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Results for “augmented feedback”

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At least 145 records · Page 8Linked to original sources

PubMed1991

Toward a movement dynamics perspective on dual-task performance.

The effect of practice on the parallel organization and control of discrete, asymmetrical bimanual movements was investigated. Subjects performed a flexion movement in the left limb together with a flexion-extension-flexion movement in the right limb. Two groups, one of which received kinematic information feedback, were instructed to produce the different patterns simultaneously. A third group performed each movement in isolation at all times, serving as the baseline condition. The degree of success in parallel action organization was assessed at the qualitative (or structural) and quantitative (or metrical) level of movement specification. Findings revealed that the bimanual groups displayed a tendency to synchronize the patterns of motor output, resulting in (mutual) interference. However,the provision of augmented kinematic information feedback resulted in more successful metrical and structural dissociation of the limb actions. The results are discussed in support of a movement dynamics perspective on motoric dual-task performance. The relevance of the approach for human factors is also emphasized.

Acceleration↗

PubMed2004

GIT1 mediates thrombin signaling in endothelial cells: role in turnover of RhoA-type focal adhesions.

Thrombin mediates changes in endothelial barrier function and increases endothelial permeability. A feature of thrombin-enhanced endothelial hyperpermeability is contraction of endothelial cells (ECs), accompanied by formation of focal adhesions (FAs). Recently, a G protein-coupled receptor kinase-interacting protein, GIT1, was shown to regulate FA disassembly. We hypothesized that GIT1 modulates thrombin-induced changes in FAs. In human umbilical vein ECs (HUVECs), thrombin recruited GIT1 to FAs, where GIT1 colocalized with FAK and vinculin. Recruitment of GIT1 to FAs was dependent on activation of the small GTPase RhoA, and Rho kinase, as demonstrated by adenoviral transfection of dominant-negative RhoA and treatment with Y-27632. Thrombin stimulated GIT1 tyrosine phosphorylation with a time course similar to FAK phosphorylation in a Rho kinase- and Src-dependent manner. Depletion of GIT1 with antisense GIT1 oligonucleotides had no effect on basal cell morphology, but increased cell rounding and contraction of HUVECs, increased FA formation, and increased FAK tyrosine phosphorylation in response to thrombin, concomitant with increased endothelial hyperpermeability. These data identify GIT1 as a novel mediator in agonist-dependent signaling in ECs, demonstrate that GIT1 is involved in cell shape changes, and suggest a role for GIT1 as a negative feedback regulator that augments recovery of cell contraction.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Association of PSD-95 with ErbB4 facilitates neuregulin signaling in cerebellar granule neurons in culture.

The growth factor neuregulin 1 (NRG) selectively induces an increase in the gamma-aminobutyric acid (GABA)(A) receptor beta2 subunit protein in rat cerebellar granule neurons in culture. We previously demonstrated that NRG acts by triggering ErbB4 receptor phosphorylation and subsequent signaling through the mitogen-activated kinase (MAPK), phosphatidyl inositol-3 kinase (PI-3K) and cyclin-dependent kinase 5 (cdk5) pathways. In this report we show that the scaffolding protein, PSD-95, plays a key role in mediating the effects of NRG and that reducing its level attenuates the NRG-induced increase in beta2 subunit expression. PSD-95 appears to facilitate the effects of NRG through its association with ErbB4, an interaction that is augmented by NRG-activated cdk signaling. Inhibition of cdk activity with roscovitine attenuates the association of PSD-95 with ErbB4. The effects of cdk5 are not blocked by U0126, an inhibitor of MAPK signaling, indicating that cdk5 functions independently of cross-talk with this pathway. These findings raise the possibility that NRG-induced activation of cdk5 works in part by recruiting PSD-95, a protein involved in regulating synaptic plasticity, to associate with ErbB4. This interaction may be a positive feedback loop that augments NRG signaling and its downstream effects on GABA(A) receptor beta2 subunit expression.

Animals↗

PubMed2006

To stabilize neutrophil polarity, PIP3 and Cdc42 augment RhoA activity at the back as well as signals at the front.

