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Related Concept Videos

Inflammation01:38

Inflammation

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Second Order systems II01:18

Second Order systems II

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In an underdamped second-order system, where the damping ratio ζ is between 0 and 1, a unit-step input results in a transfer function that, when transformed using the inverse Laplace method, reveals the output response. The output exhibits a damped sinusoidal oscillation, and the difference between the input and output is termed the error signal. This error signal also demonstrates damped oscillatory behavior. Eventually, as the system reaches a steady state, the error diminishes to zero.
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First Order Systems01:21

First Order Systems

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First-order systems, such as RC circuits, are foundational in understanding dynamic systems due to their straightforward input-output relationship. Analyzing their responses to different input functions under zero initial conditions reveals significant insights into system behavior.
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Human milk oligosaccharides attenuate bacterial endotoxin-induced fever in mice.

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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
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Fever and hypothermia in systemic inflammation.

Andras Garami1, Alexandre A Steiner2, Andrej A Romanovsky3

  • 1Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary.

Handbook of Clinical Neurology
|November 22, 2018
PubMed
Summary

Systemic inflammation causes fever or hypothermia, regulated body temperature changes beneficial for host defense. Prostaglandin E2 mediates fever, while hypothermia mediators remain unclear, though it aids severe infections.

Keywords:
LPSSIRSbody temperaturecyclooxygenaseendotoxinneuropeptideprostaglandinsepsisshocksickness syndromethermoregulation

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Area of Science:

  • Immunology
  • Emergency Medicine
  • Physiology

Background:

  • Systemic inflammation, seen in sepsis, presents challenges in emergency medicine.
  • Body temperature changes, fever (mild inflammation) and hypothermia (severe inflammation), accompany systemic inflammation.
  • Bacterial lipopolysaccharide models systemic inflammation in animals, inducing thermoeffector responses.

Purpose of the Study:

  • To explore the roles of fever and hypothermia in systemic inflammation.
  • To identify mediators of fever and hypothermia.
  • To understand the host defense benefits of these temperature changes.

Main Methods:

  • Review of animal studies and human clinical trials.
  • Analysis of inflammatory mediators, including prostaglandins and cytokines.
  • Investigation of cellular sources of mediator synthesis (macrophages, endothelial cells).

Main Results:

  • Prostaglandin E2 (PGE2), synthesized by cyclooxygenase-2 and microsomal PGE2 synthase-1, is a key mediator of fever.
  • Blood PGE2 and PGE2 synthesized at the blood-brain barrier maintain fever.
  • Mediators of hypothermia are not well-established.
  • Fever is beneficial for mild infections, while hypothermia benefits severe inflammation and infection.

Conclusions:

  • Fever and hypothermia are regulated host defense mechanisms against pathogens.
  • Understanding these thermoeffector responses is crucial for managing systemic inflammation.
  • Further research is needed to elucidate hypothermia mediators.