Functionalism and the Negative Feedback Model in Biology

1970 ◽  
Vol 1970 ◽  
pp. 225-240
Author(s):  
Edward Manier
Keyword(s):  
Negative Feedback ◽  
Feedback Model

Light adaptation in the primate retina: Analysis of changes in gain and dynamics of monkey retinal ganglion cells

1990 ◽  
Vol 4 (1) ◽  
pp. 75-93 ◽  
Author(s):  
Keith Purpura ◽  
Daniel Tranchina ◽  
Ehud Kaplan ◽  
Robert M. Shapley
Keyword(s):  
Retinal Ganglion Cells ◽  
Negative Feedback ◽  
Light Adaptation ◽  
Ganglion Cells ◽  
Human Subjects ◽  
Light Level ◽  
Retinal Ganglion ◽  
M Cell ◽  
Feedback Model ◽  
Light Levels

AbstractThe responses of monkey retinal ganglion cells to sinusoidal stimuli of various temporal frequencies were measured and analyzed at a number of mean light levels. Temporal modulation tuning functions (TMTFs) were measured at each mean level by varying the drift rate of a sine-wave grating of fixed spatial frequency and contrast. The changes seen in ganglion cell temporal responses with changes in adaptation state were similar to those observed in human subjects and in turtle horizontal cells and cones tested with sinusoidally flickering stimuli; “Weber's Law” behavior was seen at low temporal frequencies but not at higher temporal frequencies. Temporal responses were analyzed in two ways: (1) at each light level, the TMTFs were fit by a model consisting of a cascade of low- and high-pass filters; (2) the family of TMTFs collected over a range of light levels for a given cell was fit by a linear negative feedback model in which the gain of the feedback was proportional to the mean light level. Analysis (1) revealed that the temporal responses of one class of monkey ganglion cells (M cells) were more phasic at both photopic and mesopic light levels than the responses of P ganglion cells. In analysis (2), the linear negative feedback model accounted reasonably well for changes in gain and dynamics seen in three P cells and one M cell. From the feedback model, it was possible to estimate the light level at which the dark-adapted gain of the cone pathways in the primate retina fell by a factor of two. This value was two to three orders of magnitude lower than the value estimated from recordings of isolated monkey cones. Thus, while a model which includes a single stage of negative feedback can account for the changes in gain and dynamics associated with light adaptation in the photopic and mesopic ranges of vision, the underlying physical mechanisms are unknown and may involve elements in the primate retina other than the cone.

scholarly journals Flies, clocks and evolution

2001 ◽  
Vol 356 (1415) ◽  
pp. 1769-1778 ◽  
Author(s):  
Ezio Rosato ◽  
Charalambos P. Kyriacou
Keyword(s):  
Gene Regulation ◽  
Negative Feedback ◽  
Clock Gene ◽  
Circadian System ◽  
Gene Duplications ◽  
Closely Related Species ◽  
Feedback Model ◽  
Silk Moth ◽  
The Brain

The negative feedback model for gene regulation of the circadian mechanism is described for the fruitfly, Drosophila melanogaster . The conservation of function of clock molecules is illustrated by comparison with the mammalian circadian system, and the apparent swapping of roles between various canonical clock gene components is highlighted. The role of clock gene duplications and divergence of function is introduced via the timeless gene. The impressive similarities in clock gene regulation between flies and mammals could suggest that variation between more closely related species within insects might be minimal. However, this is not borne out because the expression of clock molecules in the brain of the giant silk moth, Antheraea pernyi , is not easy to reconcile with the negative feedback roles of the period and timeless genes. Variation in clock gene sequences between and within fly species is examined and the role of co-evolution between and within clock molecules is described, particularly with reference to adaptive functions of the circadian phenotype.

scholarly journals A Negative Feedback Model to Explain Regulation of SARS-CoV-2 Replication and Transcription

2020 ◽  
Author(s):  
Xin Li ◽  
Zhi Cheng ◽  
Fang Wang ◽  
Yibo Xuan ◽  
Qiang Zhao ◽  
...  
Keyword(s):  
Negative Feedback ◽  
Feedback Mechanism ◽  
The Body ◽  
Expression Level ◽  
Regulatory Sequences ◽  
Cleavage Sites ◽  
Genomic Rnas ◽  
Negative Feedback Mechanism ◽  
Feedback Model ◽  
Public Data

Abstract Background: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although a preliminary understanding of the replication and transcription mechanisms of SARS-CoV-2 has recently emerged, their regulation remains unclear.Results: Based on reanalysis of public data, we propose a negative feedback model to explain the regulation of replication and transcription in—but not limited to—CoVs. The key step leading to new discoveries was the identification of the cleavage sites of nsp15—an RNA uridylate-specific endoribonuclease, encoded by CoVs. According to this model, nsp15 regulates the synthesis of subgenomic RNAs (sgRNAs) and genomic RNAs (gRNAs) by cleaving transcription regulatory sequences in the body. The expression level of nsp15 determines the relative proportions of sgRNAs and gRNAs, which in turn change the expression level of nps15 to reach equilibrium between the replication and transcription of CoVs.Conclusions: The replication and transcription of CoVs are regulated by a negative feedback mechanism that influences the persistence of CoVs in hosts. Our findings enrich fundamental knowledge in the field of gene expression and its regulation, and provide new clues for future studies. One important clue is that nsp15 may be an important and ideal target for the development of drugs (e.g. uridine derivatives) against CoVs.