Chemoattractants like f-Met-Leu-Phe (fMLP) induce neutrophils to polarize by triggering divergent signals that promote the formation of protrusive filamentous actin (F-actin; frontness) and RhoA-dependent actomyosin contraction (backness). Frontness locally inhibits backness and vice versa. In neutrophil-like HL60 cells, blocking phosphatidylinositol-3,4,5-tris-phosphate (PIP3) accumulation with selective inhibitors of PIP3 synthesis completely prevents fMLP from activating a PIP3-dependent kinase and Cdc42 but not from stimulating F-actin accumulation. PIP3-deficient cells show reduced fMLP-dependent Rac activity and unstable pseudopods, which is consistent with the established role of PIP3 as a mediator of positive feedback pathways that augment Rac activation at the front. Surprisingly, such cells also show reduced RhoA activation and RhoA-dependent contraction at the trailing edge, leading to the formation of multiple lateral pseudopods. Cdc42 mediates PIP3's positive effect on RhoA activity. Thus, PIP3 and Cdc42 maintain stable polarity with a single front and a single back not only by strengthening pseudopods but also, at longer range, by promoting RhoA-dependent actomyosin contraction at the trailing edge.

Bridged Bicyclo Compounds, Heterocyclic↗

PubMed2000

Catheter insertion simulation with co-registered direct volume rendering and haptic feedback.

We have developed an experimental catheter insertion simulation system supporting head-tracked stereoscopic viewing of volumetric anatomic reconstructions registered with direct haptic 3D interaction. The system takes as input data acquired with standard medical imaging modalities and regards it as a visual and haptic environment whose parameters are interactively defined using look-up tables. The system's display, positioned like a surgical table, provide a realistic impression of looking down at the patient. Measuring head motion via a six degrees-of-freedom head tracker, good positions to observe the anatomy and identify the catheter insertion point are quickly established with simple head motion. By generating appropriate stereoscopic images and co-registering physical and virtual spaces beforehand, volumes appear at fixed physical positions and it is possible to control catheter insertion via direct interaction with a PHANToM haptic device. During the insertion procedure, the system provides perception of the effort of penetration and deviation inside the traversed tissues. Semi-transparent volumetric rendering augment the sensory feedback with the visual indication of the inserted catheter position inside the body.

Catheterization, Peripheral↗

PubMed1996

Dynamic synapse: a new concept of neural representation and computation.

Presynaptic mechanisms influencing the probability of neurotransmitter release from an axon terminal, such as facilitation, augmentation, and presynaptic feedback inhibition, are fundamental features of biological neurons and are cardinal physiological properties of synaptic connections in the hippocampus. The consequence of these presynaptic mechanisms is that the probability of release becomes a function of the temporal pattern of action potential occurrence, and hence, the strength of a given synapse varies upon the arrival of each action potential invading the terminal region. From the perspective of neural information processing, the capability of dynamically tuning the synaptic strength as a function of the level of neuronal activation gives rise to a significant representational and processing power of temporal spike patterns at the synaptic level. Furthermore, there is an exponential growth in such computational power when the specific dynamics of presynaptic mechanisms varies quantitatively across axon terminals of a single neuron, a recently established characteristic of hippocampal synapses. During learning, alterations in the presynaptic mechanisms lead to different pattern transformation functions, whereas changes in the postsynaptic mechanisms determine how the synaptic signals are to be combined. We demonstrate the computational capability of dynamic synapses by performing speech recognition from unprocessed, noisy raw waveforms of words spoken by multiple speakers with a simple neural network consisting of a small number of neurons connected with synapses incorporating dynamically determined probability of release. The dynamics included in the model are consistent with available experimental data on hippocampal neurons in that parameter values were chosen so as to be consistent with time constants of facilitative and inhibitory processes governing the dynamics of hippocampal synaptic transmission studied using nonlinear systems analytic procedures.

Acoustic Stimulation↗

PubMed1990

Enhancement of low-level ECG components in noise with time-sequenced adaptive filtering.

