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PubMed2002

Estrogen action and cytoplasmic signaling pathways. Part II: the role of growth factors and phosphorylation in estrogen signaling.

In recent years, distinct signaling pathways involving specific complexes of cytoplasmic proteins have been shown to orchestrate estrogen action. These pathways might supplement or augment genomic effects of estrogen that are attributable to transcriptional activation by liganded receptor. Signals might be transduced through phosphorylation of the estrogen receptors (ERs), or indirectly through effects upon transcriptional coactivators or cell receptors. Estrogen signaling is coupled to growth factor signaling with feedback mechanisms directly impacting function of growth factor receptors. These signaling pathways regulate important physiological processes, such as cell growth and apoptosis. Here, we focus on cytoplasmic signaling pathways leading to activation of ERs.

Animals↗

PubMed1994

Twitch potentiation following voluntary diaphragmatic contraction.

The purpose of this study was to determine whether twitch potentiation (a transient augmentation of twitch tension following vigorous muscular contraction) occurs in the human diaphragm in vivo. Six healthy subjects were studied. To determine whether twitch potentiation occurs, the subjects attempted to maximally activate their diaphragm by performing the combined Mueller-expulsive maneuver with visual feedback (Pdi max maneuver). Twitches were obtained before, at 10 s after the transdiaphragmatic pressure (Pdi) maneuver, and at intervals over the ensuing 10 min. We also determined whether twitch potentiation would occur following submaximal voluntary diaphragmatic contractions (33 and 66% of Pdi max). In addition, we examined whether repeated voluntary contractions would result in greater twitch potentiation compared with that observed after a single voluntary contraction. Twitch potentiation was observed in every subject. The number of maximal voluntary contractions (MVC) (one, two, or four) had no significant effect on the degree of twitch potentiation. The increase in twitch amplitude (expressed as a percentage of the control value) averaged 63 +/- 35% (SD)(pooled data from one, two, and four contraction trials). Twitch potentiation decayed in a monoexponential fashion (r = 0.99) with a time constant of 125 s (95% Cl = 100 to 160 s). Twitch potentiation was also observed after submaximal voluntary diaphragmatic contractions. Again, the number of voluntary contractions (one or four) had no significant effect on the degree of twitch potentiation. After submaximal diaphragmatic contractions of 66% of Pdi max, the degree of twitch potentiation was not significantly different, 61 +/- 36% (pooled data from one and four contraction trials) from that observed following the maximal voluntary contraction maneuvers.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1995

Cyclic nucleotide phosphodiesterase type IV participates in the regulation of IL-10 and in the subsequent inhibition of TNF-alpha and IL-6 release by endotoxin-stimulated macrophages.

We have recently shown that PGE2 inhibits the release of TNF-alpha from LPS-stimulated murine peritoneal macrophages via a feedback mechanism involving IL-10. Here we demonstrate that a rolipram-sensitive phosphodiesterase (PDE) type IV participates in the regulation of IL-10 synthesis. Selective PDE IV inhibitors (rolipram and RO-20-1724), but not selective inhibitors of other types of PDE, significantly augment marcrophage IL-10 production and contribute to the inhibition of TNF-alpha and IL-6 release. The addition of rolipram to LPS-stimulated macrophages results in the accumulation of cAMP and in the significant augmentation of IL-10 release. Competitive PCR analysis reveals that the drug dramatically increases IL-10 mRNA, but does not affect TNF-alpha mRNA. The inhibitory effect of rolipram on TNF-alpha can be significantly but incompletely reversed by anti-IL-10 Ab, whereas the effect of the drug on IL-6 can be completely reversed by anti-IL-10. In endotoxemic mice, the administration of rolipram increases serum IL-10 and reduces TNF-alpha and IL-6 levels. Northern blot analysis of spleens from these mice shows that rolipram increases IL-10 mRNA, whereas TNF-alpha mRNA remains largely unchanged. These results suggest that a rolipram-sensitive PDE type IV is involved in the production of IL-10 and in turn contributes to the inhibition of TNF-alpha and IL-6 release.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗

PubMed1996

Role of neuromedin B in the in vitro thyrotropin release in response to thyrotropin-releasing hormone from anterior pituitaries of eu-, hypo-, and hyperthyroid rats.

