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Results for “augmented feedback”

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At least 307 records · Page 17Linked to original sources

PubMed1996

Monocyte-endothelial cell interaction induces expression of adhesion molecules on human umbilical cord endothelial cells.

OBJECTIVE: The adhesive interaction of monocytes and endothelial cells has been implicated as a regulatory signal in the cell activation that is involved in the pathogenesis of atherosclerosis. We investigated the effect of monocyte-endothelial cell interaction on the expression of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), in human umbilical cord vein endothelial cells (HUVECs). METHODS: ICAM-1 and VCAM-1 protein and mRNA expression were determined by cellular ELISA and Northern blot analysis, respectively. RESULTS: The addition of unstimulated human monocytes, as well as interleukin-1 beta (IL-1 beta: 25 U/ml) and tumor necrosis factor-alpha (TNF: 100 U/ml), to HUVECs rapidly induced the expression of ICAM-1 and VCAM-1 protein and mRNA in HUVECs, whereas the addition of polymorphonuclear leukocytes (PMNs) had no significant effect on their expression. The induction of ICAM-1 and VCAM-1 by the co-culture of HUVECs and monocytes was significantly, but partially, inhibited by the combination of anti-IL-1 alpha, anti-IL-1 beta and anti-TNF Abs. Actinomycin D and genistein, but not calphostin C, also significantly inhibited the co-culture-induced adhesion molecule expression. CONCLUSIONS: These results suggest that the monocyte-endothelial cell interaction induces the expression of ICAM-1 and VCAM-1 in endothelial cells partially through the production of IL-1 and TNF. These findings also suggest that the monocyte-endothelial interaction further augments their interaction through the up-regulation of endothelial adhesion molecules, as a positive feedback mechanism.

Arteriosclerosis↗

PubMed2000

Potassium-induced enhancement of persistent inward current in hippocampal neurons in isolation and in tissue slices.

Previous work suggested a role for the voltage-dependent persistent sodium current, I(Na,P), in the generation of seizures and spreading depression (SD). Ordinarily, I(Na,P) is small in hippocampal neurons. We investigated the effect of raising external K(+) concentration, [K(+)](o), on whole-cell persistent inward current in freshly isolated hippocampal CA1 pyramidal neurons. I(Na,P) was identified by TTX-sensitivity and dependence on external Na(+) concentration. When none of the ion channels were blocked, I(Na,P) was not usually detectable, probably because competing K(+) current masked it, but after raising [K(+)](o) I(Na,P) appeared, while K(+) currents diminished. With K(+) channels blocked, I(Na,P) could usually be evoked in control solution and raising [K(+)](o) caused its reversible increase in most cells. The increase did not depend on external calcium [Ca(2+)](o). In CA1 pyramidal neurons in hippocampal slices a TTX-sensitive persistent inward current was always recorded and when [K(+)](o) was raised, it was reversibly enhanced. Strong depolarization evoked irregular current fluctuations, which were also augmented in high [K(+)](o). The findings support a role of potassium-mediated positive feedback in the generation of seizures and spreading depression.

Animals↗

PubMed2004

Epidermal growth factor receptor regulates aberrant expression of insulin-like growth factor-binding protein 3.

Epidermal growth factor receptor (EGFR) is frequently overexpressed in esophageal carcinoma and its precursor lesions. To gain insights into how EGFR overexpression affects cellular functions in primary human esophageal cells, we performed gene expression profiling and identified insulin-like growth factor-binding protein (IGFBP)-3 as the most up-regulated gene. IGFBP-3 regulates cell proliferation through both insulin-like growth factor-dependent and independent mechanisms. We found that IGFBP-3 mRNA and protein expression was increased in EGFR-overexpressing primary and immortalized human esophageal cells. IGFBP-3 was also up-regulated in EGFR-overexpressing cells in organotypic culture and in EGFR transgenic mice. Furthermore, IGFBP-3 mRNA was overexpressed in 80% of primary esophageal squamous cell carcinomas and 60% of primary esophageal adenocarcinomas. Concomitant up-regulation of EGFR and IGFBP-3 was observed in 60% of primary esophageal squamous cell carcinomas. Immunohistochemistry revealed cytoplasmic localization of IGFBP-3 in the preponderance of preneoplastic and neoplastic esophageal lesions. IGFBP-3 was also overexpressed in esophageal cancer cell lines at both mRNA (60%) and protein (40%) levels. IGFBP-3 secreted by cancer cells was capable of binding to insulin-like growth factor I. Functionally, epidermal growth factor appeared to regulate IGFBP-3 expression in esophageal cancer cell lines. Finally, suppression of IGFBP-3 by small interfering RNA augmented cell proliferation, suggesting that IGFBP-3 may inhibit tumor cell proliferation as a negative feedback mechanism. In aggregate, we have identified for the first time that IGFBP-3 is an aberrantly regulated gene through the EGFR signaling pathway and it may modulate EGFR effects during carcinogenesis.