Adiposity signals and food reward: expanding the CNS roles of insulin and leptin

2003 ◽  
Vol 284 (4) ◽  
pp. R882-R892 ◽  
Author(s):  
Dianne P. Figlewicz
Keyword(s):  
Energy Balance ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Mental Illnesses ◽  
Therapeutic Approaches ◽  
Reward Circuitry ◽  
Feedback Model ◽  
Adiposity Signals ◽  
The Central Nervous System ◽  
The Brain

The hormones insulin and leptin have been proposed to act in the central nervous system (CNS) as adiposity signals as part of a theoretical negative feedback loop that senses the caloric stores of an animal and orchestrates adjustments in energy balance and food intake. Much research has provided support for both the existence of such a feedback loop and the specific roles that insulin and leptin may play. Most studies have focused on hypothalamic sites, which historically are implicated in the regulation of energy balance, and on the brain stem, which is a target for neural and humoral signals relating to ingestive acts. More recent lines of research, including studies from our lab, suggest that in addition to these CNS sites, brain reward circuitry may be a target for insulin and leptin action. These studies are reviewed together here with the goals of providing a historical overview of the findings that have substantiated the originally hypothesized negative feedback model and of opening up new lines of investigation that will build on these findings and allow further refinement of the model of adiposity signal/CNS feedback loop. The understanding of how motivational circuitry and its endocrine or neuroendocrine modulation contributes to normal energy balance regulation should expand possibilities for future therapeutic approaches to obesity and may lead to important insights into mental illnesses such as substance abuse or eating disorders.

scholarly journals A Negative Feedback Model to Explain Regulation of SARS-CoV-2 Replication and Transcription

2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Li ◽  
Zhi Cheng ◽  
Fang Wang ◽  
Jia Chang ◽  
Qiang Zhao ◽  
...  
Keyword(s):  
Negative Feedback ◽  
Feedback Mechanism ◽  
Expression Level ◽  
Regulatory Sequence ◽  
Cleavage Sites ◽  
Fusion Model ◽  
Genomic Rnas ◽  
Negative Feedback Mechanism ◽  
Feedback Model ◽  
Protein Structure Data

BackgroundCoronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although a preliminary understanding of the replication and transcription of SARS-CoV-2 has recently emerged, their regulation remains unknown.ResultsBy comprehensive analysis of genome sequence and protein structure data, we propose a negative feedback model to explain the regulation of CoV replication and transcription, providing a molecular basis of the “leader-to-body fusion” model. The key step leading to the proposal of our model was that the transcription regulatory sequence (TRS) motifs were identified as the cleavage sites of nsp15, a nidoviral RNA uridylate-specific endoribonuclease (NendoU). According to this model, nsp15 regulates the synthesis of subgenomic RNAs (sgRNAs), and genomic RNAs (gRNAs) by cleaving TRSs. The expression level of nsp15 controls the relative proportions of sgRNAs and gRNAs, which in turn change the expression level of nsp15 to reach equilibrium between the CoV replication and transcription.ConclusionThe replication and transcription of CoVs are regulated by a negative feedback mechanism that influences the persistence of CoVs in hosts. Our findings enrich fundamental knowledge in the field of gene expression and its regulation, and provide new clues for future studies. One important clue is that nsp15 may be an important and ideal target for the development of drugs (e.g., uridine derivatives) against CoVs.

A Negative Feedback Model for a Mechanism Based Description of Longitudinal Observations

2013 ◽  
Vol 52 (06) ◽  
pp. 484-493
Author(s):  
S. Schmidt ◽  
M. A. Boroujerdi
Keyword(s):  
Differential Equation ◽  
Negative Feedback ◽  
Order Differential Equation ◽  
Bone Turnover Marker ◽  
Second Order ◽  
Controlled Clinical Trial ◽  
Mineral Density ◽  
Second Order Differential Equation ◽  
Feedback Model ◽  
Conjugated Estrogen

SummaryIn modern medicine the diagnosis and prognosis of an abnormal metabolic condition is based on blood borne measurements involving one or more biomarker.Objective: This paper reports the development of a minimal negative feedback model for the description of longitudinal biomarkers concentrations for treatment of osteoporosis in postmenopausal women.Methods: Literature data were obtained from double-blind, placebo-controlled clinical trial over three years. There were four treatment groups: 1) Placebo, 2) Alendro -nate, 3) Conjugated Estrogen, and/or 4) Combination therapy. The negative feedback model consists of a biomarker and a companion controller. By considering the above basal biomarker values it is shown that the dynamics can be described by a second order differential equation without the involvement of biomarker production rate. The second order differential equation is also analogous to classical negative feedback servomechanism model with two parameters ωn and ξ. It was assumed that the rate constants defining the negative feedback model were equal which would set ξ to 0.707 with only ωn to be estimated.Results: ωn was estimated for both lumbar spine bone mineral density (BMD) and bone-specific alkaline phosphatase (BAP) in four treatments groups. The t½ of BMD and BAP were estimated at 26.8 (0.30) and 9.4 (0.30) days respectively.Conclusions: The negative feedback model of BMD supports the mechanism whereby Conjugated Estrogen and Alendronate decrease the clearance rate constant of BMD analogous to increased apoptosis of osteoclasts. The linked negative feedback models facilitate a mechanism based prediction of BMD using the concentrations of the bone turnover marker BAP.

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