Review of Application of Artificial Neural Networks in Textiles and Clothing Industries over Last Decades

2010-2011 > Academic research: refereed > Chapter in an edited book (author

Genetic Ancestry, Social Classification, and Racial Inequalities in Blood Pressure in Southeastern Puerto Rico

The role of race in human genetics and biomedical research is among the most contested issues in science. Much debate centers on the relative importance of genetic versus sociocultural factors in explaining racial inequalities in health. However, few studies integrate genetic and sociocultural data to test competing explanations directly.We draw on ethnographic, epidemiologic, and genetic data collected in Southeastern Puerto Rico to isolate two distinct variables for which race is often used as a proxy: genetic ancestry versus social classification. We show that color, an aspect of social classification based on the culturally defined meaning of race in Puerto Rico, better predicts blood pressure than does a genetic-based estimate of continental ancestry. We also find that incorporating sociocultural variables reveals a new and significant association between a candidate gene polymorphism for hypertension (alpha(2C) adrenergic receptor deletion) and blood pressure.This study addresses the recognized need to measure both genetic and sociocultural factors in research on racial inequalities in health. Our preliminary results provide the most direct evidence to date that previously reported associations between genetic ancestry and health may be attributable to sociocultural factors related to race and racism, rather than to functional genetic differences between racially defined groups. Our results also imply that including sociocultural variables in future research may improve our ability to detect significant allele-phenotype associations. Thus, measuring sociocultural factors related to race may both empower future genetic association studies and help to clarify the biological consequences of social inequalities

Accuracy of high-density EEG electrode position measurement using an optical scanner compared with the photogrammetry method

OBJECTIVE: To determine the feasibility and accuracy of a handheld optical scanner to measure the three-dimensional (3D) EEG electrode coordinates in a high-density array of 256 electrodes. METHODS: We compared the optical scanning with a previously validated method, based on photogrammetry. Electrode coordinates were co-registered with the MRI of the patients, and mean distance error relative to the three-dimensional MRI reconstruction was determined for each patient. We included 60 patients: 30 were measured using the photogrammetry method, and 30 age and gender matched patients were measured with the optical scanner. RESULTS: Using the optical scanner, the mean distance error was 1.78 mm (95% confidence interval: 1.59–1.98 mm) which was significantly lower (p < 0.001) compared with the photogrammetry method (mean distance error: 2.43 mm; 95% confidence interval: 2.28–2.57 mm). The real-time scanning took 5–10 min per patient. CONCLUSIONS: The handheld optical scanner is more accurate and feasible, compared to the photogrammetry method. SIGNIFICANCE: Measuring EEG electrode positions in high-density array, using the optical scanner is suitable for clinical implementation in EEG source imaging for presurgical evaluation

Hyperinduction of cyclooxygenase-2-mediated proinflammatory cascade: A mechanism for the pathogenesis of avian influenza H5N1 infection

The mechanism for the pathogenesis of H5N1 infection in humans remains unclear. This study reveals that cyclooxygenase-2 (COX-2) was strongly induced in H5N1-infected macrophages in vitro and in epithelial cells of lung tissue samples obtained during autopsy of patients who died of H5N1 disease. Novel findings demonstrated that COX-2, along with tumor necrosis factor alpha and other proinflammatory cytokines were hyperinduced in epithelial cells by secretory factors from H5N1-infected macrophages in vitro. This amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. Furthermore, selective COX-2 inhibitors suppress the hyperinduction of cytokines in the proinflammatory cascade, indicating a regulatory role for COX-2 in the H5N1-hyperinduced host proinflammatory cascade. These data provide a basis for the possible development of novel therapeutic interventions for the treatment of H5N1 disease, as adjuncts to antiviral drugs