Animals↗

PubMed1999

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression.

We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a-/-,Agtr1b-/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.

Angiotensin II↗

PubMed1992

Interleukin 1 has positive and negative regulatory effects in human long-term bone marrow culture.

The observations that interleukin 1 (IL-1) increases the production of colony-stimulating factors (CSFs) by stromal cells and acts in synergy with those CSFs to stimulate the growth of progenitor cells suggest that IL-1 may have an important role in stimulating hemopoiesis. However, IL-1 also induces the synthesis by stromal cells of inhibitors of hemopoiesis including tumor necrosis factor (TNF) and prostaglandin E2. We have used long-term bone marrow culture (LTBMC) to study the effect of IL-1 on hemopoiesis in the presence of a stromal cell layer. The addition of recombinant (r)IL-1 (10 U/ml) at the initiation of the LTBMC and at each weekly feed resulted in a significant stimulation of nonadherent granulocyte-macrophage colony-forming units (CFU-GM) by week 1 and a sustained increase in colony-stimulating activity (CSA) in culture supernatants. The increased CSA activity was mainly due to granulocyte colony-stimulating factor (G-CSF) as studied by the effects of neutralizing antibodies. Following this initial stimulation, however, nonadherent layer CFU-GM became significantly suppressed by week 4, and the number of nonadherent cells was also reduced. This delayed suppression of hemopoiesis induced by continuous exposure to rIL-1 was partially abrogated by the addition of indomethacin (10(-6) M) to the cultures, but anti-TNF had no such effect and we could not detect significant TNF levels either in culture supernatants or in stromal cell extracts. Our data suggest that prostaglandin inhibitors suppress the negative feedback control of myelopoiesis induced by IL-1 and therefore may have a role in augmenting IL-1 stimulation of myelopoiesis.

Bone Marrow↗

PubMed1983

Studies on the autologous MLR in primary biliary cirrhosis: evidence that the autologous MLR is a negative feedblock response stimulated by activated B cells.

Patients with primary biliary cirrhosis (PBC) were found to have diminished suppression of pokeweed mitogen (PWM)-stimulated immunoglobulin synthesis by in vitro cultures containing autologous T and B cells. The possibility that this abnormality is due to a defect of autologous cell-cell interactions was suggested by the finding that patients with PBC have a significantly diminished proliferative response in the autologous mixed lymphocyte reaction (MLR). In studies of normal lymphocytes, it was found that T cells activated in the autologous MLR have the capacity to suppress PWM-stimulated immunoglobulin synthesis, but do not have augmented helper function. Furthermore, when T cells were activated with lymphoblastoid B cells, augmented suppressor activity was observed. These findings suggest that the autologous MLR represents a negative feedback loop in which activated B cells initiate a suppressor T cell pathway. The defect in the autologous MLR in patients with PBC may account for the diminished suppressor cell function observed in this disease.

Antigens↗

PubMed1978

Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice.

We have shown that (a) purified T-helper cells induce cells of another T-cell set-, expressing the Ly123+Qa1+ surface phenotype, to exert potent suppressive activity, (b) this T-T interaction plays an important role in regulating in vivo immune responses, and (c) this interaction represents an important barrier to protocols intended to augment the immune status of individuals by adoptive (or active) immunotherapy. Our results also indicate that the Ly123+ T-cell set mediating feedback suppression in vivo is sensitive to both low doses of cyclophosphamide and removal of the thymus in adult life. The importance of this T-T interaction to normal, physiologic regulation of the immune system is emphasized by the finding that the major T-cell deficit of NZB mice (an inbred strain of mice that spontaneously develops an autoimmune disorder) is the absence or malfunction of an Ly123+ T-cell set responsible for feedback inhibition.

Animals↗

PubMed1983

Inhibition of intraduodenal trypsin does not stimulate exocrine pancreatic secretion in man.

