Several sources of evidence, including investigations of pathogenesis and observational studies, support the hypothesis that environmental agents may have an etiologic role in idiopathic pulmonary fibrosis (IPF). Since 1990, six case-control studies have been conducted in three countries and have consistently demonstrated increased risk of IPF with exposures to a number of environmental and occupational agents. In a meta-analysis of these studies, six exposures were significantly associated with IPF (summary odds ratios [95% confidence intervals]), including ever smoking (1.58 [1.27-1.97]), agriculture/farming (1.65 [1.20-2.26]), livestock (2.17 [1.28-3.68]), wood dust (1.94 [1.34-2.81]), metal dust (2.44 [1.74-3.40]), and stone/sand (1.97 [1.09-3.55]). Although there are a number of limitations of the case-control design and these results alone do not establish a causal link, an assessment of all of the available evidence strongly suggests that IPF may be a heterogeneous disorder caused by a number of environmental and occupational exposures.

https://www.atsjournals.org/doi/pdf/10.1513/pats.200512-131TK

Is idiopathic pulmonary fibrosis an environmental disease

At the beginning of the last century, Pasteur described postoperative pulmonary atelectasis, 58 analysed postoperative pulmonary complications (PCC; see below) and noted: ‘when the true history of postoperative lung complications comes to be written, active collapse of the lung, from deficiency of inspiratory power, will be found to occupy an important position among determining causes’. 59 Indeed, atelectasis occurs regularly during general anaesthesia induction, 46 persists postoperatively 44 and may contribute to significant morbidity 78 and additional healthcare costs. 43 This review article will review the mechanism of perioperative atelectasis, discuss its clinical significance and describe preventive measures.

New concepts of atelectasis during general anaesthesia

The respiratory response to hypoxia in mammals develops from an inhibition of breathing movements in utero into a sustained increase in ventilation in the adult. This ventilatory response to hypoxia (HVR) in mammals is the subject of this review. The period immediately after birth contains a critical time window in which environmental factors can cause long-term changes in the structural and functional properties of the respiratory system, resulting in an altered HVR phenotype. Both neonatal chronic and chronic intermittent hypoxia, but also chronic hyperoxia, can induce such plastic changes, the nature of which depends on the time pattern and duration of the exposure (acute or chronic, episodic or not, etc.). At adult age, exposure to chronic hypoxic paradigms induces adjustments in the HVR that seem reversible when the respiratory system is fully matured. These changes are orchestrated by transcription factors of which hypoxia-inducible factor 1 has been identified as the master regulator. We discuss the mechanisms underlying the HVR and its adaptations to chronic changes in ambient oxygen concentration, with emphasis on the carotid bodies that contain oxygen sensors and initiate the response, and on the contribution of central neurotransmitters and brain stem regions. We also briefly summarize the techniques used in small animals and in humans to measure the HVR and discuss the specific difficulties encountered in its measurement and analysis.

The Ventilatory Response to Hypoxia in Mammals: Mechanisms, Measurement, and Analysis

Phase I study of 131I-anti-CD45 antibody plus cyclophosphamide and total body irradiation for advanced acute leukemia and myelodysplastic syndrome

Asbestosis is an inflammatory and fibrotic process of the alveolar structures mediated, at least in part, by cytokines released by “activated” alveolar macrophages. The process of phagocytosis and “activation” of alveolar macrophages is poorly understood. Are all macrophages activated or only subpopulations? Which cytokines are up-regulated? How does the local milieu modulate profibrotic and antifibrotic mediators? Is protein release accompanied by up-regulation of gene transcription? Is there an ordered sequence of cytokine activity? What roles do neutrophils and lymphocytes play? How can disease progression best be quantified absent further exposure? Answers to these questions are important to direct rational strategies at interdicting the fibrotic process.The question of cancer and asbestos is more vexing. The processes of inflammation, fibrosis, and carcinogenesis appear to be closely intertwined. For example, proto-oncogenes such as c-sis (PDGF B-chain) are up-regulated in activated alveolar macropha...

Cellular and molecular basis of the asbestos-related diseases.

This paper presents results of a study conducted with undergraduate students involved in either problemor project-based curricula (Medicine and Engineering, respectively) at the Université de Sherbrooke, Canada. The objective of the present research was to measure the impact of these innovative curricula on students’ engagement and persistence in higher education. Our research question was: What determinants better predict students’ engagement and persistence in innovative curricula such as PBL? Nine variables were examined as potential predictors of both factors (engagement and persistence). Results showed a variation in variables predicting engagement and persistence, with the most significant predictor being stress related.

/pdf/problem-based-and-project-based-learning-in-engineering-and-44b2xditl0.pdf

Problem-based and Project-based Learning in Engineering and Medicine: Determinants of Students' Engagement and Persistance

The contribution of the carotid body chemoreceptor to postnatal maturation of breathing was evaluated in lambs from 7 to 70 days of age. The study was conducted by comparing the eupneic ventilation...

Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs.

The ventilatory response to hypoxia in the newborn lamb after carotid body denervation

To analyze the clinical features of asbestos-induced alveolitis and stage its activity, we evaluated 217 asbestos workers by the usual clinical, radiological, and functional parameters and computerized gallium 67(Ga) lung scan; we obtained bronchoalveolar lavage (BAL) in 33 and lung biopsy in 6. In addition, we scored the profusion of lung rales and correlated it with other parameters of severity of asbestosis. In the 55 workers without asbestosis and normal 67Ga scan, BAL analyses were comparable to those of controls. Of the 56 without asbestosis but increased 67Ga lung uptake, BAL analyses in 8 documented a predominantly macrophagic alveolitis (confirmed on lung biopsy in 3), with the highest levels of BAL fibronectin. In the 106 workers with asbestosis, 67Ga lung uptake was increased in 75; BAL in 17 demonstrated a macrophagic and neutro-philic alveolitis with elevated fibronectin levels. Lung biopsy in 3 of the latter workers documented peribronchiolar fibrosing alveolitis. Rale scores in all workers or in those without asbestosis did not correlate with 67Ga scores; they correlated fairly well with profusion of parenchymal opacities (Rs = 0.42) and rigidity of the lung pressure-volume curve (Rs = 0.39). Thus, 67Ga lung uptake is an early indicator of chronic macrophagic alveolitis in asbestos workers, which usually progresses to asbestosis. In the disease, profusion of lung rales constitutes a simple clinical mode of assessment of disease severity that correlates better with radiological and functional parameters than with parameters of alveolitis.

Daniel Dalle

Papers

Problem-based and Project-based Learning in Engineering and Medicine: Determinants of Students' Engagement and Persistance

Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs.

The ventilatory response to hypoxia in the newborn lamb after carotid body denervation

Clinical features to stage alveolitis in asbestos workers.

Computer analysis of bowel sounds.