15 research outputs found

    Quantitative Scanning Electron Microscopy (SEM) to Study the Adhesion and Spreading of Human Endothelial Cells to Surface-Modified Poly(Carbonate Urethane)s

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    The polymers currently in use as vascular prostheses are, in the native state, poor substrates for endothelial cell (EC) adhesion and growth. This has a negative effect on the success of pre-seeding regimes. One attempt to improve the polymer substrate is to covalently couple reactive molecules to the surface, which can be used as anchorage points for EC or serve as spacer molecule to couple biological signal molecules such as oligopeptides. We have used a digitized image analysis system coupled to a scanning electron microscope to study the adhesion and spreading of human venous EC to unmodified poly(carbonate urethane) (uPCU), hydroxyl- functionalized PCU (mPCU) and to mPCU surfaces with succinyl or adipoyl dichloride coupled to it. Although the uPCU did not promote EC growth over a 5 day period, the early (30 minutes) adhesion and spreading behaviour on this surface was comparable to that of some modified surfaces which gave good promotion of EC growth in the longer term studies. Adhesion, but not spreading data at 4 hours gave a good correlation with the longer term studies of EC growth on the polymer surfaces. This study not only presents new directions in polymer development for vascular grafts, but also indicates the dangers associated with using early cell adhesion behaviour as a parameter of bifunctionality of biomaterial surfaces

    Two-photon absorption and up-converted emission in blue-emitting stilbene dye

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    We have carried out investigations into the two-photon absorption properties of a novel blue emitting molecule; 1,4-bis(4-diphenylaminostyryl) benzene. The open aperture z-scan technique was employed to measure the two-photon absorption coefficient of this material in solution over a range of concentrations in chloroform at 800 nm. We measured the two-photon absorption cross-section to be 197 × 10-50 cm4 s photon -1. We have also demonstrated strong up-converted emission in solutions of the same molecule highlighting the potential of this material for applications such as up-conversion and two-photon fluorescence microscopy

    Decoding Pedophilia: Increased Anterior Insula Response to Infant Animal Pictures

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    Previous research found increased brain responses of men with sexual interest in children (i.e., pedophiles) not only to pictures of naked children but also to pictures of child faces. This opens the possibly that pedophilia is linked (in addition to or instead of an aberrant sexual system) to an over-active nurturing system. To test this hypothesis we exposed pedophiles and healthy controls to pictures of infant and adult animals during functional magnetic resonance imaging of the brain. By using pictures of infant animals (instead of human infants), we aimed to elicit nurturing processing without triggering sexual processing. We hypothesized that elevated brain responses to nurturing stimuli will be found – in addition to other brain areas – in the anterior insula of pedophiles because this area was repeatedly found to be activated when adults see pictures of babies. Behavioral ratings confirmed that pictures of infant or adult animals were not perceived as sexually arousing neither by the pedophilic participants nor by the heathy controls. Statistical analysis was applied to the whole brain as well as to the anterior insula as region of interest. Only in pedophiles did infants relative to adult animals increase brain activity in the anterior insula, supplementary motor cortex, and dorsolateral prefrontal areas. Within-group analysis revealed an increased brain response to infant animals in the left anterior insular cortex of the pedophilic participants. Currently, pedophilia is considered the consequence of disturbed sexual or executive brain processing, but details are far from known. The present findings raise the question whether there is also an over-responsive nurturing system in pedophilia

    Education and coronary heart disease: mendelian randomisation study

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    Objective\ua0To determine whether educational attainment is a causal risk factor in the development of coronary heart disease.Design\ua0Mendelian randomisation study, using genetic data as proxies for education to minimise confounding.Setting\ua0The main analysis used genetic data from two large consortia (CARDIoGRAMplusC4D and SSGAC), comprising 112 studies from predominantly high income countries. Findings from mendelian randomisation analyses were then compared against results from traditional observational studies (164 170 participants). Finally, genetic data from six additional consortia were analysed to investigate whether longer education can causally alter the common cardiovascular risk factors.Participants\ua0The main analysis was of 543 733 men and women (from CARDIoGRAMplusC4D and SSGAC), predominantly of European origin.Exposure\ua0A one standard deviation increase in the genetic predisposition towards higher education (3.6 years of additional schooling), measured by 162 genetic variants that have been previously associated with education.Main outcome measure\ua0Combined fatal and non-fatal coronary heart disease (63 746 events in CARDIoGRAMplusC4D).Results\ua0Genetic predisposition towards 3.6 years of additional education was associated with a one third lower risk of coronary heart disease (odds ratio 0.67, 95% confidence interval 0.59 to 0.77; P=3 710(-8)). This was comparable to findings from traditional observational studies (prevalence odds ratio 0.73, 0.68 to 0.78; incidence odds ratio 0.80, 0.76 to 0.83). Sensitivity analyses were consistent with a causal interpretation in which major bias from genetic pleiotropy was unlikely, although this remains an untestable possibility. Genetic predisposition towards longer education was additionally associated with less smoking, lower body mass index, and a favourable blood lipid profile.Conclusions\ua0This mendelian randomisation study found support for the hypothesis that low education is a causal risk factor in the development of coronary heart disease. Potential mechanisms could include smoking, body mass index, and blood lipids. In conjunction with the results from studies with other designs, these findings suggest that increasing education may result in substantial health benefits
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