Observation of low amplitude components in the ECG motivated our interest in time-sequenced adaptive filtering. This technique is applicable to signals that are cyclic in nature. Two simultaneously acquired signals are used in the technique. It is assumed that the underlying signal is correlated and that noise is uncorrelated between the two channels. Instead of one enhancer that continuously adjusts its characteristics over the time course of the signal, each cycle is subdivided into intervals; a given enhancer is used only on the same corresponding interval in successive cycles. This minimizes the signal range over which the enhancer must adjust its characteristics. In the time-sequenced approach, it is important that the enhancers adapt at the same rate. Thus, each has its own feedback coefficient derived from an average of 10 consecutive ECG cycles and an estimate of noise in intervals where no signal is present. Each feedback coefficient is augmented over the first 10 beats. To improve adaptation, a means to update each filter on the preceding beat and the current beat was developed. Lastly, a weight averaging scheme was developed to circumvent weight stalling. The procedure has enabled observation of both His activity and late potentials in individual beats from signals acquired from the chest surface.

Electrocardiography↗

PubMed2003

Interplay between brain-derived neurotrophic factor and signal transduction modulators in the regulation of the effects of exercise on synaptic-plasticity.

This study was designed to identify molecular mechanisms by which exercise affects synaptic-plasticity in the hippocampus, a brain area whose function, learning and memory, depends on this capability. We have focused on the central role that brain-derived neurotrophic factor (BDNF) may play in mediating the effects of exercise on synaptic-plasticity. In fact, this impact of exercise is exemplified by our finding that BDNF regulates the mRNA levels of two end products important for neural function, i.e. cAMP-response-element binding (CREB) protein and synapsin I. CREB and synapsin I have the ability to modify neuronal function by regulating gene-transcription and affecting synaptic transmission, respectively. Furthermore, we show that BDNF is capable of concurrently increasing the mRNA levels of both itself and its tyrosine kinaseB (TrkB) receptor, suggesting that exercise may employ a feedback loop to augment the effects of BDNF on synaptic-plasticity. The use of a novel microbead injection method in our blocking experiments and Taqman reverse transcription polymerase reaction (RT-PCR) for RNA quantification, have enabled us to evaluate the contribution of different pathways to the exercise-induced increases in the mRNA levels of BDNF, TrkB, CREB, and synapsin I. We found that although BDNF mediates exercise-induced hippocampal plasticity, additional molecules, i.e. the N-methyl-D-aspartate receptor, calcium/calmodulin protein kinase II and the mitogen-activated protein kinase cascade, modulate its effects. Since these molecules have a well-described association to BDNF action, our results illustrate a basic mechanism through which exercise may promote synaptic-plasticity in the adult brain.

Analysis of Variance↗

PubMed1993

Endogenous glucocorticoids restrain catecholamine synthesis and release at rest and during immobilization stress in rats.

Cardiovascular and metabolic adjustments during stress involve participation of the sympatho-adrenal and hypothalamic-pituitary-adrenocortical systems, which interact at several levels. The present study investigated the effects of removal of endogenous glucocorticoids on indices of norepinephrine release and metabolism and of catecholamine biosynthesis in sympathetic nerves, at baseline and in response to immobilization stress (IMMO) in rats. Plasma levels of the catecholamine precursor dihydroxyphenylalanine, norepinephrine (NE), the NE metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol, dopamine, and the dopamine metabolites dihydroxyphenylacetic acid and homovanillic acid were measured in adrenalectomized, adrenal-medullectomized, or sham-operated conscious rats, with or without glucocorticoid treatment (25 mg/kg.24 h cortisol for 7 days by osmotic minipumps), at rest and after 5, 20, 60, and 120 min of IMMO. Adrenalectomy eliminated plasma levels of epinephrine and corticosterone and augmented IMMO-induced increments in levels of NE, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, dihydroxyphenylalanine, dihydroxyphenylacetic acid, and homovanillic acid. Adrenal-medullectomy reduced plasma epinephrine, but not corticosterone, to undetectable levels at baseline and did not augment stress-induced responses of any of the measured compounds. Cortisol administration (plasma levels approximately 600 pmol/ml) reversed the augmentation of catecholaminergic responses in adrenalectomized rats. The results indicate that adrenalectomy stimulates several aspects of sympatho-neural function, including stress-induced increments in NE release, reuptake, metabolism, and turnover and in catecholamine biosynthesis. This augmentation was absent in adreno-medullectomized rats, indicating that the loss of adrenomedullary hormones after adrenalectomy does not appear to contribute to the augmentation. Since cortisol treatment reversed or prevented this augmentation, loss of feedback inhibition by endogenous glucocorticoids appears to be the basis of the enhanced responses. Thus, the results suggest that endogenous glucocorticoids restrain responses of catecholamine turnover, synthesis, release, reuptake, and metabolism in sympathetic nerves in this stress model.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Overexpression of a human transforming growth factor-alpha (TGF alpha) transgene reveals a dual antagonistic role of TGF alpha in female sexual development.

