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PubMed1999

Effect of stress-like concentrations of cortisol on gonadotroph function in orchidectomized sheep.

The effect of stress-like concentrations of cortisol (C) on the feedback potency of estradiol (E2) was assessed using 32 orchidectomized sheep (wethers) assigned at random to 1 of 4 treatment groups in a 2 x 2 factorial design. Wethers received C (3. 6 mg/50 kg per hour; groups 2 and 4) or a comparable volume of C delivery vehicle (groups 1 and 3) as a continuous infusion for 7 days. During the final 48 h of infusion, wethers received E2 (0.3 microg/50 kg/h; groups 3 and 4) or E2 delivery vehicle (groups 1 and 2). The pattern of LH secretion was assessed during a 4-h period of intensive blood collection beginning 44 h after initiation of E2 infusion. Gonadotroph responsiveness (LH secretion induced by GnRH challenge [500 ng, i.v.]) was determined 48 h after E2 delivery was begun. Although the frequency of secretory episodes of LH was not affected (p > 0.05) by infusion of C or E2 alone, LH pulse frequency was significantly decreased in wethers receiving C and E2 in combination. In contrast, neither the magnitude of basal gonadotroph responsiveness nor the extent of E2-dependent augmentation of responsiveness was significantly affected by stress-like concentrations of C. In a second experiment, the effect of C on the magnitude of E2-induced increase in pituitary concentration of GnRH receptor and GnRH receptor mRNA was assessed using 32 additional wethers. Continuous infusion of E2 for 48 h increased (p < 0.05) tissue concentrations of GnRH receptor and GnRH receptor mRNA. Concurrent delivery of C did not affect (p > 0.05) E2-induced increase in GnRH receptor mRNA but significantly reduced the magnitude of the E2-dependent increase in pituitary concentration of GnRH receptor. Collectively, these data indicate that stress-like concentrations of C enhance the negative feedback potency of E2 and reduce estrogen-dependent augmentation of the concentration of GnRH receptor in pituitary tissue.

Animals↗

PubMed1994

Disparity vergence eye movements exhibit preprogrammed motor control.

To determine the control strategy used to mediate disparity vergence eye movements, an optical technique was employed which eliminated the visual feedback normally associated with a vergence movement. The resulting "open-loop" vergence responses from four subjects exhibited multiple step-like movements. This finding augments previous demonstrations of multiple-step tracking strategies in vergence eye movements and supports the theory that the initial portion of the vergence response is under preprogrammed control. Additional evidence for preprogramming is given by the similarity of the initial dynamics between open- and closed-loop responses as evidenced by similar ratios of peak velocity to amplitude (i.e. "main sequence" plots).

Convergence, Ocular↗

PubMed1996

Histamine H3-receptor-mediated inhibition of calcitonin gene-related peptide release from cardiac C fibers. A regulatory negative-feedback loop.

Antidromic stimulation of cardiac sensory C fibers releases calcitonin gene-related peptide (CGRP), which increases heart rate, contractility, and coronary flow. C-fiber endings are closely associated with mast cells, and CGRP may release mast-cell histamine. Because prejunctional histamine H3-receptors inhibit transmitter release from autonomic nerves, we tested the hypothesis that H3-receptors modulate CGRP release in the heart. CGRP released by bradykinin in the electrically paced guinea pig left atrium and by capsaicin in the spontaneously beating isolated heart caused marked positive inotropic and chronotropic effects, respectively. Capsaicin significantly enhanced the overflow of CGRP (fivefold) and histamine (twofold) into the coronary effluent. All of these effects were prevented by prior chemical destruction of C fibers in vivo. The H3-receptor agonist imetit attenuated the inotropic response to bradykinin by 50%. Imetit also decreased the capsaicin-induced tachycardia and the increase in CGRP overflow by 50%. Imetit, however, did not modify the response to exogenous CGRP. The effects of imetit were blocked by the H3-receptor antagonist thioperamide. Notably, thioperamide by itself potentiated the capsaicin-evoked increases in heart rate and CGRP overflow (by 25% and 50%, respectively). Thus, our findings identify a negative-feedback loop, whereby CGRP releases histamine from cardiac mast cells and histamine in turn inhibits CGRP releases by activating H3-receptors on C-fiber terminals. Because CGRP release is augmented in pathophysiological conditions, such as septic shock, heart failure, and acute myocardial infarction, modulation of CGRP release may be clinically relevant.