A role of neuromedin B (NB), a bombesin-like peptide, as an inhibitory paracrine/autocrine regulator of thyrotropin secretion has been suggested. We previously reported (10) that basal thyroid-stimulating hormone (TSH) release in vitro was decreased by NB and increased in the presence of a highly potent antiserum against NB (aNB). In these experiments, we studied the effects of NB (10(-11) - 10(-7) M) and antiserum against NB (aNB, 1:2000 dilution) on basal TSH release and the response to thyrotropin-releasing hormone (TRH) (0.5 x 10(-8) M) from incubated anterior pituitaries from eu-, hypo-, and hyperthyroid rats. As expected, in euthyroid rats NB decreased basal and TRH-stimulated TSH release, but only at the highest concentration tested (10(-7) M). Incubation of the pituitaries from euthyroid rats with the antiserum against NB increased basal TSH release above that from glands of normal rabbit serum-incubated controls, as anticipated based on the concept that NB inhibits TSH release from the pituitary glands of euthyroid animals. The antiserum did not augment the response to TRH, suggesting that NB released in this situation, although suppressing basal release, had no effort on the stimulated release induced by TRH. Glands from hypothyroid rats had a slightly lower basal TSH release and decreased response to TRH than glands from euthyroid rats. They responded with a decrease in basal TSH release at a much lower concentration of NB (10(-9) M) than pituitaries from euthyroid animals. Surprisingly, pituitaries from hypothyroid rats showed a paradoxical increased release of TSH in response to the lowest concentration of NB (10(-11) M), which decreased with increasing concentrations and was not distinguishable from control release in the presence of TRH at the highest concentration of NB (10(-7) M). We hypothesize that the increased responsiveness to the inhibition of basal TSH release by NB in the hypothyroid pituitaries may be related to an upregulation of NB receptors in this situation, in which the release of NB is diminished because of loss of feedback via thyroid hormones. The view that NB secretion was reduced in the hypothyroid situation was supported by the fact that there was no change in TSH release or the response to TRH following treatment with aNB in these animals. Remarkably, in the glands from the hyperthyroid rats, although basal TSH secretion was significantly lower than that from euthyroid pituitaries and response to TRH was also decreased, NB (10(-11)-10(-7) M) instead of decreasing TSH release augmented it significantly. Also, the response to TRH was significantly augmented but only at the lowest concentration of NB tested (10(-11 M). That NB was probably being secreted in vitro from the hyperthyroid pituitaries was indicated by an increased basal TSH release as well as a higher TSH medium concentration after TRH in the presence of the aNB. These results support the concept that the glands from the hyperthyroid animals secrete more NB because of positive feedback of thyroid hormones directly on the thyrotropes to increase NB synthesis and release which downregulates NB receptors on the gland. This downregulation of receptors in some manner reverses the inhibitory action of NB on basal and TRH-stimulated TSH release. In conclusion, the results provide further evidence for an important role of NB as an autocrine regulator of TSH release, which is modulated by increased release of NB induced by thyroid hormones.

Animals↗

PubMed1998

Interplay between cytoplasmic Ca2+ and the ATP/ADP ratio: a feedback control mechanism in mouse pancreatic islets.

In pancreatic beta cells, the increase in the ATP/ADP ratio that follows a stimulation by glucose is thought to play an important role in the Ca2+-dependent increase in insulin secretion. Here we have investigated the possible interactions between Ca2+ and adenine nucleotides in mouse islets. Measurements of both parameters in the same single islet showed that the rise in the ATP/ADP ratio precedes any rise in the cytoplasmic free-Ca2+ concentration ([Ca2+]i) and is already present during the initial transient lowering of [Ca2+]i produced by the sugar. Blockade of Ca2+ influx with nimodipine did not prevent the concentration-dependent increase in the ATP/ADP ratio produced by glucose and even augmented the ratio at all glucose concentrations which normally stimulate Ca2+ influx. In contrast, stimulation of Ca2+ influx by 30 mM K+ or 100 microM tolbutamide lowered the ATP/ADP ratio. This lowering was of rapid onset and reversibility, sustained and prevented by nimodipine or omission of extracellular Ca2+. It was, however, not attenuated after blockade of secretion by activation of alpha2-adrenoceptors. The difference in islet ATP/ADP ratio during blockade and stimulation of Ca2+ influx was similar to that observed between threshold and submaximal glucose concentrations. The results suggest that the following feedback loop could control the oscillations of membrane potential and [Ca2+]i in beta cells. Glucose metabolism increases the ATP/ADP ratio in a Ca2+-independent manner, which leads to closure of ATP-sensitive K+ channels, depolarization and stimulation of Ca2+ influx. The resulting increase in [Ca2+]i causes a larger consumption than production of ATP, which induces reopening of ATP-sensitive K+ channels and arrest of Ca2+ influx. Upon lowering of [Ca2+]i the ATP/ADP ratio increases again and a new cycle may start.

