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Related Concept Videos

Atypical Pneumonia01:14

Atypical Pneumonia

Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...
Pneumonia I: Introduction01:29

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...
Pneumonia I: Introduction01:30

Pneumonia I: Introduction

Pneumonia is an acute respiratory infection that targets the lungs, specifically the alveoli. These tiny air sacs, essential for oxygen exchange, become engorged with pus and fluid, severely hindering breathing, decreasing oxygen absorption, and causing significant pain and discomfort during respiration.
Risk Factors
Various factors influence the likelihood of developing pneumonia. Age plays a crucial role, with infants, children under two, and individuals over 65 at increased risk due to their...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.

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Related Experiment Video

Updated: May 21, 2026

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
07:27

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

Published on: July 12, 2018

[Amyloidosis in pneumology].

Lars Hagmeyer1, S Stieglitz, C Röcken

  • 1Krankenhaus Bethanien gGmbH, Klinik für Pneumologie und Allergologie, Zentrum für Schlaf- und Beatmungsmedizin, Solingen. lars.hagmeyer@klinikbethanien.de

Pneumologie (Stuttgart, Germany)
|June 14, 2012
PubMed
Summary

Amyloidosis, a rare lung disorder, is often missed in diagnosis due to varied symptoms. Early biopsy and protein subtyping are crucial for identifying treatable causes and guiding therapy.

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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice

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The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats
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The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats

Published on: March 8, 2019

Related Experiment Videos

Last Updated: May 21, 2026

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
07:27

Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa

Published on: July 12, 2018

Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
15:43

Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice

Published on: March 17, 2014

The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats
07:29

The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats

Published on: March 8, 2019

Area of Science:

  • Pneumology and rare diseases
  • Protein misfolding disorders
  • Systemic and localized manifestations

Context:

  • Amyloidosis is infrequently considered in respiratory diagnostics.
  • Unreported cases may be significant.
  • Diverse clinical presentations challenge diagnosis.

Purpose:

  • To review the pathophysiology, classification, diagnostics, and therapeutics of amyloidosis.
  • To highlight pulmonary manifestations and treatment options.
  • To increase awareness of amyloidosis in clinical practice.

Summary:

  • Amyloidosis diagnosis requires awareness of its varied clinical signs.
  • Early tissue biopsy and Congo red staining are key diagnostic steps.
  • Subtyping amyloid protein identifies treatable causes and guides therapy.

Impact:

  • Improved diagnostic rates for pulmonary amyloidosis.
  • Timely initiation of appropriate systemic or local treatments.
  • Enhanced understanding of amyloidosis management strategies.