Validity and reliability of the multidimensional health locus of control scale for college students

<p>Abstract</p> <p>Background</p> <p>The purpose of the present study was to assess the validity and reliability of Form A of Multidimensional Health Locus of Control scales in Iran. Health locus of control is one of the most widely measured parameters of health belief for the planning of health education programs.</p> <p>Methods</p> <p>496 university students participated in this study. The reliability coefficients were calculated in three different methods: test-retest, parallel forms and Cronbach alpha. In order to survey validity of the scale we used three methods including content validity, concurrent validity and construct validity.</p> <p>Results</p> <p>We established the content validity of the Persian translation by translating (and then back-translating) each item from the English version into the Persian version. The concurrent validity of the questionnaire, as measured by Levenson's IPC scale was .57 (P < .001), .49 (P < .01) and .53 (P < .001) for IPC, respectively. Exploratory principal components analysis supported a three-factor structure that items loading adequately on each factor. Moreover, the approximate orthogonal of the dimensions were obtained through correlation analyses. In addition, the reliability results were acceptable, too.</p> <p>Conclusion</p> <p>The results showed that the reliability and validity of Persian Form A of MHLC was acceptable and respectable and is suggested as an applicable criterion for similar studies in Iran.</p

Identification of a Common Gene Expression Response in Different Lung Inflammatory Diseases in Rodents and Macaques

To identify gene expression responses common to multiple pulmonary diseases we collected microarray data for acute lung inflammation models from 12 studies and used these in a meta-analysis. The data used include exposures to air pollutants; bacterial, viral, and parasitic infections; and allergic asthma models. Hierarchical clustering revealed a cluster of 383 up-regulated genes with a common response. This cluster contained five subsets, each characterized by more specific functions such as inflammatory response, interferon-induced genes, immune signaling, or cell proliferation. Of these subsets, the inflammatory response was common to all models, interferon-induced responses were more pronounced in bacterial and viral models, and a cell division response was more prominent in parasitic and allergic models. A common cluster containing 157 moderately down-regulated genes was associated with the effects of tissue damage. Responses to influenza in macaques were weaker than in mice, reflecting differences in the degree of lung inflammation and/or virus replication. The existence of a common cluster shows that in vivo lung inflammation in response to various pathogens or exposures proceeds through shared molecular mechanisms

Transcriptional profiling of the acute pulmonary inflammatory response induced by LPS: role of neutrophils

<p>Abstract</p> <p>Background</p> <p>Lung cancer often develops in association with chronic pulmonary inflammatory diseases with an influx of neutrophils. More detailed information on inflammatory pathways and the role of neutrophils herein is a prerequisite for understanding the mechanism of inflammation associated cancer.</p> <p>Methods</p> <p>In the present study, we used microarrays in order to obtain a global view of the transcriptional responses of the lung to LPS in mice, which mimics an acute lung inflammation. To investigate the influence of neutrophils in this process, we depleted mice from circulating neutrophils by treatment with anti-PMN antibodies prior to LPS exposure.</p> <p>Results</p> <p>A total of 514 genes was greater than 1.5-fold differentially expressed in the LPS induced lung inflammation model. 394 of the 514 were up regulated genes mostly involved in cell cycle and immune/inflammation related processes, such as cytokine/chemokine activity and signalling. Down regulated genes represented nonimmune processes, such as development, metabolism and transport. Notably, the number of genes and pathways that were differentially expressed, was reduced when animals were depleted from circulating neutrophils, confirming the central role of neutrophils in the inflammatory response. Furthermore, there was a significant correlation between the differentially expressed gene list and the promutagenic DNA lesion M₁dG, suggesting that it is the extent of the immune response which drives genetic instability in the inflamed lung. Several genes that were specifically regulated by the presence of activated neutrophils could be identified and these were mostly involved in interferon signalling, oxidative stress response and cell cycle progression. The latter possibly refers to a higher rate of cell turnover in the inflamed lung with neutrophils, suggesting that the neutrophil influx is associated with a higher risk for the accumulation and fixation of mutations.</p> <p>Conclusion</p> <p>Gene expression profiling identified specific genes and pathways that are related to neutrophilic inflammation and could be associated to cancer development and indicate an active role of neutrophils in mediating the LPS induced inflammatory response in the mouse lung.</p

Systems biology ter verbreding van de toepasbaarheid van in vitro testen in de toxicologie

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