Animals↗

PubMed2003

Cortisol, DHEAS and aging: resistance to cortisol suppression in frail institutionalized elderly.

Convincing evidences has linked the hypothalamus-pituitary-adrenal (HPA) axis to aging patterns. F excess is implicated in the development of frailty characteristics whereas DHEAS is positively correlated to successful aging. We compared serum F and DHEAS levels of independent community-living (successful group, 19 M and 28 F, 69 to 87 yr) with those of institutionalized elderly (frail group, 20 M and 30 F, 65 to 95 yr). Serum F was determined at 1) baseline (08:00 h, 16:00 h and 23:00 h), 2) after 2 overnight dexamethasone (DEX) suppression tests (DST, using 0.25 and 1.0 mg doses), and 3) 60 min after ACTH stimulation (250 microg i.v. bolus); serum DHEAS was determined at 08:00 h. Basal serum F at 08:00 h, 16:00 h and 23:00 h and serum DHEAS levels were similar in both groups; however F: DHEAS ratio at 08:00 h was higher in the frail, compared to the successful group (mean +/- SD: 0.55 +/- 0.53 and 0.35 +/- 0.41, respectively; p = 0.04). In response to DST, F suppression was less effective in frail elderly after either 0.25 or 1.0 mg doses (9.0 +/- 6.0 and 2.0 +/- 0.9 microg/dl), as compared to the successful group (5.8 +/- 4.4 and 1.5 +/- 0.5 microg/dl) (p = 0.01). In addition, a significant correlation was observed between post-DEX F levels (both doses) and parameters of cognitive and physical frailty. Normal and similar F levels were observed after ACTH stimulation in both groups. Our data suggest a deficient feedback regulation of the HPA axis in frail institutionalized elderly, as demonstrated by a higher set point for F suppression. This augmented HPA tonus enforces the hypothesis that even milder F excess may be related to characteristics of frailty in the elderly.

Activities of Daily Living↗

PubMedDate not supplied

Combat burn life support: a military burn-education program.

The Advanced Burn Life Support Course has been used to train military physicians and nurses for more than 16 years. Although it useful for teaching the fundamentals of burn care, the course is designed for a civilian audience, covers only the first 24 hours of burn care, and presumes the availability of a burn center for patient transfer. In preparation for hostilities in Iraq, we developed several add-on modules to the standard Advanced Burn Life Support course to meet specific needs of military audiences. These modules cover the treatment of white phosphorus burns; the treatment of mustard gas exposure; the long-range aeromedical transfer of burn patients; the management of burn patients beyond the first 24 hours; and the delivery of burn care in austere environments. These add-on modules are termed Combat Burn Life Support. Between January 22, 2003, and May 12, 2003, Advanced Burn Life Support and/or Combat Burn Life Support courses were provided to a total of 1035 military health care providers in the United States, Germany, and the Middle East. Student feedback was largely positive and is being used for further course refinement. The Combat Burn Life Support Course is designed to augment, rather than replace, the Advanced Burn Life Support Course. Although intended for a military audience, the course material is equally applicable to civilian terrorist or mass casualty situations.

Burn Units↗

PubMed2003

Coupling fields and underlying space curvature: an augmented Lagrangian approach.

We demonstrate a systematic implementation of coupling between a scalar field and the geometry of the space which carries the field. This naturally gives rise to a feedback mechanism between the field and the geometry. We develop a systematic model for the feedback in a general form, inspired by a specific implementation in the context of molecular dynamics (the so-called Rahman-Parrinello molecular dynamics, or RP-MD). We use a generalized Lagrangian that allows for the coupling of the space's metric tensor to the scalar field, and add terms motivated by RP-MD. We present two implementations of the scheme: one in which the metric is only time-dependent (which gives rise to an ordinary differential equation for its temporal evolution), and the other with spatiotemporal dependence (wherein the metric's evolution is governed by a partial differential equation). Numerical results are reported for the (1+1)-dimensional model with a nonlinearity of the sine-Gordon type.