The importance of transforming growth factor-alpha (TGF alpha) in female reproductive development was assessed using transgenic mice bearing a human TGF alpha complementary DNA under the control of a mouse metallothionein-1 promoter (MT1-hTGF alpha). Examination of the brain and ovaries 5 h after a single sc injection of zinc chloride, administered to activate the MT1-hTGF alpha transgene, revealed that prominent sites of human TGF alpha messenger RNA expression within these tissues were the hypothalamus and ovarian follicles, respectively. In vitro experiments showed that acute transgene activation increased hypothalamic release of LH-releasing hormone. In contrast, the ovarian steroidal response to gonadotropins, examined in vitro, was markedly attenuated. Chronic activation of transgene expression by daily administration of zinc chloride delayed the time of first estrus (an index of peripubertal estrogen secretion), but shortened the interval between first estrus and the onset of estrous cyclicity (an index of reproductive competence). Accumulation of small antral follicles, accompanied by thecal hypertrophy and enhanced androgen production, preceded the acquisition of ovulatory capacity. These changes were accompanied by reduced serum LH levels, suggesting that the relative inability of small antral follicles to develop further in TGF alpha-overexpressing mice is at least in part due to inappropriate gonadotropin support. Serum LH levels in these animals may be reduced by an augmented androgen negative feedback signal. Nontransgenic mouse ovaries, placed under the control of a transgenic hypothalamus by heterologous grafting, rapidly ovulated and initiated estrous cyclicity. In contrast, acquisition of reproductive capacity was severely delayed in nontransgenic mice bearing transgenic ovarian grafts. The results indicate that TGF alpha regulates female reproductive development through two opposing mechanisms: within the brain, it facilitates the neuroendocrine activation of the process; at the ovarian level, modulates the stimulatory effect of gonadotropin hormones on follicular growth and steroidogenesis.

Animals↗

PubMed2005

Anesthetic preconditioning: the role of free radicals in sevoflurane-induced attenuation of mitochondrial electron transport in Guinea pig isolated hearts.

Cardioprotection by anesthetic preconditioning (APC) can be abolished by nitric oxide (NO*) synthase inhibitors or by reactive oxygen species (ROS) scavengers. We previously reported attenuated mitochondrial electron transport (ET) and increased ROS generation during preconditioning sevoflurane exposure as part of the triggering mechanism of APC. We hypothesized that NO* and other ROS mediate anesthetic-induced ET attenuation. Cardiac function and reduced nicotinamide adenine dinucleotide (NADH) fluorescence, an index of mitochondrial ET, were measured online in 68 Langendorff-prepared guinea pig hearts. Hearts underwent 30 min of global ischemia and 120 min of reperfusion. Before ischemia, hearts were temporarily perfused with superoxide dismutase, catalase, and glutathione to scavenge ROS or N(G)-nitro-L-arginine-methyl-ester (L-NAME) to inhibit NO* synthase in the presence or absence of 1.3 mM sevoflurane (APC). APC temporarily increased NADH before ischemia, i.e., it attenuated mitochondrial ET. Both this NADH increase and the cardioprotection by APC on reperfusion were prevented by superoxide dismutase, catalase, and glutathione and by N(G)-nitro-L-arginine-methyl-ester. Thus, ROS and NO*, or reaction products including peroxynitrite, mediate sevoflurane-induced ET attenuation. This may lead to a positive feedback mechanism with augmented ROS generation to trigger APC secondary to altered mitochondrial function.

Anesthesia↗

PubMed2000

Microbial and T cell-derived stimuli regulate antigen presentation by dendritic cells in vivo.

