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Biomedical subjects

R Hajela

Publications and source records attributed to R Hajela.

12 recordsLinked to original sources
PubMed1996

Family physicians and smoking cessation. Survey of practices, opinions, and barriers.

OBJECTIVES: To assess what family physicians need to promote smoking cessation by looking at current knowledge, attitudes, and behaviours and to examine the barriers facing physicians in implementing an effective antismoking strategy. DESIGN: Cross-sectional study involving face-to-face interviews and mailed questionnaires. SETTING: Family practices in Kingston, Ont, and surrounding areas. PARTICIPANTS: All family physicians (n = 155) in the City of Kingston and the counties of Frontenac, Lennox, and Addington. MAIN OUTCOME MEASURES: Knowledge, attitudes, beliefs, and practices concerning smoking cessation; barriers and practices recommended in the literature. RESULTS: Response rate was 77%. Many physicians know about smoking cessation, and many actively counsel their patients to quit. Brief advice, nicotine replacement therapy, self-help materials, and follow-up appointments are the most common methods. Although many report that they are already knowledgeable, many are willing to learn more. Many physicians have unrealistically high estimates of the probability of success, and many find poor compliance among patients to be the greatest barrier. CONCLUSIONS: Family physicians in this are recognize the need to help their patients to quit and are identifying and counseling smokers in their practices. The main educational need could be to appreciate smoking as an addictive behaviour.

Cross-Sectional Studies↗
PubMed1991

Effects of smoke inhalation on surfactant phospholipids and phospholipase A2 activity in the mouse lung.

The effects of smoke inhalation on the pulmonary surfactant system were examined in mice exposed for 30 minutes to smoke generated from the burning of polyurethane foam. At 8 or 12 hours after exposure, surfactants were isolated separately from lung lavage (extracellular surfactant) and residual lung tissue (intracellular surfactant) for phospholipid analysis. Calcium-dependent phospholipase A2 (PLA2) was measured on a microsomal fraction prepared from the tissue homogenate. Smoke inhalation produced a twofold increase in extracellular surfactant total phospholipid. While there was no change in the total phospholipid or phosphatidylcholine (PC) content of the intracellular surfactant, smoke inhalation significantly decreased the disaturated species of PC (DSPC). The specific activity of PLA2 was reduced by more than 50% in both groups of exposed mice. Smoke inhalation appears to result in selective depletion of the DSPC of intracellular surfactant and PLA2 involved in its synthesis. This depletion may be compensated for by increased secretion or slower breakdown of the material present in the extracellular compartment.

Animals↗
PubMed1990

Fatal pulmonary edema due to nitric acid fume inhalation in three pulp-mill workers.

Three young men died of rapidly progressive pulmonary edema of delayed onset after inhalation of fumes from an accidental nitric acid explosion. Electron microscopy revealed altered neutrophils and necrotic endothelial cells in alveolar capillaries. Immunohistochemistry showed small and large serum proteins, including immunoglobulin M, in the edema fluid and hyaline membranes. Increased permeability is a consequence of direct microvascular injury by inhaled nitrogen dioxide. However, our findings, implicating neutrophils and serum-derived mediators in the pathogenesis of the pulmonary edema, are consistent with recent proposals on their roles in the maintenance and/or progression of edema initiated by toxic inhalations.

Accidents, Occupational↗