Publications by authors named "P Bernardi"

Background: Polymethylmethacrylate (PMMA) fillers are permanent fillers known for their possible side effects. In case of complications, the only possible treatment is surgical removal, followed by procedures to minimize resulting deformity. The aims of this study were (1) to analyse the morphology of the PMMA material in the nodules, (2) to demonstrate that treatment by acoustic wave therapy (AWT) can help the removal of the nodules, and (3) to present an easy procedure to solve deformities.

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Natural history museum collections harbour a record of wild species from the past centuries, providing a unique opportunity to study animals as well as their infectious agents. Thousands of great ape specimens are kept in these collections, and could become an important resource for studying the evolution of DNA viruses. Their genetic material is likely to be preserved in dry museum specimens, as reported previously for monkeypox virus genomes from historical orangutan specimens.

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Cyclophilin (CyP) D is a regulator of the mitochondrial F-ATP synthase. Here we report the discovery of a form of CyPD lacking the first 10 (mouse) or 13 (human) N-terminal residues (ΔN-CyPD), a protein region with species-specific features. NMR studies on recombinant human full-length CyPD (FL-CyPD) and ΔN-CyPD form revealed that the N-terminus is highly flexible, in contrast with the rigid globular part.

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Article Synopsis
  • Pre-clinical trials show that transplanted human neural stem cells (hNSCs) have neuroprotective effects after brain ischemia, but the mechanisms behind this are still not fully understood.
  • The study explores whether hNSCs use tunneling nanotubes (TNTs) to communicate and transfer functional mitochondria, highlighting their role in protecting neurons from damage.
  • Findings reveal that hNSCs can form nestin-positive TNTs for mitochondrial transfer, which helps rescue damaged neurons from apoptosis and restore their function when in direct contact with hNSCs.
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Aim: Parvalbumin (PV) is a primary calcium buffer in mouse fast skeletal muscle fibers. Previous work showed that PV ablation has a limited impact on cytosolic Ca ([Ca]) transients and contractile response, while it enhances mitochondrial density and mitochondrial matrix-free calcium concentration ([Ca]). Here, we aimed to quantitatively test the hypothesis that mitochondria act to compensate for PV deficiency.

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