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Related Concept Videos

Epistaxis01:30

Epistaxis

478
Epistaxis, or nosebleeds, occurs when small, swollen blood vessels in the nasal mucous membrane rupture. Typically, the anterior septum is the primary site of occurrence.
Etiology
Possible causes of this condition include high blood pressure, trauma, low humidity, upper respiratory tract infections, allergies, foreign bodies, nasal inhalation of corticosteroids or illicit drugs, excessive use of decongestant nasal sprays, facial or nasal surgery, anatomic malformation, tumors, or systemic...
478

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Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
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Arginase Isoform Expression in Chronic Rhinosinusitis.

Diana Vlad1,2, Silviu Albu3,4

  • 1Second Department of Otolaryngology, University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca 400489, Romania. diagav@yahoo.com.

Journal of Clinical Medicine
|November 6, 2019
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Summary

Chronic rhinosinusitis (CRS) is linked to low nitric oxide (NO). This study found higher arginase II (ARG2) activity in CRS patients, suggesting ARG2 upregulation contributes to specific CRS types.

Keywords:
arginasearginase isoformchronic rhinosinusitisnitric oxide

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Area of Science:

  • Immunology
  • Otolaryngology
  • Biochemistry

Background:

  • Nitric oxide (NO) is crucial for upper airway inflammation control.
  • Increased arginase activity reduces NO by limiting L-arginine availability.
  • Chronic rhinosinusitis (CRS) is associated with diminished nasal NO (nNO).

Purpose of the Study:

  • Investigate arginase I (ARG1) and arginase II (ARG2) activity in CRS.
  • Determine the role of arginase activity in CRS pathogenesis.
  • Explore the link between arginase expression and nNO levels in CRS.

Main Methods:

  • Collected sinonasal mucosa samples from CRS patients (n=36) and controls (n=29).
  • Quantified arginase I and II mRNA levels using real-time PCR.
  • Analyzed ARG2 expression in relation to CRS phenotypes (e.g., non-polypotic, non-allergic, non-asthmatic).

Main Results:

  • Arginase I activity was low across all samples.
  • ARG2 mRNA levels were significantly elevated in CRS patients compared to controls (FR 2.22 vs. 1.31, p=0.016).
  • Increased ARG2 expression was observed in specific CRS phenotypes: without nasal polyposis (FR 3.14), non-allergic CRS (FR 2.55), and non-asthmatic CRS (FR 2.42).

Conclusions:

  • Upregulation of ARG2 is implicated in the pathogenesis of certain CRS phenotypes.
  • Elevated ARG2 may contribute to reduced NO levels in CRS.
  • Further research is warranted to explore ARG2 as a therapeutic target in CRS.