinase can have additional regulatory effects on G(betagamma)-stimulated pathways, possibly through direct binding and regulation of the receptor-G(betagamma) complex.

Animals↗

Orexin receptor type-1 couples exclusively to pertussis toxin-insensitive G-proteins, while orexin receptor type-2 couples to both pertussis toxin-sensitive and -insensitive G-proteins.

Signal transduction pathways of orexin receptors were examined using a nerve-like cell line transfected with orexin receptor type-1 (OX1R) and orexin receptor type-2 (OX2R). Forskolin-stimulated cyclic adenosine 3,5-monophosphate (cAMP) accumulation in OX2R-expressing cells was inhibited by orexin in a dose-dependent manner, and the effect was abolished by pretreatment with pertussis toxin (PTX). The inhibitory effect of orexin on forskolin-stimulated cAMP accumulation was not observed in OX1R-expressing cells. Administration of orexin to these cells resulted in a transient increase of intracellular calcium concentration ([Ca(2+)](i)). Orexin-stimulated increases in [Ca(2+)](i) in OX1R- or OX2R-expressing cells were not affected by the PTX pretreatment. These observations suggest that OX1R couples exclusively to PTX-insensitive G-proteins, while OX2R couples to both PTX-sensitive and -insensitive G-proteins. To examine the relative contributions of these G-proteins in OX2R-mediated activation of neurons, we used histaminergic tuberomammillary nucleus neurons, in which OX2R is abundantly expressed. We found that a phospholipase C (PLC)-inhibitor, U73122, inhibits orexin-mediated neuronal activation, but PTX showed no effect on it. This suggests that although OX2R couples to multiple G-proteins, activation of neurons by orexins through OX2R is mediated via a PTX-insensitive, PLC dependent pathway.

Animals↗

Analysis of the coupling of G12/13 to G protein-coupled receptors using a luciferase reporter assay.

G protein-coupled receptors (GPCRs) transduce signals from cell surface to intracellular effectors through various G proteins. In this chapter, a luciferase reporter gene assay system is described for the study of the coupling of GPCRs to G alpha 12/13. This assay system, in which ligand-stimulated production of the reporter luciferase under the control of a modified serum-responsive element (SRE) in a cell line derived from mice lacking G alpha q/11 that are transfected with a GPCR of interest, allows for easy, fast, and valid determination of the coupling of the GPCR to G alpha 12/13.

Animals↗

Palladium-catalyzed cross-coupling reactions of silanolates: a paradigm shift in silicon-based cross-coupling reactions.

This paper chronicles the conceptual development, proof of principle experiments, and recent advances in the palladium-catalyzed cross-coupling reactions of the conjugate bases of organosilanols. The discovery that led to the design and refinement of this process represents a classical illustration of how mechanistic studies can provide a fertile ground for the invention of new reactions. On the basis of a working hypothesis (which ultimately proved to be incorrect) and the desire to effect silicon-based cross-coupling without the agency of fluoride activation, a mild and practical palladium-catalyzed cross-coupling of alkenyl-, aryl-, and heteroaryl silanolates has been developed. The mechanistic underpinnings, methodological extensions, and the successful applications of this technology to the synthesis of complex molecules are described.

Butanols↗

[Couple relations and couple dynamics in the sterile marriage].

Only if the couple can accept that both their wish to have a child and their infertility are deeply rooted in their relationship will they be prepared to undergo and tolerate the stresses and strains involved in fertility treatment without allowing it to govern their lives completely. If both sides - the doctor and the couple - refuse to admit that there are limits and cannot acknowledge their feelings of inadequacy and impotence, and the anger and sadness which are inevitably linked with these, the couple will have no chance to mourn and finally give up their desire for a child, if that becomes necessary.

Adaptation, Psychological↗