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Related Concept Videos

Dose Response Curve: Conventional Versus Nonmonotonic01:21

Dose Response Curve: Conventional Versus Nonmonotonic

The correlation between a drug's dosage and its impact on a biological system is a cornerstone of pharmacology and toxicology. Conventional dose–response curves, which include graded and quantal relationships, are key to this understanding. Graded dose–response curves depict the spectrum of a biological reaction to different doses within an individual, indicating that as the drug dosage increases, so does the intensity of the response. On the other hand, quantal dose–response relationships...
Dose-Response Relationship: Overview01:03

Dose-Response Relationship: Overview

Agonists can bind with and activate receptors, resulting in the formation of drug-receptor complexes. Once formed, these complexes catalyze many biochemical processes at the cellular level and subsequently induce a pharmacologic response. The degree of response is directly proportional to the fraction of activated receptors, which in turn, depends on the concentration of the drug at the receptor site as well as the sensitivity of the receptor. An increase in the administered dose contributes to...
Dose-Response Relationship: Potency and Efficacy01:22

Dose-Response Relationship: Potency and Efficacy

The potency of a drug is the measure of its ability to produce a biological response and can be compared by looking at the half-maximum effective concentration or EC50 values of different drugs. A lower EC50 value indicates higher potency of the drug. In the dose–response curve of two antihypertensive drugs, candesartan and irbesartan, a significant difference is observed in their EC50 values. A lower EC50 value for candesartan indicates that it is more potent than irbesartan, as it produces...
Pharmacokinetic–Pharmacodynamic Relationship: Intensity of Dose-Effect Relationship01:23

Pharmacokinetic–Pharmacodynamic Relationship: Intensity of Dose-Effect Relationship

Pharmacodynamics explores the relationship between drug concentration and its effect. In a quantal response drug, the duration of action better correlates with drug concentration, while for graded effect drugs, the intensity of response is more relevant. This intensity depends on the dose, drug removal rate, and the region of the concentration–response curve.The concentration–response curve can be divided into three regions. Region 3 (80–100% maximum response) demonstrates that even as drug...
Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Pharmacokinetic–Pharmacodynamic Relationship: Dose to Pharmacological Effect01:28

Pharmacokinetic–Pharmacodynamic Relationship: Dose to Pharmacological Effect

A drug’s dosage and pharmacokinetic properties determine how quickly it acts, how intense its effects are, and how long it lasts. Higher doses increase drug concentration at receptor sites, producing a hyperbolic curve when pharmacologic response is plotted against drug dose. Converting this scale to a log-linear format results in a sigmoidal curve, better representing dose–response relationships.For drugs following a one-compartment model, the pharmacologic response is directly proportional to...

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Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis
08:11

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Published on: November 14, 2016

Dose-response thresholds for progressive diseases.

Louis Anthony Tony Cox1

  • 1Cox Associates and University of Colorado.

Dose-Response : a Publication of International Hormesis Society
|June 29, 2012
PubMed
Summary
This summary is machine-generated.

Diseases like cancer and heart disease may stem from disrupted feedback control systems. Alternative-equilibria (AE) theory explains how exposure can create new disease states, with a threshold triggering spontaneous progression.

Keywords:
crystalline silicadose-response thresholdexposure-response thresholdlung cancermathematical modelsilicosis

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Area of Science:

  • Systems biology
  • Disease pathogenesis
  • Homeostasis and feedback control

Background:

  • Many diseases, including cancers and heart diseases, arise from disruptions in normal feedback control systems that maintain tissue and cell population homeostasis.
  • Excessive exposure can destabilize these feedback control loops, leading to sustained variable elevation and clinical consequences like chronic inflammation, tissue destruction, and cell proliferation.

Purpose of the Study:

  • To propose a theoretical framework, alternative-equilibria (AE) theory, for understanding how environmental exposures can destabilize homeostatic feedback control systems.
  • To explain the development of sustained imbalances and elevated disease-related variables, leading to chronic diseases.

Main Methods:

  • Development of a dynamic systems model based on feedback control principles.
  • Introduction of the concept of alternative, locally stable equilibria to represent disease states.
  • Analysis of the model's implications for disease progression following exposure.

Main Results:

  • The proposed alternative-equilibria (AE) theory suggests that destabilizing exposures can create a new, stable disease equilibrium alongside the normal homeostatic one.
  • AE theory predicts an exposure threshold; exceeding this threshold initiates spontaneous progression to the disease state, even without continued exposure.
  • This model may explain observed patterns in diseases such as COPD, silicosis, and inflammation-mediated lung cancer.

Conclusions:

  • Alternative-equilibria (AE) theory provides a novel framework for understanding disease initiation and progression as a shift in system dynamics.
  • The theory highlights the critical role of exposure thresholds in transitioning from homeostasis to a disease state.
  • This framework offers potential explanations for epidemiological and experimental observations in various chronic diseases.