Journal Article↗

PubMed2002

Hypoxia-induced secretion of serotonin from intact pulmonary neuroepithelial bodies in neonatal rabbit.

We examined the effects of hypoxia on the release of serotonin (5-HT) from intact neuroepithelial body cells (NEB), presumed airway chemoreceptors, in rabbit lung slices, using amperometry with carbon fibre microelectrodes. Under normoxia (P(O2) ~155 mmHg; 1 mmHg approximately 133 Pa), most NEB cells did not exhibit detectable secretory activity; however, hypoxia elicited a dose-dependent (P(O2) range 95-18 mmHg), tetrodotoxin (TTX)-sensitive stimulation of spike-like exocytotic events, indicative of vesicular amine release. High extracellular K(+) (50 mM) induced a secretory response similar to that elicited by severe hypoxia. Exocytosis was stimulated in normoxic NEB cells after exposure to tetraethylammonium (20 mM) or 4-aminopyridine (2 mM). Hypoxia-induced secretion was abolished by the non-specific Ca(2+) channel blocker Cd(2+) (100 microM). Secretion was also largely inhibited by the L-type Ca(2+) channel blocker nifedipine (2 microM), but not by the N-type Ca(2+) channel blocker omega-conotoxin GVIA (1 microM). The 5-HT(3) receptor blocker ICS 205 930 also inhibited secretion from NEB cells under hypoxia. These results suggest that hypoxia stimulates 5-HT secretion from intact NEBs via inhibition of K(+) channels, augmentation of Na(+)-dependent action potentials and calcium entry through L-type Ca(2+) channels, as well as by positive feedback activation of 5-HT(3) autoreceptors.

Animals↗

PubMed1984

Role of prejunctional alpha 2-adrenergic receptors in the regulation of myocardial performance during exercise in conscious dogs.

We examined, in conscious dogs, the potential role of prejunctional alpha 2-adrenergic receptors for the regulation of heart rate and contractility response to exercise through modulation of the neurotransmitter release. Changes in heart rate and left ventricular pressure with time during comparable exercise levels, together with changes in norepinephrine concentration in the coronary sinus, were compared before and after the intravenous administration of: prazosin (0.5 mg/kg), a preferential postjunctional alpha 1-adrenergic receptor blocking agent; phentolamine (1 mg/kg), a nonselective alpha-adrenergic blocking agent; and yohimbine (0.3 mg/kg), a preferential prejunctional alpha 2-adrenergic receptor blocking agent. During exercise after phentolamine or yohimbine, changes in heart rate and left ventricular dP/dt were markedly potentiated compared to the control exercise, as well as to exercise after prazosin, whereas the norepinephrine concentration in the coronary sinus was substantially elevated. After intracoronary administration of phentolamine (0.1 mg/kg) or yohimbine (0.03 mg/kg), heart rate and contractility response to exercise were also potentiated, compared to the control exercise. These observations indicate that, in the intact conscious animal, prejunctional alpha 2-adrenoreceptors are stimulated during exercise, thereby modulating the norepinephrine release through a negative feedback inhibitory mechanism. Blocking these receptors by phentolamine or yohimbine results in an uncontrolled norepinephrine release during exercise associated with an augmented beta-adrenergic receptor-mediated end organ response, i.e., a potentiation in heart rate and contractility response.

Adrenergic alpha-Antagonists↗

PubMed1993

Adrenalectomy augments in vivo release of norepinephrine in the paraventricular nucleus during immobilization stress.