Adenosine Diphosphate↗

PubMed1999

Evidence for a feedback inhibition of NO synthesis in enteric synaptosomes via a nitrosothiol intermediate.

The exact mechanisms controlling nitric oxide synthase (NOS) activity within enteric neurons are largely unknown. In this study, the effect of exogenous nitric oxide (NO) on NOS activity was investigated in enteric synaptosomes of rat ileum. 3-Morpholinosydnonimine (SIN-1; 10(-4) M) and S-nitroso-N-acetylpenicillamine (SNAP; 10(-4) M) significantly inhibited NOS activity by 53% and 48%, respectively. However, superoxide dismutase (SOD; 160 U/ml) as well as the NO scavenger oxyhemoglobin (10(-3) M) did not influence NO donor-induced inhibition. In contrast, the inhibitory effect was antagonized by diethyldithiocarbamate (3 x 10(-4) M), an inhibitor of endogenous Cu/Zn SOD. Inhibition of NOS by exogenous NO was dependent on glutathione (GSH), since the inhibitory effect was augmented in the presence of GSH (5 x 10(-4) M) and antagonized by the GSH-depletor DL-buthionine-SR-sulfoximine (5 x 10(-4) M), suggesting that NO might be protected from extracellular breakdown by reaction with GSH. The reaction product of SIN-1/SNAP and GSH was identified as a nitrosothiol. In the presence of the Cu(+)-chelator neocuproine (10(-5) M), inhibition of NOS by SNAP/SIN-1 was reversed, suggesting that nitrosothiol formation is intermediary. These findings are indicative of a feedback inhibition of enteric NOS, presumably via formation of a nitrosothiol intermediate.

Animals↗

PubMed2006

Auditory biofeedback substitutes for loss of sensory information in maintaining stance.

The importance of sensory feedback for postural control in stance is evident from the balance improvements occurring when sensory information from the vestibular, somatosensory, and visual systems is available. However, the extent to which also audio-biofeedback (ABF) information can improve balance has not been determined. It is also unknown why additional artificial sensory feedback is more effective for some subjects than others and in some environmental contexts than others. The aim of this study was to determine the relative effectiveness of an ABF system to reduce postural sway in stance in healthy control subjects and in subjects with bilateral vestibular loss, under conditions of reduced vestibular, visual, and somatosensory inputs. This ABF system used a threshold region and non-linear scaling parameters customized for each individual, to provide subjects with pitch and volume coding of their body sway. ABF had the largest effect on reducing the body sway of the subjects with bilateral vestibular loss when the environment provided limited visual and somatosensory information; it had the smallest effect on reducing the sway of subjects with bilateral vestibular loss, when the environment provided full somatosensory information. The extent that all subjects substituted ABF information for their loss of sensory information was related to the extent that each subject was visually dependent or somatosensory-dependent for their postural control. Comparison of postural sway under a variety of sensory conditions suggests that patients with profound bilateral loss of vestibular function show larger than normal information redundancy among the remaining senses and ABF of trunk sway. The results support the hypothesis that the nervous system uses augmented sensory information differently depending both on the environment and on individual proclivities to rely on vestibular, somatosensory or visual information to control sway.

Adaptation, Physiological↗

PubMed1992

Modulation of slow cortical potentials by instrumentally learned blood pressure responses.

We assessed whether instrumentally-learned pressor responses inhibit electrocortical activity, as predicted by learning theories of idiopathic hypertension. Subjects received beat-by-beat feedback for increases and decreases in mean arterial pressure measured from the finger (Peñáz method). Slow potentials were recorded from the midsagittal line during the final training session. Also recorded at this time were heart rate, eye movements, respiration, and post-session verbal reports of the subject's control strategies. Thirteen of 14 subjects differentiated blood pressure increases and decreases at p less than .05 or better during the final session (within-subject discriminative operant procedure). Slow potentials were less negative on blood pressure increase compared to decrease trials at all midsagittal sites (p less than .02), indicating relative cortical inhibition by pressor responses. This effect occurred even though subjects reported tensing of muscles on increase trials (p less than .01), a behavioral activity previously associated with augmented rather than diminished cortical negativity. On increase trials slow potentials shifted toward positivity just prior to heart rate deceleration (the latter effect confirming activation of the baroreceptors).

Adult↗

PubMed2004

Intelligent training system integrated in an echocardiography simulator.

