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Toward the therapy of AUNA1 auditory neuropathy – Diaphanous
The Diaphanous homolog 3 (DIAPH3) gene is responsible for the autosomal dominant nonsyndromic auditory neuropathy 1 (AUNA1). DIAPH3 belongs to the formin related family, i.e, it is activated by Rho-GTPases and stabilizes the cytoskeleton. Strikingly, the DIAPH3 gene mutation leads to the overexpression of the DIAPH3 protein. <br />Here, we propose to decipher the mechanism responsible for AUNA1 from the molecular signaling pathways to the system level in order to envision future therapies. <br />
Toward the Rebirth of Aromatic Cope Rearrangement – ArCopeRebirth
The Aromatic Cope Rearrangement (ArCopeR) is a challenging transformation that has been the subject to very few studies considering the huge thermodynamic and kinetic predicaments inherent to this tra
Toward quantitative epistemology - Reconstructing the long term evolution of science through large scale analysis of science productions – EPIQUE
The evolution of scientific knowledge is directly related to the history of humanity. Document archives and bibliographic sources like the “Web Of Science” or PubMed contain a valuable source for the
Toward offering healthy food products better adapted to elderly people – AlimaSSenS
AlimaSSenS' project proposes to design innovative food products for elderly population living at home. These food products combine high nutritional quality on one side and enjoyment for eating on the other. It will also take into account the senior environment via its purchasing and culinary practices.
Toward industrailisation of ultrathin CIGSe based solar cells – ULTRACIS_M
The aim of this project is to settle a disruptive CIGS solar cell technology based on ultrathin CIGS layers with thicknesses down to 0.1 µm while maintaining, or even increasing, the cells and module
Toward immune Biomarkers for Tolerance and GvHD in Humans – BioGvHD
Graft-versus-Host Disease (GVHD), is the most frequent and severe complication of allogeneic hematopoietic stem cell transplantation (HSCT). Much of our knowledge on the pathophysiology of GVHD has been gained from experimental models but far less from the study of the disease in humans.