Adrenalectomy (ADX) activates CRH neurons in the paraventricular nucleus (PVN) of the hypothalamus and increases hypothalamic norepinephrine (NE) turnover in vitro. Immobilization (IMMO) markedly increases the release of NE into extracellular fluid in the PVN. The present study assessed whether ADX affects the release of NE in the PVN in vivo in conscious rats at baseline and during IMMO and whether cortisol (CORT) treatment attenuates the effects of ADX. Concentrations of NE, the NE metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol, and the dopamine metabolite dihydroxyphenylacetic acid were measured in microdialysate samples beginning 24 h after implantation of a microdialysis probe in the PVN. Seven to 10 days after ADX or ADX plus CORT (20 mg/kg.day via osmotic minipump), animals underwent IMMO for 2 h. Adrenalectomized rats had slightly higher baseline microdialysate NE, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, and dihydroxyphenylacetic acid levels and much larger IMMO-induced responses of these compounds than did sham-operated rats. CORT treatment abolished the ADX-induced augmentation of these responses. The results indicate that ADX, by removing endogenous glucocorticoids, augments IMMO-induced release and turnover of NE and amplifies the responses of catecholamine synthesis. Glucocorticoids, therefore, appear to exert feedback inhibition on stress-induced increments in the release of NE and catecholamine biosynthesis in the PVN.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Streptozocin-diabetes modifies acetylcholine release from mouse phrenic nerve terminal and presynaptic sensitivity to succinylcholine.

Acetylcholine (ACh) release from the motor nerve terminal in the streptozocin-induced diabetic state was studied in mouse phrenic nerve-diaphragm muscle preparations. Electrically evoked release of 3H-ACh from the preparation preloaded with 3H-choline was measured during two consecutive periods of stimulation (S1 and S2). In diabetic mice, the amount of 3H-ACh release during S2 was decreased, and the evoked ACh release declined more steeply with successive stimulation periods than in normal ddY mice. The decrease in release was restored when the presynaptic autoreceptors were stimulated by accumulating ACh under the irreversible inhibition of junctional cholinesterase by methanesulfonyl fluoride. This effect was abolished by the administration of (+)-tubocurarine (5 microM). In diabetic mice, the biphasic (acceleration and suppression) effect by succinylcholine on evoked ACh release was caused at 3- to 10-fold lower concentrations than in normal mice. The degree of enhancement of resting 3H-overflow by succinylcholine (10 and 30 microM) was greater in the diabetic state. These results indicated that in the diabetic state, the decrease in evoked ACh release interferes with its presynaptic action on inducing further release (positive feedback modulation) via the presynaptic nicotinic ACh receptor (n-AChR). The presynaptic hypersensitivity to succinylcholine may be due to the augmentation of presynaptic n-AChR sensitivity caused by the reduction of evoked ACh release in the diabetic state.

Acetylcholine↗

PubMed1993

Endogenous nitric oxide inhibits NMDA- and kainate- responses by a negative feedback system in rat hippocampal neurons.

Involvement of endogenous nitric oxide (NO) on glutamate receptor-mediated response was investigated in neuronal cells cultured from embryonic rat hippocampus. L-NG-Nitroarginine (NOARG), a NO synthase inhibitor, augmented NMDA- and kainate-induced increase in intracellular Ca2+ concentration ([Ca2+]i) measured by fura-2 fluorometry. However, quisqualate-induced response was not affected. The potentiating effect of NOARG was blocked by L-arginine, a substrate for NO synthase. NOARG was also effective when added after glutamate-induced response had reached a steady-state. Hemoglobin itself increased the basal level of [Ca2+]i at concentrations higher than 10 mM, and treatment of the cells with 1.0 mM hemoglobin had no effect on NMDA response. 8-Bromo-cyclic GMP was not effective on NMDA response. These results suggest that endogenous NO inhibits NMDA- and kainate-induced increase in [Ca2+]i as a negative feedback system independent of guanylate cyclase activation.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1993

A pentapeptide from type I procollagen promotes extracellular matrix production.

The NH2 and COOH propieces of fibril-forming collagens are cleaved off extracellularly and have been implicated in feedback regulation of their own synthesis. Recently, we showed that a subfragment of the carboxyl-terminal propeptide of type I collagen (residues 197-241) dramatically augments extracellular matrix production in subconfluent fibroblasts. This stimulation of type I collagen, type III collagen, and fibronectin production occurred in a dose- and time-dependent manner with no effect on total protein synthesis or on the ratio of secreted proteins to cell-associated proteins (Katayama, K., Seyer, J.M., Raghow, R., and Kang, A.H. (1991) Biochemistry 30, 7097-7104). In the present report, we have extensively dissected this subfragment of the propeptide and found that the pentapeptide Lys-Thr-Thr-Lys-Ser (residues 212-216) is the minimum sequence necessary for potent stimulation of collagen and fibronectin production in a variety of mesenchymal cells. We postulate that the extracellular matrix production in fibroblasts may be subject to either positive or negative feedback regulation depending on the repertoire of specific proteases during postinflammatory tissue regeneration and fibrosis.