Computer simulators play an important role in medical education. We have extended our simulator EchoComJ with an intelligent training system (ITS) to support trainees adjusting echocardiographic standard views. EchoComJ is an augmented reality application that combines real three-dimensional ultrasound data with a virtual heart model enabling one to simulate an echocardiographic examination. The ITS analyzes the image planes according to their position, orientation and the visualization of anatomical landmarks using fuzzy rules. An adaptive feedback is provided that colors the specific anatomic landmarks within the contours of the virtual model based on the quality of the image plane.

Artificial Intelligence↗

PubMed1985

Lipoxygenase and calcium entry in vascular smooth muscle.

In the canine saphenous vein, inhibitors of cyclo-oxygenase augment contractile responses to acetylcholine, potassium chloride and partial alpha-adrenergic activation. This augmentation is prevented by inhibitors of lipoxygenase, and abolished by calcium entry blockers. These observations suggest that when Ca2+ enters the smooth muscle cells it activates the metabolism of arachidonic acid. If cyclo-oxygenase is inhibited, end-products of lipoxygenase exert a positive feedback on calcium entry. A similar mechanism may explain the hypoxic contractions observed in various blood vessels, including coronary arteries.

Acetylcholine↗

PubMed1995

Influence of alterations in the oral environment on speech production.

We examined the influence on temporal aspects of three consonants, /k/, /c/ and /s/, of alterations in the oral environment produced by either palatal augmentation or by an increase in the vertical dimension of occlusion. Voice onset time (V.O.T.) for /k/ and /c/ was influenced more than aspiration time by the palatal augmentation. Consonant duration for /s/ was also influenced by palatal augmentation. Significant influence of an increase in vertical dimension on the timing was not recognized. Speech disorder caused by the malformation of palate seems to be more frequent than that caused by vertical dimension. Adaptation to prostheses would seem to be definitely concerned with orosensory feedback.

Adaptation, Physiological↗

PubMed1999

Actions of estrogen on pulsatile, nyctohemeral, and entropic modes of growth hormone secretion.

The neuroendocrine mechanisms by which estradiol drives growth hormone (GH) secretion in the human are poorly defined. Here we investigate estrogen's specific regulation of the 24-h pulsatile, nyctohemeral, and entropic modes of GH secretion in healthy postmenopausal women. Volunteers (n = 9) received randomly ordered placebo versus estradiol-17beta (1 mg micronized steroid twice daily orally) treatment for 7-10 days and underwent blood sampling at 10-min intervals for 24 h to capture GH release profiles quantitated in a high-sensitivity chemiluminescence assay. Pulsatile GH secretion was appraised via deconvolution analysis, nyctohemeral GH rhythms by cosinor analysis, and the orderliness of GH release patterns via the approximate entropy statistic. Mean (+/-SE) 24-h serum GH concentrations approximately doubled on estrogen treatment (viz., from 0.31 +/- 0.03 to 0.51 +/- 0.07 microgram/l; P = 0.033). Concomitantly, serum insulin-like growth factor-I (IGF-I), luteinizing hormone, and follicle-stimulating hormone concentrations fell, whereas thyroid-stimulating hormone and prolactin levels rose (P < 0.01). The specific neuroendocrine action of estradiol included 1) a twofold amplified mass of GH secreted per burst, with no significant changes in basal GH release, half-life, pulse frequency, or duration; 2) an augmented amplitude and mesor of the 24-h rhythm in GH release, with no alteration in acrophase; and 3) greater disorderliness of GH release (higher approximate entropy). These distinctive and dynamic reactions to estrogen are consistent with partial withdrawal of IGF-I's negative feedback and/or accentuated central drive to GH secretion.

Aged↗

PubMed2004

Urinary potassium excretion and sodium sensitivity in blacks.

Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle's loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure.

Animals↗

PubMed1992

EEG-dependent modulation of response dynamics of cat dLGN relay cells and the contribution of corticogeniculate feedback.

Single unit recordings were made extracellularly from the dorsal lateral geniculate nucleus (dLGN) in the anaesthetized and paralysed cat. The impulse rates of phasic (peak) and tonic components of visual responses to stimulation of the receptive field center by a flashing spot were determined during different states of the EEG, during local cortical cooling and during micro-iontophoretic application of the excitatory amino acid receptor agonists, quisqualate (QUIS) and N-methyl-D-aspartate (NMDA). Typically, visual responses were phasic during low frequency/high amplitude EEG patterns, resembling slow wave sleep (SWS). During high frequency EEG patterns (non-SWS) visual responses of X- and Y-cells exhibited a prominent tonic response component. This tonic component could be clearly reduced during ipsilateral cortical cooling in the non-SWS state. QUIS or NMDA, applied in order to mimic corticofugal activity, augmented the tonic response component, most efficiently during SWS EEG. The effects did not differ significantly for X- and Y-cells. During non-SWS EEG Y-cells exhibited a tonic response component similar to X-cells, but because of their higher peak rates the responses of Y-cells were on average more phasic than those of X-cells. Our results indicate that state-dependent changes in CNS activity modulate dL'GN responsiveness in part via the corticogeniculate feedback, and that predominantly the tonic response component is modulated.

