University of Aberdeen

About: University of Aberdeen is a education organization based out in Aberdeen, United Kingdom. It is known for research contribution in the topics: Population & Health care. The organization has 21174 authors who have published 49962 publications receiving 2105479 citations. The organization is also known as: Aberdeen University.

Diet as a risk factor for atopy and asthma.

Abstract: It has been hypothesized that decreasing antioxidant (fruit and vegetables), increased n-6 polyunsaturated fatty acid (PUFA; (margarine, vegetable oil), and decreased n-3 PUFA (oily fish) intakes have contributed to the recent increases in asthma and atopic disease. Epidemiologic studies in adults and children have reported beneficial associations between dietary antioxidants and lipids and parameters of asthma and atopic disease. The associations with n-6 and n-3 PUFA appear to be very complex and might differ between asthma and atopic dermatitis. Dietary antioxidants are probably exerting antioxidant and nonantioxidant immunomodulatory effects. Dietary lipids exert numerous complex effects on proinflammatory and immunologic pathways. It has also been suggested that atopic dermatitis is associated with an enzyme defect in lipid metabolism. In spite of this, the results of interventional supplementation studies in established disease have been disappointing, and there is now increasing interest in the possibility that dietary antioxidant and lipid intakes might be important in determining expression of disease during pregnancy and early childhood and that dietary interventions should be targeted at these groups. It also seems likely that there is individual variation in the responses of individuals to lipid, and probably antioxidant, supplementation. Further research to determine whether dietary intervention can reduce the risk of asthma and atopic disease is justified.

Polymorphisms in Genes Involved in Folate Metabolism and Colorectal Neoplasia: A HuGE Review

Abstract: Epidemiologic and mechanistic evidence suggests that folate is involved in colorectal neoplasia. Some polymorphic genes involved in folate metabolism--methylenetetrahydrofolate reductase (MTHFR C677T and A1298C), methionine synthase (MTR A2756G), methionine synthase reductase (MTRR A66G), cystathionine beta-synthase (CBS exon 8, 68-base-pair insertion), and thymidylate synthase (TS enhancer region and 3' untranslated region)--have been investigated in colorectal neoplasia. For MTHFR C677T and A1298C, the variant allele is associated with reduced enzyme activity in vitro. For the other polymorphisms, functional data are limited and/or inconsistent. Genotype frequencies for all of the polymorphisms show marked ethnic and geographic variation. In most studies, MTHFR 677TT (10 studies, >4,000 cases) and 1298CC (four studies, >1,500 cases) are associated with moderately reduced colorectal cancer risk. In four of five genotype-diet interaction studies, 677TT subjects who had higher folate levels (or a "high-methyl diet") had the lowest cancer risk. In two studies, 677TT homozygote subjects with the highest alcohol intake had the highest cancer risk. Findings from six studies of MTHFR C677T and adenomatous polyps are inconsistent. There have been only one or two studies of the other polymorphisms; replication is needed. Overall, the roles of folate-pathway genes, folate, and related dietary factors in colorectal neoplasia are complex. Research priorities are suggested.

Entrepreneurship education within the enterprise culture: Producing reflective practitioners

Abstract: The enterprise culture is founded on the premise that entrepreneurship is the engine that drives the economy One aspect of this cultural pervasion is the increase in the numbers of educational institutions teaching entrepreneurship courses Yet this hegemony of the encouragement of new business start‐up, almost for its own sake, needs to be critically reviewed One aspect is the enigmatic nature of entrepreneurship itself; what is it, and can it be taught? Another aspect is the very different expectations of those stakeholders promoting entrepreneurship education Argues that the process of entrepreneurship involves both art and science; consequently our students need more than SME management skills Graduating enterprise students must be innovative and creative to satisfy the need for entrepreneurial novelty ‐ the art Yet, paradoxically they also need to be competent and multifunctional managers ‐ the science Explores both these areas to argue that theory can bridge the art and science The final section explains briefly how the recent research and practice at Aberdeen University attempts this synthesis The intended outcome of our educational process are reflective practitioners, fit for an entrepreneurial career

Dynorphin 1-8 and dynorphin 1-9 are ligands for the κ-subtype of opiate receptor

Abstract: It is generally accepted that there are three subtypes of opiate receptor: µ, δ and κ. The main endogenous ligands for the µ-and δ-sites are Met5-enkephalin, Leu5-enkephalin and β-endorphin, whereas the putative endogenous ligands for the κ-binding site were unknown until recent observations suggested that dynorphin1–13 might be a candidate. The most convincing evidence for this view has been presented by Goldstein and his colleagues who showed that dynorphin1–13 is a specific endogenous ligand for the κ-receptor and has a high potency and long duration of action1–13. We show here that the sequences Leu5-enkephalyl-Arg-Arg-Ile (dynorphin1–8) and, particularly, Leu5-enkephalyl-Arg-Arg-Ile-Arg (dynorphin1–9) are selective ligands for the κ-binding site. Whereas dynorphin1–13 and dynorphin1–17 are relatively resistant to the action of peptidase and have a long duration of action in vitro after wash-out, dynorphin1–8 and dynorphin1–9 are readily degraded by peptidases and their duration of action is much shorter. For this and other reasons, the possibility will have to be considered that dynorphin1–8 or dynorphin1–9 may be transmitters or modulators at the κ-binding site while dynorphin1–13 and dynorphin1–17 may act hormonally, that is, at a distance from the site of release.