B cells and dendritic cells (DC) internalize and degrade exogenous Ags and present them as peptides bound to MHC class II molecules for scrutiny by CD4(+) T cells. Here we use an Ab specific for a processed form of the model Ag, hen egg lysozyme (HEL), to demonstrate that this protein is not efficiently presented by lymph node DC following s.c. immunization. HEL presentation by the DC can be dramatically enhanced upon coinjection of a microbial adjuvant, which appears to act by enhancing peptide loading onto MHC class II. CD40 cross-linking or the presence of a high frequency of T cells specific for HEL can similarly improve presentation by DC in vivo. For any of these activating stimuli, CD8alpha(+) DC consistently display the highest proportion of HEL-loaded MHC class II molecules. These data indicate that exogenous Ags can be displayed to T cells in lymphoid tissues by a large cohort of resident DC whose presentation is regulated by innate and adaptive stimuli. Our data further reveal the existence of a feedback mechanism that augments Ag presentation during cognate APC-T cell interactions.

Adjuvants, Immunologic↗

PubMed2002

NF-kappa B and TNF-alpha: a positive autocrine loop in human lung mast cells?

The generation of cytokines, particularly TNF-alpha, by mast cells is crucial for the initiation of the allergic response. A key transcription factor involved in the synthesis of TNF-alpha is NF-kappaB. Using a mAb specific for the activated form of NF-kappaB, immunocytochemistry, confocal microscopy, and gel shift assays have been used in conjunction to localize this transcription factor to human lung mast cells and to study its activation. Activation of mast cells with stem cell factor (10 ng/ml) and anti-IgE (1 micro g/ml) induced maximal activation of NF-kappaB at 4 and 2 h, respectively. In contrast, with TNF-alpha (5 ng/ml) maximal activation occurred within 15 min. Parallel falls in IkappaB were demonstrated. Confocal microscopy demonstrated the localization of the activated form of NF-kappaB to the nuclei of activated mast cells. NF-kappaB activation was verified using a gel shift assay. A supershift assay showed mast cell NF-kappaB to be composed primarily of p50 with smaller amounts of p65. No interaction with Abs for Rel-A, c-Rel, Rel-B, and p52 was seen. Immunocytochemistry and ELISAs showed TNF-alpha to be stored within mast cells and released into the extracellular environment following activation. The possible participation of TNF-alpha generated by mast cells in NF-kappaB activation by anti-IgE was investigated using a blocking Ab for TNF-alpha. The blocking Ab reduced NF-kappaB activation by anti-IgE by >50%, suggesting that the release of preformed mast cell-associated TNF-alpha acts as a positive autocrine feedback signal to augment NF-kappaB activation and production of further cytokine, including GM-CSF and IL-8.

Active Transport, Cell Nucleus↗

PubMed2003

Notch signaling augments T cell responsiveness by enhancing CD25 expression.

Notch receptors signal through a highly conserved pathway to influence cell fate decisions. Notch1 is required for T lineage commitment; however, a role for Notch signaling has not been clearly defined for the peripheral T cell response. Notch gene expression is induced, and Notch1 is activated in primary CD4(+) T cells following specific peptide-Ag stimulation. Notch activity contributes to the peripheral T cell response, as inhibition of endogenous Notch activation decreases the proliferation of activated T cells in a manner associated with the diminished production of IL-2 and the expression of the high affinity IL-2R (CD25). Conversely, forced expression of a constitutively active Notch1 in primary T cells results in increased surface expression of CD25, and renders these cells more sensitive to both cognate Ag and IL-2, as measured by cell division. These data suggest an important role for Notch signaling during CD4(+) T cell responses, which operates through augmenting a positive feedback loop involving IL-2 and its high affinity receptor.

Adjuvants, Immunologic↗

PubMed2006

Mathematical modeling identifies inhibitors of apoptosis as mediators of positive feedback and bistability.