Inhibition of intraduodenal trypsin stimulates pancreatic secretion in rats and swine. This finding is controversial in healthy humans. The present study was designed to find whether a 'negative-feedback' mechanism exists in man. A 7-lumen tube equipped with two balloons was passed into the duodenum in 18 healthy volunteers. During a constant intravenous infusion of secretin (0.1 CU/kg/h) the duodenum was perfused with 0.9% NaCl solution (20 ml/10 min). Polyethylene glycol (10 g/l) served as nonabsorbable marker. Aprotinin (0.5 X 10(6) KIU/10 min or 1 X 10(6) KIU/10 min) was perfused intraduodenally during periods of constant pancreatic enzyme secretion for 30 min. During perfusion of the trypsin inhibitor aprotinin an almost complete inhibition of trypsin could be observed. However, at the same time or following the perfusion of aprotinin a significant augmentation of amylase, lipase or volume secretion did not occur. Thus, in the present study a negative-feedback control of pancreatic exocrine secretion by the intraduodenal trypsin concentration in man could not be demonstrated.

Adult↗

PubMed1982

Delayed hypersensitivity granuloma formation and modulation around Schistosoma mansoni eggs in vitro. II. Regulatory T cell subsets.

Schistosoma mansoni granuloma modulation was first described in an in vivo murine model of schistosomiasis and was characterized as a diminished cellular responsiveness to newly formed eggs in chronic infections. This phenomenon of modulation was studied using an in vitro model of granuloma formation. Negative selection procedures using anti-Lyt-1.2, 2.2, and Qa-1 sera and complement on spleen cell populations from normal or S. mansoni-infected C57BL/6 or (C57BL/6 X A/J)F1 mice were examined for their effect on in vitro granuloma formation or modulation. These data suggest that there is a Lyt-1+2-, Qa-1+ T cell present in chronically infected spleen cells that is capable of inducing feedback suppression. In addition, selective removal of a population of Lyt-1-2+ T cells from chronically infected spleen cells augmented the ability of that population to form granulomas in vitro. The selective removal of Lyt-1+2- cells ablated the ability of chronically infected spleen cells to form in vitro granulomas. Granuloma formation is primarily dependent on a population of Lyt-1+, Qa-1+ cells, and modulation is dependent on 2 populations, 1 acting directly (Lyt-1-2+) and the other through a (Lyt-1+2-, Qa-1+) feedback mechanism of suppression.

Acute Disease↗

PubMed1998

Pindolol augmentation of antidepressant therapy.

BACKGROUND: Antidepressant therapy is not always effective and is slow to take effect. In theory, these shortfalls may be caused by induction of neuronal negative feedback via pre-synaptic 5-HTIA receptors. Pindolol, an antagonist at somatodentritic pre-synaptic 5-HTIA receptors has been investigated as a potential accelerator and augmentor of antidepressant response. METHOD: A Medline search was conducted in November 1997. RESULTS: Six open-label studies and six controlled studies were identified for review. CONCLUSIONS: Open-label studies strongly suggest that pindolol may accelerate and augment antidepressant response, but controlled studies do not wholly support these findings: only three of six studies clearly demonstrate benefit. Larger, well-designed, controlled trials are needed to determine definitively the effectiveness of pindolol in this context.

Adrenergic beta-Antagonists↗

PubMed2006

The effects of observational feedback and verbal cues on the motor learning of an aimed reach-and-point task.

PURPOSE: Current technology allows the recording of movement for both motion analysis and providing observational feedback. The most effective type of observational feedback is under debate. We compared a child's reach-and-point performance after viewing a videotaped playback of a model's performance and after viewing a split-screen comparison of the model's and child's performances while simultaneously receiving verbal cues. METHODS: A PTVision system provided observational feedback and recorded spatial trajectory, target accuracy, movement time, and joint angles while a 13 year-old boy with cerebral palsy reached for three targets. RESULTS: The split-screen comparison had the largest effect on reach performance, including slower-yet-more-accurate movements and a more extended wrist, curved spatial trajectories, and an ulnar-deviated wrist. CONCLUSIONS: Feedback using split-screen comparison between a model's and the child's performance with verbal cues appears to promote motor learning. When using technology to augment therapy, the intervention should be designed considering current motor learning principles.

Adolescent↗

PubMed1986

Auditory biofeedback in spastic diplegia.

