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1.
International Journal of Occupational Safety and Health ; 12(3):163-170, 2022.
Article in English | Scopus | ID: covidwho-1963341

ABSTRACT

Introduction: Doctors are at increased risk of exposure to the SARS-CoV-2 virus, and the use of N95 respirators has emerged as a critical preventive measure. We studied the real-world experiences, practices, and adverse effects of N95 respirator usage amongst Indian physicians. Methods: We conducted an analytical, cross-sectional online survey between November 2020 and January 2021. Real-world usage characteristics of N-95 respirators were collected via a pre-validated questionnaire and compared amongst different sub-cohorts. Results: A total of 453 responses from physicians were analyzed. The most important adjunct to the N95 respirator perceived by the respondents was the full-face shield (81.9%). Most doctors had to purchase extra masks per month (median = 5 ± 8), which was more among the medical specialties (p = 0.006). The highest mean VAS scores for adverse events reported were for breathing on exertion (6.62 ± 2.25) and ear pain (6.34 ± 2.69). VAS ear pain was higher in ages < 40 and doctors working in the public sector (p = 0.017 and p = 0.019 respectively). Conclusion: Despite many inadequacies regarding proper mask removal, doffing techniques, and multiple reported prolonged mask usage-related adverse effects, there is generally good adherence to protocols and good practices of mask usage amongst physicians in the hospital setting. This journal is licensed under a Creative Commons Attribution-Non Commercial 4.0 International License.

2.
Mol Med ; 26(1): 98, 2020 10 30.
Article in English | MEDLINE | ID: covidwho-894987

ABSTRACT

BACKGROUND: Mechanical ventilation, in combination with supraphysiological concentrations of oxygen (i.e., hyperoxia), is routinely used to treat patients with respiratory distress, such as COVID-19. However, prolonged exposure to hyperoxia compromises the clearance of invading pathogens by impairing macrophage phagocytosis. Previously, we have shown that the exposure of mice to hyperoxia induces the release of the nuclear protein high mobility group box-1 (HMGB1) into the pulmonary airways. Furthermore, extracellular HMGB1 impairs macrophage phagocytosis and increases the mortality of mice infected with Pseudomonas aeruginosa (PA). The aim of this study was to determine whether GTS-21 (3-(2,4-dimethoxybenzylidene) anabaseine), an α7 nicotinic acetylcholine receptor (α7nAChR) agonist, could (1) inhibit hyperoxia-induced HMGB1 release into the airways; (2) enhance macrophage phagocytosis and (3) increase bacterial clearance from the lungs in a mouse model of ventilator-associated pneumonia. METHOD: GTS-21 (0.04, 0.4, and 4 mg/kg) or saline were administered by intraperitoneal injection to mice that were exposed to hyperoxia (≥ 99% O2) and subsequently challenged with PA. RESULTS: The systemic administration of 4 mg/kg i.p. of GTS-21 significantly increased bacterial clearance, decreased acute lung injury and decreased accumulation of airway HMGB1 compared to the saline control. To determine the mechanism of action of GTS-21, RAW 264.7 cells, a macrophage-like cell line, were incubated with different concentrations of GTS-21 in the presence of 95% O2. The phagocytic activity of macrophages was significantly increased by GTS-21 in a dose-dependent manner. In addition, GTS-21 significantly inhibited the cytoplasmic translocation and release of HMGB1 from RAW 264.7 cells and attenuated hyperoxia-induced NF-κB activation in macrophages and mouse lungs exposed to hyperoxia and infected with PA. CONCLUSIONS: Our results indicate that GTS-21 is efficacious in improving bacterial clearance and reducing acute lung injury via enhancing macrophage function by inhibiting the release of nuclear HMGB1. Therefore, the α7nAChR represents a possible pharmacological target to improve the clinical outcome of patients on ventilators by augmenting host defense against bacterial infections.


Subject(s)
Benzylidene Compounds/pharmacology , Hyperoxia/immunology , Macrophages, Alveolar/drug effects , Pseudomonas Infections/drug therapy , Pyridines/pharmacology , Ventilator-Induced Lung Injury/drug therapy , alpha7 Nicotinic Acetylcholine Receptor/antagonists & inhibitors , Animals , Disease Models, Animal , HMGB1 Protein/metabolism , Hyperoxia/diet therapy , Macrophages, Alveolar/immunology , Macrophages, Alveolar/metabolism , Male , Mice , Mice, Inbred C57BL , Phagocytosis/drug effects , Pseudomonas aeruginosa , RAW 264.7 Cells
3.
Mol Med ; 26(1): 63, 2020 06 29.
Article in English | MEDLINE | ID: covidwho-617382

ABSTRACT

BACKGROUND: Oxygen therapy, using supraphysiological concentrations of oxygen (hyperoxia), is routinely administered to patients who require respiratory support including mechanical ventilation (MV). However, prolonged exposure to hyperoxia results in acute lung injury (ALI) and accumulation of high mobility group box 1 (HMGB1) in the airways. We previously showed that airway HMGB1 mediates hyperoxia-induced lung injury in a mouse model of ALI. Cholinergic signaling through the α7 nicotinic acetylcholine receptor (α7nAChR) attenuates several inflammatory conditions. The aim of this study was to determine whether 3-(2,4 dimethoxy-benzylidene)-anabaseine dihydrochloride, GTS-21, an α7nAChR partial agonist, inhibits hyperoxia-induced HMGB1 accumulation in the airways and circulation, and consequently attenuates inflammatory lung injury. METHODS: Mice were exposed to hyperoxia (≥99% O2) for 3 days and treated concurrently with GTS-21 (0.04, 0.4 and 4 mg/kg, i.p.) or the control vehicle, saline. RESULTS: The systemic administration of GTS-21 (4 mg/kg) significantly decreased levels of HMGB1 in the airways and the serum. Moreover, GTS-21 (4 mg/kg) significantly reduced hyperoxia-induced acute inflammatory lung injury, as indicated by the decreased total protein content in the airways, reduced infiltration of inflammatory monocytes/macrophages and neutrophils into the lung tissue and airways, and improved lung injury histopathology. CONCLUSIONS: Our results indicate that GTS-21 can attenuate hyperoxia-induced ALI by inhibiting extracellular HMGB1-mediated inflammatory responses. This suggests that the α7nAChR represents a potential pharmacological target for the treatment regimen of oxidative inflammatory lung injury in patients receiving oxygen therapy.


Subject(s)
Acute Lung Injury/etiology , Acute Lung Injury/metabolism , Benzylidene Compounds/pharmacology , HMGB1 Protein/metabolism , Hyperoxia/complications , Nicotinic Agonists/pharmacology , Pyridines/pharmacology , Acute Lung Injury/drug therapy , Acute Lung Injury/pathology , Animals , Biomarkers , Disease Susceptibility , HMGB1 Protein/blood , HMGB1 Protein/genetics , Immunohistochemistry , Male , Mice , Models, Biological
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