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Jim Secord - Eureka! How the history of science became a story

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Cambridge Darwins in Conversation

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Professor Helen Anne Curry - Securing Crop Diversity from the Cold War through the Internet Age


Professor Gerry Gilmore - The Milky Way Galaxy - from beginning to end - Larmor Lecture

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Professor Duncan McFarlane - Should we automate?

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13

02

Building your life-support system; a new paradigm for human placental development

Professor Graham Burton

  • 18:00 - 19:00 Bristol-Myers Squibb Lecture Theatre

Growth during the intrauterine period is a critical determinant of life-long health. During this period the placenta acts as the baby’s life-support system, transferring nutrients and orchestrating maternal adaptations to the pregnancy. But what stimulates formation of the placenta? Development of the human placenta is precocious, and for many years was considered the pinnacle of evolutionary advance amongst mammals by providing early and intimate access to the maternal circulation. Over the last two decades our understanding of the physiology of early pregnancy has undergone radical revision. It is now appreciated that for the first three months the placenta is nourished by the secretory lining of the uterus rather than maternal blood. Furthermore, evidence from domestic species and recently derived human organoid cultures indicates that a signalling dialogue operates between the placenta and the uterus, increasing the release of growth factors and nutrients by the latter. In this way, the placenta stimulates its own development, ready to support the baby. Evidence for this concept will be presented, and the clinical implications discussed.

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27

02

Mitigating mitochondrial mutational meltdown: can we save the species?

Professor Patrick Chinnery

  • 18:00 - 19:00 Bristol-Myers Squibb Lecture Theatre

Mitochondria are sub-microscopic organelles present in every cell. They convert the breakdown products of food into a form of energy the cell needs to function and survive. An unfortunate by-product is the generation of toxic oxygen free radicals that can damage DNA within each mitochondrion. With a limited capacity for repair, these mutations are passed down the maternal line, where they predispose to disease, can shorten our lifespan, and are threatening our own survival. New biological insights have cast light on the mechanisms involved, but is Homo sapiens facing mutational meltdown?  

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