Amino Acid Sequence↗

PubMed1995

Effects of serotonin precursors on the negative feedback effects of glucocorticoids on hypothalamic-pituitary-adrenal axis function in depression.

In order to investigate the relationships between brain serotonergic turnover and hypothalamic-pituitary-adrenal (HPA) axis function in unipolar depression, the authors measured intact adrenocorticotropic hormone (ACTH) and cortisol levels in baseline conditions and after combined dexamethasone (1 mg PO) and L-5-hydroxytryptophan (L-5-HTP, 200 mg PO) administration in 13 minor, 17 simple major, and 17 melancholic subjects. L-5-HTP significantly enhanced post-DST ACTH and cortisol secretion in major--but not in minor--depressed subjects. Major depressed subjects with or without melancholia exhibited significantly higher post-DST ACTH and cortisol responses to L-5-HTP than minor depressed subjects. L-5-HTP administration converted some major depressed ACTH or cortisol suppressors into nonsuppressors. L-5-HTP stimulated ACTH or cortisol secretion to the same extent in major depressed HPA-axis suppressors and nonsuppressors. It is concluded that L-5-HTP loading may augment ACTH and, consequently, cortisol escape from suppression by dexamethasone in major but not in minor depressed subjects. The findings show that serotonergic mechanisms modulate the negative feedback of glucocorticoids on central HPA-axis regulation. It is hypothesized that the higher L-5-HTP-induced post-DST HPA-axis hormone responses in major depression reflect upregulated 5-HT2 receptor-driven breakthrough secretion of pituitary ACTH from suppression by dexamethasone.

Adrenocorticotropic Hormone↗

PubMed1991

Psychophysiological response patterns to positive and negative film stimuli.

The aim of the present study was to investigate differential emotional response patterns to film stimuli by multimodal assessment of mood ratings, perception of bodily sensations, salivary cortisol, autonomic variables and facial electromyogram (EMG). Film stimuli, chosen to elicit positive and negative emotional states, were presented to 12 subjects with general anxiety disorder and 12 controls. Changes in mood, bodily sensations, autonomic activity (heart rate, respiration rate and skin conductance), facial EMG activity (corrugator and zygomatic muscle region) and salivary cortisol were measured. Analyses revealed differential changes in all response systems except for respiration rate and salivary cortisol. Although high-anxious subjects did not differ from controls in their average responses to the negative film stimuli, there is a tendency of a greater coherence of emotional response components in generalized anxiety subjects. However, spontaneous facial expressions to positive and negative film stimuli were associated with augmented electrodermal activity within both groups. Results are interpreted in light of directional response fractionation, dimensional approaches of emotion, and the facial feedback literature.

Adult↗

PubMed2006

IFN-gamma suppresses IL-10 production and synergizes with TLR2 by regulating GSK3 and CREB/AP-1 proteins.

The control of IL-10 production and mechanisms that mediate synergy between IFN-gamma and TLR ligands are not well understood. We report that IFN-gamma augments induction of TNFalpha by TLR ligands, immune complexes, and zymosan by suppressing IL-10 production and thereby interrupting Stat3-mediated feedback inhibition. IFN-gamma altered TLR2-induced signal transduction by increasing GSK3 activity and suppressing MAPK activation, leading to diminished IL-10 production. Inhibition of GSK3 or ablation of the GSK3beta gene ameliorated TLR2-induced peritonitis and arthritis. IFN-gamma suppressed the activity of CREB and AP-1, transcription factors that induce IL-10 expression and are regulated in part by MAPKs and GSK3. These results yield insight into mechanisms by which IFN-gamma regulates IL-10 production and TLR2-mediated inflammatory responses and identify inhibition of CREB and AP-1 as part of the macrophage response to IFN-gamma. GSK3 and CREB/AP-1 are key players in integrating IFN-gamma and TLR2 responses in innate immunity and inflammation.

