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Ciccone, M.

Publications and source records attributed to Ciccone, M..

2 recordsLinked to original sources

Adapting to visuomotor rotations in stepped increments increases implicit motor learning

Human motor adaptation relies on both explicit conscious strategies and implicit unconscious updating of internal models to correct motor errors. Implicit adaptation is powerful, requiring less preparation time before executing adapted movements, but recent work suggests it is limited to some absolute magnitude regardless of the size of a visuomotor perturbation when the perturbation is introduced abruptly. It is commonly assumed that gradually introducing a perturbation should lead to improved implicit learning beyond this limit, but outcomes are conflicting. We tested whether introducing a perturbation in two distinct gradual methods can overcome the apparent limit and explain past conflicting findings. We found that gradually introducing a perturbation in a stepped manner, where participants were given time to adapt to each partial step before being introduced to a larger partial step, led to [~]80% higher implicit aftereffects of learning, but introducing it in a ramped manner, where participants adapted larger rotations on each subsequent reach, did not. Our results clearly show that gradual introduction of a perturbation can lead to substantially larger implicit adaptation, as well as identify the type of introduction that is necessary to do so.

neuroscience↗

Pregnancy reprograms the enhancer landscape of mammary epithelial cells and alters the response to cMYC-driven oncogenesis

Pregnancy leaves a series of cellular and molecular modifications on mammary epithelial cells (MECs). Pregnancy is also known for decreasing the predisposition of rodent and human MECs to oncogenesis. Here, in order to understand the molecular basis for this effect, we analyzed epigenetic changes in the enhancer landscape of murine post-pregnancy MECs, together with their effect on gene regulation, tissue development and oncogenesis. Using in vivo and in vitro analyses, we found that completion of a pregnancy cycle changed the dynamics of cellular proliferation and gene expression in response to a second pregnancy. Our results also demonstrated that post-pregnancy MECs are resistant to the initial molecular programs driven by cMYC overexpression, a response that blocked MEC proliferation but did not perturb the pregnancy-induced epigenomic landscape. Overall, our findings suggest that pregnancy-induced mammary cancer prevention involves the epigenomic changes in MECs brought about by pregnancy.

molecular biology↗