Animals↗

PubMed1975

The effect of ovarian steroid feedback upon radioimmunoreactive luteinizing hormone releasing hormone in the hypothalamus.

A radioimmunoassay (RIA) method for luteinizing hormone (LH) releasing hormone (RH) utilizing rabbit antiserum against synthetic (Glu1)-LH-RH coupled with human serum albumin at the N-terminus, is described. This assay system for LH-RH also cross-reacted with several LH-RH analogues or fragments, but not with pituitary trophic hormones. The assay was performed on the hypothalamic extracts of adult ovariectomized rats and female immature rats which had been treated with estradiol. The FSH and LH levels in the pituitary gland and serum of the same animals were determined by RIA. The radioimmunoreactive LH-RH content of the stalk median eminence markedly increased seven days after ovariectomy. The serum levels and the pituitary contents of FSH and LH of the same rats were also significantly augmented. In immature rats, the hypothalamic content of LH-RH, as measured by RIA, was significantly increased one hour after the injection of estradiol. The FSH and LH levels in the pituitary showed a significant rise after 7 hours.

Animals↗

PubMed1991

Age-related changes in rates of basal secretion of immunoreactive vasoactive intestinal polypeptide and dopamine into pituitary stalk blood from the hypothalamus in anesthetized male rats.

Age-related changes in prolactin (PRL) in systemic blood plasma, and in secretions of hypothalamic vasoactive intestinal polypeptide (VIP), an important candidate for PRL-releasing factor, and dopamine, a PRL-inhibiting factor, into the pituitary stalk blood were investigated. The experiments were performed on male urethane-chloralose-anesthetized Wistar rats of three different ages, i.e., (1) adult rats 5-8 months old, (2) middle-aged rats 12-15 months old, and (3) aged rats 24-26 months old. The concentration of immunoreactive PRL (iPRL) in systemic blood plasma of the aged rats was significantly higher than that of the adult rats (p less than 0.01). The secretion rate of hypothalamic immunoreactive VIP (iVIP) into the pituitary stalk blood was unchanged during aging, while that of dopamine was markedly increased in the aged rats in comparison with the value in both adult and middle-aged rats (p less than 0.01). These results indicate that the basal secretion of hypothalamic VIP is well maintained, while that of hypothalamic dopamine is augmented in aged rats with hyperprolactinemia. It can be assumed that the increase in the pituitary PRL secretion is a primary event during aging in rats, and that a high circulating level of PRL may facilitate the hypothalamic dopamine secretion through the activation of a negative feedback system of the hormone.

Aging↗

PubMed2006

New tools for sculpting cranial implants in a shared haptic augmented reality environment.

New volumetric tools were developed for the design and fabrication of high quality cranial implants from patient CT data. These virtual tools replace time consuming physical sculpting, mold making and casting steps. The implant is designed by medical professionals in tele-immersive collaboration. Virtual clay is added in the virtual defect area on the CT data using the adding tool. With force feedback the modeler can feel the edge of the defect and fill only the space where no bone is present. A carving tool and a smoothing tool are then used to sculpt and refine the implant. To make a physical evaluation, the skull with simulated defect and the implant are fabricated via stereolithography to allow neurosurgeons to evaluate the quality of the implant. Initial tests demonstrate a very high quality fit. These new haptic volumetric sculpting tools are a critical component of a comprehensive tele-immersive system.

Computer-Aided Design↗

PubMed1985

Chromatic and spatial information processing by red cones and L-type horizontal cells in the turtle retina.

Flash sensitivities to red (694 nm) and green (546 nm) light were measured intracellularly from red cones and L-type horizontal cells in the turtle retina. The horizontal cells' sensitivity to short wavelength light was significantly larger than expected from the model where horizontal cells receive input mainly from red cones. The red cone responses to chromatic stimuli were strongly dependent upon the flash colour and size. Increasing the spot size reduced the sensitivity to green relative to red and augmented the differences in kinetics between the response to red light and that evoked by green light. It was concluded that L-type horizontal cells received a short wavelength input in addition to the input from red cones. This additional green input coupled with the negative feedback pathway from horizontal cells onto red cones determined the differential spatial properties of the red cone responses to red and green test flashes.

Animals↗