Women with ACS were more likely to have cardiovascular disease risk factors and atypical symptoms such as nausea compared with men, but were more likely to have normal/mild angiographic coronary artery disease. Further study regarding sex differences related to disease severity is warranted.
Late-preterm infants have greater morbidity and total health care costs than term infants, and these differences persist throughout the first year of life. Management strategies and guidelines to reduce morbidity and costs in late-preterm infants should be investigated.
Gliadins, here defined as those proteins of defatted wheat endosperm which dissolve in 70% (v/v) ethanol at room temperature, were fractionated by gel filtration using Sephadex G-100. The protein which eluted with the void volume of the column, often described as high-molecular-weight (HMW) gliadin, was fractionated by the two different, two dimensional gel electrophoresis procedures of O'Farrell (1975) and O'Farrell et al. (1977). The next two fractions to elute from the gel column, ω-gliadin and α-, β-, γ-gliadin, were analysed similarly. The subunits of HMW gliadin and the classical (i.e. non-aggregated) gliadins map at distinctive positions on the electrophoregrams, the majority of the HMW gliadin subunits being more basic and having a slightly slower electrophoretic mobility than the α-, β-, γ-gliadins. These experiments demonstrate that those gliadins which aggregate to form HMW gliadin are distinct molecular entities and thus coded by different genes to those gliadins which do not aggregate. Glutenin, here prepared by a modification of the pH 6.4 precipitation procedure of Orth and Bushuk (1973), was also analysed by two-dimensional electrophoresis. The low-molecular-weight subunits were found to correspond exactly with the HMW gliadin subunits. Using the nullisomic-tetrasomic lines and the ditelocentric lines of 'Chinese Spring', the genes controlling the synthesis of all the major HMW gliadin subunits were shown to be located on the short arms of chromosomes 1A, 1B and 1D, as are the genes coding for the ω-gliadins and the majority of the γ-gliadins.
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