Lung disease structure

Cor pulmonale Right-sided heart failure, usually due to structural lung disease (e.g., pulmonary fibrosis or emphysema). 

Fig.l. Expression of CC and CXC chemokine receptors by inflammatory and structural cells in allergic lung disease. Eos, eosinophil Mac, macrophage Mono, monocyte. 

Expression of Chemokine Receptors by Leukocytes and Structural Cells in Allergic Lung Disease... 

A variety of cell culture systems for the modelling of the tracheo-bronchial epithelium are available. These include primary cultures and cell lines of human and animal origins, plus airway cells with characteristics of lung disease such as CF. The advantages and limitations of using a simple culture system compared to one that recreates to a greater extent the epithelial structure and function in vitro should be considered according to the pre-clinical application required. However, this choice is complicated by the lack of comparative data, both between the different cell systems and for in vitro-in vivo correlation, upon which to base such decisions. 

Models of Lung Disease Microscopy and Structural Methods, edited by J. Gil... 

These results indicated that clinical PA isolates from various infections display marked heterogeneity with respect to the acylation state of their lipid A, reflecting differences in selective pressure that these infections impose on PA lipid A synthesis and structural modifications. Further study of the synthesis and regulation of lipid A modifications that are associated with CF lung disease is needed to understand their role in antibiotic resistance and other adaptations that are relevant to this specialized niche. 

Mandel, G. and Mandel, N., The structure of crystalline Si02, In Silica and Silica-Induced Lung Diseases, Castranova, V., Vallyathan, V., and Wallace, W.E., Eds., CRC Press, Boca Raton, FL, 1996, p. 63. 

Harrison NK, Myers AR, Corrin B, Soosay G,DewarA,etal. 1991. Structural features of interstitial lung disease in systemic sclerosis. Am. Rev. Respir. Dis. 144 706-13... 

Hopkins N, McLoughlin P. The structural basis of pulmonary hypertension in chronic lung disease remodeling, rarefaction or angiogenesis J Anat 2002 201(4) 335-48. 

Mechanisms based on electron transfer and active oxygen species have been proposed to explain asbestos-induced toxicity and lung disease. Fisher et al. (1987) studied the effect of heat treatment on chrysotile asbestos toxicity. The in vitro study showed that heat treatment reduced cytotoxicity. Infra red spectra indicated a reduction of external hydroxyl group population, which repopulated after irradiation. There is, apparently, an electron transfer from the asbestos matrix to biological receptors. In an earlier study, Fisher and coworkers (1985) reported that irradiation of chrysotile samples heated to 400°C (752°F) restored the biological activity to near-control values. X-ray diffraction pattern showed no change in the crystal structure. Brucite, present as a surface contaminant, was removed by heating. 

Draw a chemical structure for diacetyl (2,3-butanedione), a diketone (see Table 1.6) with the C4H6O2 chemical formula. Diacetyl is used as a flavoring for microwave popcorn, but has been under scrutiny of late as a possible causative agent for bronchiolitis obliterans, often referred to as popcorn lung disease. 

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