Disparity pattern-based autostereoscopic 3D metrology system for in situ measurement of microstructured surfaces.

This paper presents a disparity pattern-based autostereoscopic (DPA) 3D metrology system that makes use of a microlens array to capture raw 3D information of the measured surface in a single snapshot through a CCD camera. Hence, a 3D digital model of the target surface with the measuring data is generated through a system-associated direct extraction of disparity information (DEDI) method. The DEDI method is highly efficient for performing the direct 3D mapping of the target surface based on tomography-like operation upon every depth plane with the defocused information excluded. Precise measurement results are provided through an error-elimination process based on statistical analysis. Experimental results show that the proposed DPA 3D metrology system is capable of measuring 3D microstructured surfaces with submicrometer measuring repeatability for high precision and in situ measurement of microstructured surfaces.

Progression of atherosclerosis is associated with variation in the alpha1-antitrypsin gene.

OBJECTIVE: Alpha1-Antitrypsin (AAT) protects elastic tissue and may play a role in atherogenesis. The association of atherosclerosis progression with common AAT variants was considered in 2 clinical trials. METHODS AND RESULTS: We examined the association of AAT V213A, S and Z deficiency alleles, and the functional 3' UTR 11478G>A with change in minimal luminal diameter, a measure of focal disease, in the Lopid Coronary Angiography Trial gemfibrozil study of post-bypass men. S or Z carriers (n=14) showed strong progression of disease on placebo (11.5%) but responded well to treatment (3% regression). 11478A carriers treated with placebo or gemfibrozil showed significantly more disease progression (n=8, -14.5% and n=16, -4.0%, respectively) than 11478GG men (n=107, -7.0% and n=108, -1.4%, respectively; overall, P=0.003). VV213 men treated with gemfibrozil (n=68) showed -4.8% progression, whereas A213 carriers (n=55) showed +1.4% regression of disease (P=0.001). No V213A effect was seen on placebo (P=0.11). In the Diabetes Atherosclerosis Intervention Study fenofibrate trial of angiographic progression in type 2 diabetes, the association of 11478A with increased disease progression was confirmed in the treatment group, but not the gemfibrozil-treated A213 association with regression, suggesting a pharmacogenetic difference. CONCLUSIONS: Disease progression is associated with variation in AAT, and low AAT levels promote atherogenesis.

Surface geometry, miniaturization and metrology.

Ultra-precision engineering has at its core the size, shape and texture of the components used. This study examines how the relationship between them and their role is changing with respect to manufacture, function and characterization, with particular emphasis on aspects of miniaturization and ultra-precision engineering. Surface geometry has traditionally been linked to the generation of part size. This is changing: the study shows that it is now possible to separate shape and texture from the size generation and to design them independently for function. In addition, with miniaturization, the roles and properties of shape and texture that affect performance change considerably, especially those tribological functions involving contact and flow. This study reveals these changes and shows how the characterization of the surfaces making up a surface system can take these into account.

Recombination hotspots and block structure of linkage disequilibrium in the human genome exemplified by detailed analysis of PGM1 on 1p31.

The distribution of linkage disequilibrium (LD) in the human genome has important consequences for the design of experiments that infer susceptibility genes for complex disease using association studies. Recent studies have shown a non-random distribution of human meiotic recombination associated with intervening tracts of LD. Little is known about the processes, patterns and frequency of reciprocal meiotic recombination in humans. However, this phenomenon can be better understood by the fine structure analysis of several genomic regions by mapping hotspots and characterizing regions with variable LD. Here, we report clustered hotspot activity with intervening blocks of LD within the human PGM1 gene (1p31) using data derived from meiotic and population studies. Earlier work has suggested a high recombination rate in two regions within the PGM1 gene, site A (exons 4-8) and site B (exons 1A-4). Sequencing of eight individuals across 6 kb of targeted regions in site B identified 18 informative SNPs. Individuals from three distinct populations, Caucasian (n=264), Chinese (n=222) and Vietnamese (n=187), were genotyped, and haplotypes were determined using estimate of haplotypes, ldmax and Arlequin. Allelic association and haplotype analysis in these samples revealed variable recombination rates across PGM1, demonstrating the presence of: (i) three hotspots and (ii) three haplotype blocks. The spatial arrangement of haplotype blocks was identical in all populations studied. The pattern of association within PGM1 represents a region decomposed into small blocks of LD, where increased recombination activity has disrupted the ancestral chromosome. Additionally, crossovers in phased data mapped preferentially to regions where LD collapses, which also overlap with sequence motifs.

Alpha1-antitrypsin as a risk for infant and adult respiratory outcomes in a national birth cohort.

Reduced alpha1-antitrypsin (AAT) encoded by the gene SERPINA1 is a potential risk for pulmonary disease. We investigated SERPINA1 polymorphism as a risk for infant and adult pulmonary morbidity, and adult respiratory function and its change between 43 and 53 yr. We used data on a British national representative sample (n = 5,362) studied since birth in 1946 to age 53 yr (when n = 3,035), when DNA was first obtained. SERPINA1 Z and, to a lesser extent, S carriers had an increased risk of infant lower respiratory infection compared with those who were neither S nor Z carriers (Z carriers: odds ratio = 2.32, 95% confidence interval = 1.37-3.92; S but not Z carriers odds ratio = 1.58, 95% confidence interval = 1.10-2.28) after adjustment for environmental, socioeconomic, and developmental factors, and breast-feeding. There was no difference in the adult outcomes at 53 yr according to genotype, nor was there any association of genotype with change in forced expiratory volume at 1 s between 43 and 53 yr. Lower alpha1-antitrypsin, as indicated by carrier status for the Z and S alleles, was a risk for infant lower respiratory infection, but not for adult respiratory outcomes.