An open systems approach to risk assessment

1994 ◽  
Vol 26 (3) ◽  
pp. 427-427 ◽  
Author(s):  
Sheldon Wilfred Samuels
1994 ◽  
Vol 25 (3) ◽  
pp. 447-453 ◽  
Author(s):  
Sheldon Wilfred Samuels

2011 ◽  
Vol 21 (6) ◽  
pp. 789-818 ◽  
Author(s):  
Roxanne M. Mitchell ◽  
C. John Tarter

This study replicated an earlier study conducted by Tarter and Hoy (2004) in which an open systems model was used to test a series of hypotheses that explained elements of school performance. Four internal system elements (structure, individual, culture, and politics) of the school were used to explain two sets of school outcomes (student achievement and teachers’ assessment of overall school effectiveness) in a sample of 110 Catholic elementary schools in one Northeastern city. Correlational and multiple regression analyses were used to test the relationships. The results of this study further confirmed the usefulness of this model in understanding the factors that contribute to quality in elementary schools.


2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Anita R. Iskandar ◽  
Florian Martin ◽  
Marja Talikka ◽  
Walter K. Schlage ◽  
Radina Kostadinova ◽  
...  

Capturing the effects of exposure in a specific target organ is a major challenge in risk assessment. Exposure to cigarette smoke (CS) implicates the field of tissue injury in the lung as well as nasal and airway epithelia. Xenobiotic metabolism in particular becomes an attractive tool for chemical risk assessment because of its responsiveness against toxic compounds, including those present in CS. This study describes an efficient integration from transcriptomic data to quantitative measures, which reflect the responses against xenobiotics that are captured in a biological network model. We show here that our novel systems approach can quantify the perturbation in the network model of xenobiotic metabolism. We further show that this approach efficiently compares the perturbation upon CS exposure in bronchial and nasal epithelial cellsin vivosamples obtained from smokers. Our observation suggests the xenobiotic responses in the bronchial and nasal epithelial cells of smokers were similar to those observed in their respective organotypic models exposed to CS. Furthermore, the results suggest that nasal tissue is a reliable surrogate to measure xenobiotic responses in bronchial tissue.


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