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Mismatch Repair01:36

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Related Experiment Video

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Surfactant Dysfunction in ARDS and Bronchiolitis is Repaired with Cyclodextrins.

Mustafa Al-Saiedy1, Lasantha Gunasekara1, Francis Green1,2

  • 1Snyder Institute of Chronic Diseases, University of Calgary, Calgary, Alberta, Canada T2N 4Z6.

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Cyclodextrins can restore surfactant function impaired in acute respiratory distress syndrome (ARDS) and bronchiolitis. This drug may offer a novel treatment for ARDS caused by various injuries.

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Area of Science:

  • Pulmonary Medicine
  • Biochemistry

Background:

  • Acute respiratory distress syndrome (ARDS) involves surfactant dysfunction, leading to alveolar collapse and hypoxemia.
  • Causes of ARDS include toxic inhalation, barotrauma, aspiration, and burns.

Purpose of the Study:

  • To investigate mechanisms of surfactant dysfunction in ARDS and bronchiolitis.
  • To evaluate the therapeutic potential of cyclodextrins in restoring surfactant function.

Main Methods:

  • Utilized in vitro models, a mouse model of ARDS, and human patient samples.
  • Measured surface tension using captive bubble surfactometry.
  • Assessed the effects of methyl-β-cyclodextrin (MβCD) on surfactant function.

Main Results:

  • Surfactant inhibition was observed in patient samples and ARDS mice.
  • Elevated cholesterol and oxidized phospholipids contributed to surfactant impairment.
  • Methyl-β-cyclodextrin (MβCD) successfully restored surfactant function in both human and animal models.
  • MβCD demonstrated anti-inflammatory effects.

Conclusions:

  • Inhaled cyclodextrins show promise for treating ARDS.
  • Potential application in managing ARDS following combat-related injuries or exposures.