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Example Abstracts

  • Popular Press Audience Example


'Rewarding Sucks'

Animals can be trained to learn associations between a signal presentation (such as. a light or tone) and a reward (such as food).  They exhibit particular behaviours in response to the signal.  Depending on the animal, these behaviours frequently take the form of pecking, as in pigeons, or licking, as in rats, and are not necessarily under the animal’s conscious control.  Displaying these behaviours in response to a signal is known as autoshaping. Cambridge scientists are hoping to develop autoshaping protocols in human research.  It has recently been identified that humans exhibit a propensity to suck in anticipation of the delivery of an appetitive or rewarding liquid through a tube or straw.  This ‘anticipatory sucking’ is thought to be independent of conscious control and can be detected (using equipment which identifies pressure changes in the mouth) before the onset of the conscious suck, used to consume the liquid.  Anticipatory sucking has been found to decrease if an aversive liquid is expected. Three human studies are planned which involve participants learning associations between a signal (a picture) and the delivery of a juice reward.  Briefly these are: i) The effects of Ketamine on reconsolidation of rewarding memories (reconsolidation is a process thought to be important for updating long term memories). ii) Differences in anticipation and consummation of reward in Anhedonia patients (these patients exhibit an inability to experience pleasure). iii) The responses of obese patients to expected and unexpected rewards, in comparison to healthy participants. Anticipatory sucking will be measured as an example of autoshaping behaviour.


    • General Research Scientist Audience


    'Poor maternal nutrition enhances levels of pro-inflammatory cytokines and accelerates splenic ageing in the offspring.'

    Environmental factors such as nutrition during very early life can influence long-term health.  Initial focus was directed towards the effects on metabolic health but more recent studies have demonstrated that early nutrition can also influence non-metabolic parameters including ageing and lifespan.  Given that immunosenescence is responsible for increased infection, neoplasia and autoimmune diseases in the elderly, developmental programming of the adaptive immune system could play an important role in mediating the effect of early nutrition on lifespan.  In the current study we used the low protein mouse model of nutritionally-induced fetal growth restriction and postnatal catch-up growth (recuperated) which display reduced lifespan, to test the hypothesis that a suboptimal diet in early life leads to accelerated ageing of the immune system.  We focused on pro-inflammatory cytokines which increase with age, and the spleen, the major secondary lymph organ and site of peripheral antigen recognition.  Here we observed significantly higher levels of TNF-α and IL-1β (p=0.007) in sera from recuperated mice at 18 months compared to controls. Using confocal microscopy of splenic sections we demonstrated that 12-week old recuperated animals displayed disrupted T cell and B cell zonal architecture, a feature observed in aged control animals.  Spleen from recuperated mice had increased staining of fibroblasts, which characterises the age-associated phenomenon of fibroblast infiltration in the spleen.  We conclude that low birth weight and catch up growth leads to enhanced peripheral inflammation and accelerated ageing of the spleen, which in turn could contribute towards the effects of early growth on lifespan.