Publications by authors named "P Ursi"

Background: Laparoscopic cholecystectomy is the gold standard in the treatment of symptomatic gallstones. The large number of gallbladders removed every year is not fully consistent with the excessively high incidence of iatrogenic bile duct injury (IBDI). Several strategies have been suggested to reduce this risk.

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  • HIV-1 matrix protein p17 (p17) can alter the activity of different cells and is released from infected cells, with variants (vp17s) found more in patients with lymphoma displaying specific amino acid changes that promote B cell growth.
  • These vp17s are unstable and their growth-promoting activity is linked to misfolding that reveals a functional site interacting with protease-activated receptor 1 (PAR-1), whereas the well-folded reference p17 (refp17) does not affect B cell functions.
  • Computational studies reveal that the clonogenic ability of vp17s stems from shifts in protein structure and H-bond networks, highlighting key residues Trp16 and Tyr29 that are critical for maintaining
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The characterization of modifications of microbial proteins is of primary importance to dissect pathogen lifecycle mechanisms and could be useful in identifying therapeutic targets. Attempts to solve this issue yielded only partial and non-exhaustive results. We developed a multidisciplinary approach by coupling in vitro infection assay, mass spectrometry (MS), protein 3D modelling, and surface plasma resonance (SPR).

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  • Two siblings with symptoms resembling Rothmund-Thomson syndrome, including fragile hair and cataracts, were investigated genetically due to their shared ancestry as children of first cousins.
  • Whole exome sequencing identified significant variations in the nucleoporin 98 (NUP98) gene, particularly one variant that suggested higher pathogenicity and potential alteration of protein function.
  • The mutations potentially disrupt the normal behavior of the NUP98 protein, which could affect its role in cellular processes, revealing a new constitutional disorder linked to NUP98 and its relation to cancer.
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Cystic fibrosis is a hereditary disease mainly caused by the deletion of the Phe 508 (F508del) of the cystic fibrosis transmembrane conductance regulator (CFTR) protein that is thus withheld in the endoplasmic reticulum and rapidly degraded by the ubiquitin/proteasome system. Cystic fibrosis remains a potentially fatal disease, but it has become treatable as a chronic condition due to some CFTR-rescuing drugs that, when used in combination, increase in their therapeutic effect due to a synergic action. Also, dietary supplementation of natural compounds in combination with approved drugs could represent a promising strategy to further alleviate cystic fibrosis symptoms.

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