The intrinsic, or mitochondrial, pathway of caspase activation is essential for apoptosis induction by various stimuli including cytotoxic stress. It depends on the cellular context, whether cytochrome c released from mitochondria induces caspase activation gradually or in an all-or-none fashion, and whether caspase activation irreversibly commits cells to apoptosis. By analyzing a quantitative kinetic model, we show that inhibition of caspase-3 (Casp3) and Casp9 by inhibitors of apoptosis (IAPs) results in an implicit positive feedback, since cleaved Casp3 augments its own activation by sequestering IAPs away from Casp9. We demonstrate that this positive feedback brings about bistability (i.e., all-or-none behaviour), and that it cooperates with Casp3-mediated feedback cleavage of Casp9 to generate irreversibility in caspase activation. Our calculations also unravel how cell-specific protein expression brings about the observed qualitative differences in caspase activation (gradual versus all-or-none and reversible versus irreversible). Finally, known regulators of the pathway are shown to efficiently shift the apoptotic threshold stimulus, suggesting that the bistable caspase cascade computes multiple inputs into an all-or-none caspase output. As cellular inhibitory proteins (e.g., IAPs) frequently inhibit consecutive intermediates in cellular signaling cascades (e.g., Casp3 and Casp9), the feedback mechanism described in this paper is likely to be a widespread principle on how cells achieve ultrasensitivity, bistability, and irreversibility.

Apoptosis↗

PubMed1980

Pursuit rotor learning of mildly retarded children under supplementary feedback conditions.

A rotary pursuit task employing a supplementary feedback paradigm was used to study the effects of augmenting, task-inherent information (feedback) in enhancing motor acquisition of mildly retarded children. 119 subjects were trained on the task under control and six differential applications of supplementary visual, tactile or auditory feedback. Task acquisition was facilitated by supplementary feedback in specific treatments. Also, task acquisition was favored under conditions where the locus of the supplementary feedback was juxtaposed with the "correct" response behavior. Those feedback treatments which were juxtaposed with incorrect or "error" behavior did not serve to facilitate acquisition of the pursuit task with mildly retarded subjects. A tenable explanation for the consistency of the difference between treatments could be an increase in habit state, created by the locus of the feedback which served to reinforce the elicited response.

Adolescent↗

PubMed2003

GABA(B) receptor activation augments TASK-1 in MAH cells and mediates autoreceptor feedback during hypoxia.

Previously, we demonstrated an autoregulatory feedback loop in the rat carotid body (CB), involving presynaptic GABA(B) receptor-mediated activation of the background K(+) channel TASK-1. Here, we examined the effects of the selective GABA(B) receptor agonist baclofen on K(+) currents in immortalised adrenomedullary chromaffin (MAH) cells, which share the same sympathoadrenal lineage as CB type I cells. Under symmetrical K(+) conditions, 50 microM baclofen enhanced a K(+) current which was linear and reversed close to 0 mV. Under physiological K(+) conditions, baclofen enhanced outward K(+) current and caused membrane hyperpolarisation, effects inhibited by 100 nM CGP 55845. Current enhancement was virtually abolished in the presence of 300 microM Zn(2+), a selective inhibitor of TASK-1. When recording membrane potential from MAH cells in clusters, hypoxic depolarisation was augmented by 100 nM CGP 55845. These data demonstrate that GABA(B) receptors mediate autoreceptor feedback in the adrenal medulla presumably via TASK-1, demonstrating a common autoregulatory feedback pathway in neurosecretory, chemosensitive cells.

Adaptation, Physiological↗

PubMed1992

Decrease in lung volume-related feedback enhances laryngeal reflexes to negative pressure.

Negative pressure applied to the upper airway has an excitatory effect on the activity of upper airway muscles and an inhibitory effect on thoracic inspiratory muscles. The role of lung volume feedback in this response was investigated in 10 anesthetized spontaneously breathing adult rabbits. To alter lung volume feedback, the lower airway was exposed to SO2 (250 ppm for 15 min), thereby blocking slowly adapting receptors (SARs). Negative pressure pulses (5, 10, and 20 cmH2O, 300-ms duration) were applied to the functionally isolated upper airway before and after SAR blockade. Tracheal airflow and electromyogram (EMG) of the genioglossus and alae nasi were recorded. Peak EMG, peak inspiratory flow, tidal volume, and respiratory timing of control breaths (3 breaths immediately preceding test) and test breaths were determined. Analysis of variance was used to determine the significance of the effects. Negative pressure pulses increased peak EMG of genioglossus and alae nasi and inspiratory duration and decreased peak inspiratory flow. These effects were larger after SAR blockade. We conclude that a decrease in volume feedback from the lung augments the response to upper airway pressure change.

Animals↗