Using a simple auditory feedback device that produces a continuous buzzing signal on heel contact, we studied the effects of augmented auditory biofeedback on the gait of four spastic diplegic children. The purpose of the biofeedback was to attempt to increase dorsiflexion at heel strike without causing other compensatory changes at the knee and hip, which might lead to crouch gait. We measured velocity, stride length, and thigh, knee, and ankle angles at the heel strike, midswing, and toe-off phases of gait. Four subjects, aged 5-8 years, were given a standard gait training program, supplemented with biofeedback two times per week in a clinical setting and 1 h daily in a home program over an 8-week period. Three computer video gait analyses of the sagittal plane were conducted without biofeedback in the pre- and posttraining conditions and twice with biofeedback over the course of treatment. We performed linear regression analysis of joint angles at heel strike, midswing, and toe-off as a function of days into the study for each patient. Angle-angle diagrams for a test subject before, during, and after treatment indicate changes toward a normal gait pattern with biofeedback. The linear regression analysis showed a statistically significant (p less than 0.01) shift toward dorsiflexion at heel strike with repeated exposure to biofeedback. A compensatory crouch gait was not induced. The linear regression analyses for hip and knee angles were not statistically significant (p greater than 0.25), indicating a disassociation of movement among hip, knee, and ankle.

Acoustic Stimulation↗

PubMed1998

Involvement of 26-kDa membrane-bound tumour necrosis factor precursor in bidirectional feedback regulation on 17-kDa tumour necrosis factor production after stimulation by lipopolysaccharide.

The authors have previously shown that 26-kDa membrane-bound tumour necrosis factor precursor (proTNF) on the cell-surface of primed human monocytic cell line THP-1 is involved in positive feedback regulation of lipopolysaccharide (LPS)-dependent TNF-production. Here, we provide direct evidence for modulation of responsiveness of the THP-1 cells against LPS by membrane-bound pro-TNF. When THP-1 cells were cocultivated with a heterogeneous cell line (proTNF/3T3 cells) which constitutively expressed membrane-bound proTNF, LPS-dependent TNF-production by THP-1 cells was significantly suppressed and the normal level was restored by the presence of anti-TNF antibody during cocultivation. The proTNF-3T3-induced decline of TNF-production of THP-1 was observed primarily at the mRNA level, although no difference was observed in the mRNA level of interleukin 1 beta, another LPS-inducible cytokine. These results suggest that proTNF could also be involved in the negative feedback regulation of LPS-dependent TNF-production through cell-to-cell contact. The augmentation of LPS-dependent TNF-production accompanied by the production of endogenous proTNF induced by exogenous agent was inhibited by protein kinase C inhibitor, whereas proTNF/3T3-induced suppression of TNF-production could not be restored to the normal level. It thus seems possible that proTNF might act on macrophages as a bidirectional regulator of its production by THP-1 cells depending on co-induced signals.

3T3 Cells↗

PubMed2005

Atrazine and the hypothalamo-pituitary-gonadal axis in sexually maturing precocial birds: studies in male Japanese quail.

The herbicide atrazine is a putative endocrine disruptor. The present studies investigated the effects of atrazine in male Japanese quail during sexual maturation. Atrazine was administered for two weeks in the diet or systemically to birds under long photoperiods. Atrazine had no effect on mortality but depressed both feed intake and growth (average daily gain [ADG] in g/day) at dietary concentrations of 1000 ppm. Atrazine in the diet at 10 ppm, but at no other concentrations, increased testes weight and gonadal-somatic-index and decreased the seminiferous tubule diameter-to-testis weight ratio. However, there were no effects on absolute tubule diameter, relative stage of testicular development, or the presence of a lumen. Atrazine in the diet at 1000 ppm increased circulating concentrations of testosterone but this effect was not observed consistently in all studies. Dietary atrazine at 10 ppm increased circulating concentrations of estradiol. Moreover, in one study, atrazine at 1000 ppm in the diet decreased circulating concentrations of luteinizing hormone. Atrazine administered systemically exerted no effect on indices of growth or reproduction. Atrazine did not mimic the effects of either estradiol or tamoxifen in male quail; thus, atrazine did not exhibit overt estrogenic or anti-estrogenic activity. Conversely, atrazine augmented the effects of testosterone and estradiol on testis regression, presumably by increasing the negative-feedback effects of these sex-steroids on follicle stimulating hormone secretion. It is concluded that atrazine up to 1000 ppm in the diet may exert some effects on reproductive development in sexually maturing male birds, but these are inconsistent and modest.

Animals↗

PubMed1983

Influence of testosterone and/or luteinizing hormone releasing hormone analogue on precocious sexual development in the juvenile rainbow trout.