Animals↗

PubMed2004

Visual and motor constraints on trajectory planning in pointing movements.

The aim of the present study was to show that planning and controlling the trajectory of a pointing movement is influenced not solely by physical constraints but also by visual constraints. Subjects were required to point towards different targets located at 20 degrees , 40 degrees , 60 degrees and 80 degrees of eccentricity. Movements were either constrained (i.e. two-dimensional movements) or unconstrained (i.e. three-dimensional movements). Furthermore, movements were carried out either under a direct or a remote visual control (use of a video system). Results revealed that trajectories of constrained movements were nearly straight whatever the eccentricity of the target and the type of visual control. A different pattern was revealed for unconstrained movements. Indeed, under direct vision the trajectory curvature increased as the eccentricity augmented, whereas under indirect vision, trajectories remained nearly straight whatever the eccentricity of the target. Thus, movements controlled through a remote visual feedback appear to be planned in extrinsic space as constrained movements.

Adolescent↗

PubMed1980

Implication of endogenous prostaglandin system in the antihypertensive effect of captopril, SQ 14225, in low renin hypertension.

The role of endogenous prostaglandins in the antihypertensive mechanism of orally active angiotensin I-converting enzyme inhibitor in low renin hypertension was investigated. In the SQ 14225-responders with low renin hypertension, blood pressure was elevated to control level and antihypertensive effect of SQ 14225 was attenuated after the inhibition of endogenous prostaglandin synthesis with indomethacin, while no significant change in blood pressure was found in the SQ 14225-responders with normal renin hypertension. Urinary prostaglandin E excretion was not significantly increased after the SQ 14225 administration but significantly decreased after the administration of indomethacin. There was no significant difference in urinary prostaglandin E excretion between normal renin hypertension and low renin hypertension. These results suggest that SQ 14225 may potentiate extrarenal vasodilating prostaglandin system, probably vascular prostaglandin system, contributing to the antihypertensive mechanism in SQ 14225-responders with low renin hypertension. The augmented renin release following SQ 14225 administration was inhibited by indomethacin, suggesting that endogenous prostaglandin system may contribute to the negative short feedback mechanism of renin release.

Adult↗

PubMed2007

Bidirectional regulation of upstream IGF-I/insulin receptor signaling and downstream FOXO1 in cardiomyocytes.

Signaling pathways of IGF-I and insulin receptors play important roles in the regulation of myocardial function. FOXO1 is a member of the forkhead transcriptional factor family, but how insulin and IGF-I receptor signaling regulate FOXO1 in cardiomyocytes is not well understood. This study was carried out to elucidate how IGF-I and insulin receptor signaling modulate FOXO1 in cardiomyocytes. In cardiomyocytes, activation of IGF-I receptor and insulin receptor lead to rapid phosphorylation of FOXO1. Inhibition of phosphatidylinositol 3-kinase/Akt pathway suppressed the effect of insulin and IGF-I on FOXO1 phosphorylation. Prolonged incubation with IGF-I increased ubiquitination of FOXO1 and down-regulated the abundance of FOXO1 proteins, which suggested that IGF-I might modulate FOXO1 degradation. To explore whether FOXO1 could modulate IGF-I and insulin signaling, a constitutively active FOXO1 was overexpressed in cardiomyocytes. The abundance of insulin receptor and IGF-I receptor was significantly upregulated in the cells overexpressing active FOXO1, accompanied by increased receptor phosphorylation upon insulin/IGF-I stimulation. Interestingly, overexpression of constitutively active FOXO1 also led to activation of MEK and Akt phosphorylation. IGF-I-stimulated MEK and Akt phosphorylation were augmented byoverexpression of constitutively active FOXO1. These findings indicate bidirectional regulation of insulin/IGF-I receptor signaling and FOXO1 in cardiomyocytes. FOXO1 may provide feedback control through upregulation of insulin and IGF-I receptor signaling.

Adenoviridae↗