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Respiratory Protection (respiratory + protection)

Distribution by Scientific Domains
Medical Sciences50%

Selected Abstracts

Respiratory protection of nitrogenase in Azotobacter species: is a widely held hypothesis unequivocally supported by experimental evidence?

FEMS MICROBIOLOGY REVIEWS, Issue 4 2000
Jürgen Oelze
Abstract The hypothesis of respiratory protection, originally formulated on the basis of results obtained with Azotobacter species, postulates that consumption of O2 at the surface of diazotrophic prokaryotes protects nitrogenase from inactivation by O2. Accordingly, it is assumed that, at increased ambient O2 concentrations, nitrogenase activity depends on increased activities of a largely uncoupled respiratory electron transport system. The present review compiles evidence indicating that cellular O2 consumption as well as both the activity and the formation of the respiratory system of Azotobacter vinelandii are controlled by the C/N ratio, that is to say the ratio at which the organism consumes the substrate (i.e. the source of carbon, reducing equivalents and ATP) per source of compound nitrogen. The maximal respiratory capacity which can be attained at increased C/N ratios, however, is controlled, within limits, by the ambient O2 concentration. When growth becomes N-limited at increased C/N ratios, cells synthesize nitrogenase and fix N2. Under these diazotrophic conditions, cellular O2 consumption remains constant at a level controlled by the O2 concentration. Control by O2 has been studied on the basis of both whole cell respiration and defined segments of the respiratory electron transport chain. The results demonstrate that the effect of O2 on the respiratory system is restricted to the lower range of O2 concentrations up to about 70 ,M. Nevertheless, azotobacters are able to grow diazotrophically at dissolved O2 concentrations of up to about 230 ,M indicating that respiratory protection is not warranted at increased ambient O2 concentrations. This conclusion is supported and extended by a number of results largely excluding an obvious relationship between nitrogenase activity and the actual rate of cellular O2 consumption. On the basis of theoretical calculations, it is assumed that the rate of O2 diffusion into the cells is not significantly affected by respiration. All of these results lead to the conclusion that, in the protection of nitrogenase from O2 damage, O2 consumption at the cell surface is less effective than generally assumed. It is proposed that alternative factors like the supply of ATP and reducing equivalents are more important. [source]

Upper and lower respiratory diseases after occupational and environmental disasters

MOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 2 2008
David J. Prezant MD
Abstract Respiratory consequences from occupational and environmental disasters are the result of inhalation exposures to chemicals, particulate matter (dusts and fibers) and/or the incomplete products of combusion that are often liberated during disasters such as fires, building collapses, explosions and volcanoes. Unfortunately, experience has shown that environmental controls and effective respiratory protection are often unavailable during the first days to week after a large-scale disaster. The English literature was reviewed using the key words,disaster and any of the following: respiratory disease, pulmonary, asthma, bronchitis, sinusitis, pulmonary fibrosis, or sarcoidosis. Respiratory health consequences after aerosolized exposures to high-concentrations of particulates and chemicals can be grouped into 4 major caterogies: 1) upper respiratory disease (chronic rhinosinusitis and reactive upper airways dysfunction syndrome), 2) lower respiratory diseases (reactive [lower] airways dysfunction syndrome, irritant-induced asthma, and chronic obstructive airways diseases), 3) parenchymal or interstitial lung diseases (sarcoidosis, pulmonary fibrosis, and bronchiolitis obliterans, and 4) cancers of the lung and pleura. This review describes several respiratory consequences of occupational and environmental disasters and uses the World Trade Center disaster to illustrate in detail the consequences of chronic upper and lower respiratory inflammation. Mt Sinai J Med 75:89,100, 2008. © 2008 Mount Sinai School of Medicine [source]

Occupational tuberculosis following extremely short exposure

THE CLINICAL RESPIRATORY JOURNAL, Issue 1 2009
Zaza Kamper-Jørgensen
Abstract Introduction:, Transmission of Mycobacterium tuberculosis (MT) in most cases requires extended exposure. Objectives:, To document that MT transmission may occur even after very short exposure. Material and Methods:, All first-time culture-confirmed tuberculosis (TB) cases in Denmark have since 1992 been subjected to genotyping, using the IS6110 -Restriction Fragment Length Polymorphism (RFLP) technique. A young nurse with no risk factors developed pulmonary TB: the DNA pattern of her MT strain was compared to The Danish TB Subtyping Database, comprising >6000 DNA patterns from TB patients nationwide. Results:, Only one single MT DNA pattern matched the DNA profile of the isolate from the nurse. The pattern originated from a patient shortly admitted to the department where she worked at the time. MT transmission had occurred in spite of very short exposure. Conclusion:, By adding modern molecular epidemiological methods to traditional epidemiological surveys, a more detailed picture of MT-transmission pathways can be obtained, showing that MT transmission can occur even after extremely short exposure. This stresses the necessity for adequate respiratory protection among hospital staff taking care of patients with pulmonary symptoms suspected for TB. Please cite this paper as: Kamper-Jørgensen Z, Lillebaek T and Andersen ÅB. Occupational tuberculosis following extremely short exposure. The Clinical Respiratory Journal 2009; 3: 55,57. [source]