The influence of testosterone, luteinizing hormone releasing hormone (LHRH) agonist and combinations of these hormones on gonadotropic hormone (GtH) levels in the sexually immature trout was investigated. Both the steroid and releasing hormone preparations, testosterone in Silastic capsules and cholesterol-pelleted LHRH-A, were formulated for sustained release and long-term biological action following a single hormone implantation. Marked increases in pituitary GtH followed testosterone and/or testosterone and LHRH analogue treatment combined, but the low pituitary GtH level in controls remained unchanged after LHRH analogue administration alone. Plasma GtH titers increased with time after testosterone treatment, indicating a positive steroid feedback effect by androgen on GtH in the juvenile rainbow trout. When combined with testosterone treatment, LHRH analogue augmented plasma GtH levels compared to fish receiving testosterone treatment alone. In males the elevated plasma GtH levels were associated with testes stimulation and onset of spermatogenesis; in females, however, no significant stimulation of the ovaries was observed. It can be concluded from these studies that the testosterone stimulus is sufficient to induce onset of sexual development in immature males but not females. Whereas LHRH analogue releases GtH from the testosterone-primed trout pituitary, LHRH treatment alone under these conditions fails to stimulate the juvenile trout reproductive system.

Animals↗

PubMed2002

Aromatase inhibition for ovarian stimulation: future avenues for infertility management.

Ovarian stimulation is applied during infertility management either alone or in conjunction with intrauterine insemination and assisted reproductive technologies. At the present time, the two main medications used for ovarian stimulation include an oral antiestrogen, clomiphene citrate, and injectable gonadotropins. In spite of the high ovulation rate with the use of clomiphene citrate, the pregnancy rate is much lower. In clomiphene citrate failures, gonadotropin injections have generally been used as the next treatment option. Treatment with gonadotropins is difficult to control and characteristically associated with increased risk of severe ovarian hyperstimulation syndrome and high multiple pregnancies. Therefore, an effective oral treatment that could be used without risk of hyperstimulation and with minimal monitoring is the preferred therapy. We hypothesize that aromatase inhibitors can be administered early in the follicular phase to induce ovulation by releasing the hypothalamus or pituitary from estrogen negative feedback. Based on this hypothesis, we have reported the success of aromatase inhibitors in induction and augmentation of ovulation in addition to improving ovarian response to gonadotropin stimulation. Moreover, there are other potential applications for aromatase inhibitors in infertility management, including improving implantation in assisted reproduction and in-vitro maturation.

Anastrozole↗

PubMed1999

Control of parturition in ruminants.

Parturition is a process which, when set into motion, occurs to completion. This review concerns the control of parturition in ruminants. Parturition is an endocrine event, dependent upon the activation of the fetal hypothalamus-pituitary-adrenal (HPA) axis. In sheep and other ruminants, increases in plasma concentrations of cortisol induce the activity of 17-hydroxylase and 17,20 lyase in the placenta, increasing the biosynthesis of oestrogen relative to progesterone. The increase in the so-called E:P ratio increases myometrial activity and culminates in labour and delivery. Much work has been done to identify the mechanism of the endogenous activation of the fetal HPA axis. Recent work suggests that production of prostanoids within the fetal brain influences fetal ACTH secretion, and that induction of prostanoid biosynthesis at the end of gestation might be important in the process of parturition. Oestrogen and androgens, secreted by the placenta at the end of gestation, augment activity of the fetal HPA axis by increasing fetal ACTH secretion and by decreasing negative feedback sensitivity to cortisol. Although significant progress has been made concerning the neuroendocrinology of parturition, many significant questions remain. Is parturition regulated or simply programmed? Is parturition the ultimate result of neuronal maturation within the fetal hypothalamus, or is there a complex interplay between the placenta and fetal hypothalamus? Answers to these and other important questions await further research, but may provide key information which will prove useful in understanding general principles of parturition in many mammalian species.

Adrenocorticotropic Hormone↗

PubMed1980

The biogenesis of erythropoietin.

Aerobic living demands a constant supply of oxygen at the cellular mitochondrial level. Numerous interlocking feedback mechanisms insure the constancy of this supply by adapting the supply lines to changes in the intra and extracellular milieu. Among these mechanisms is the feedback circuit which, triggered by an intracellular decrease in oxygen supply, initiates the production of a polypeptide hormone, erythropoietin, which in turn augments the production of an oxygen carrier, the hemoglobin-containing red cell. The biogenesis of this hormone is an important biologic process which is being studied intensively and slowly unravelled.

Animals↗