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Negative feedback

About: Negative feedback is a research topic. Over the lifetime, 2804 publications have been published within this topic receiving 66052 citations. The topic is also known as: Negative feedback mechanism.


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Journal ArticleDOI
TL;DR: This paper provided a conceptual analysis of feedback and reviewed the evidence related to its impact on learning and achievement, and suggested ways in which feedback can be used to enhance its effectiveness in classrooms.
Abstract: Feedback is one of the most powerful influences on learning and achievement, but this impact can be either positive or negative. Its power is frequently mentioned in articles about learning and teaching, but surprisingly few recent studies have systematically investigated its meaning. This article provides a conceptual analysis of feedback and reviews the evidence related to its impact on learning and achievement. This evidence shows that although feedback is among the major influences, the type of feedback and the way it is given can be differentially effective. A model of feedback is then proposed that identifies the particular properties and circumstances that make it effective, and some typically thorny issues are discussed, including the timing of feedback and the effects of positive and negative feedback. Finally, this analysis is used to suggest ways in which feedback can be used to enhance its effectiveness in classrooms.

7,222 citations

Journal ArticleDOI
TL;DR: The outlines of a model that integrates autonomic, attentional, and affective systems into a functional and structural network that may help to guide us in the understanding of emotion regulation and dysregulation are presented.

2,217 citations

Journal ArticleDOI
18 Apr 2005-Oncogene
TL;DR: The p53 pathway responds to stresses that can disrupt the fidelity of DNA replication and cell division by activation of the p53 protein as a transcription factor that initiates a program of cell cycle arrest, cellular senescence or apoptosis.
Abstract: The p53 pathway responds to stresses that can disrupt the fidelity of DNA replication and cell division. A stress signal is transmitted to the p53 protein by post-translational modifications. This results in the activation of the p53 protein as a transcription factor that initiates a program of cell cycle arrest, cellular senescence or apoptosis. The transcriptional network of p53-responsive genes produces proteins that interact with a large number of other signal transduction pathways in the cell and a number of positive and negative autoregulatory feedback loops act upon the p53 response. There are at least seven negative and three positive feedback loops described here, and of these, six act through the MDM-2 protein to regulate p53 activity. The p53 circuit communicates with the Wnt-beta-catenin, IGF-1-AKT, Rb-E2F, p38 MAP kinase, cyclin-cdk, p14/19 ARF pathways and the cyclin G-PP2A, and p73 gene products. There are at least three different ubiquitin ligases that can regulate p53 in an autoregulatory manner: MDM-2, Cop-1 and Pirh-2. The meaning of this redundancy and the relative activity of each of these feedback loops in different cell types or stages of development remains to be elucidated. The interconnections between signal transduction pathways will play a central role in our understanding of cancer.

1,881 citations

Journal ArticleDOI
01 Jun 2000-Nature
TL;DR: Simple gene circuits consisting of a regulator and transcriptional repressor modules in Escherichia coli are designed and constructed and the gain of stability produced by negative feedback is shown.
Abstract: The genetic and biochemical networks which underlie such things as homeostasis in metabolism and the developmental programs of living cells, must withstand considerable variations and random perturbations of biochemical parameters These occur as transient changes in, for example, transcription, translation, and RNA and protein degradation The intensity and duration of these perturbations differ between cells in a population The unique state of cells, and thus the diversity in a population, is owing to the different environmental stimuli the individual cells experience and the inherent stochastic nature of biochemical processes (for example, refs 5 and 6) It has been proposed, but not demonstrated, that autoregulatory, negative feedback loops in gene circuits provide stability, thereby limiting the range over which the concentrations of network components fluctuate Here we have designed and constructed simple gene circuits consisting of a regulator and transcriptional repressor modules in Escherichia coli and we show the gain of stability produced by negative feedback

1,551 citations

Journal ArticleDOI
TL;DR: There is some evidence that suggests that whereas comparator elements are not reset during stress, a comparator element is reset during the course of the circadian rhythm so that different basal levels of steroid are achieved.
Abstract: THE LEVEL of activity within the adrenocortical system is determined by endogenous (circadian) and exogenous (stress) excitatory inputs, by inhibitory neural modulation and also by corticosteroid negative feedback control. Although corticosteroid feedback on (CRF and) ACTH secretion is easily demonstrated by treatment of mammals with exogenous glucocorticoids and subsequent measurement of either basal or stimulated activity in the system, the physiological role of this negative feedback is not so easily discerned. It is likely that most disagreement about feedback regulation of ACTH secretion has arisen because of three characteristics of the system. First, it now appears that there are at least three distinct time domains in which negative feedback by glucocorticoids on ACTH secretion are exerted. These can be distinguished at the level of the corticotrope in vitro by the different cellular effects of glucocorticoid action. Thus, interpretation of results of in vivo experiments is critically dependent on...

1,177 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202374
2022123
202161
202090
2019117
2018104