Archivio Istituzionale della Ricerca- Università del Piemonte Orientale
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Lipid recovery and bioactive compounds profiling from cocoa bean shells
Cocoa bean shells (CBS), a major chocolate industry by-product, rich in dietary fibres and bioactive compound, represent a promising target for upcycling in sustainable food systems. This study evaluates the CBS lipidic fraction extracted by Soxhlet using four apolar solvents: dichloromethane (DE), petroleum ether (PE), diethyl ether (EE), and hexane (HE). The extracts were analysed for yield and chemical composition, including phenolics, methylxanthines, phytosterols, tocopherols, and volatile organic compounds (VOCs). Results showed a significant variation in extraction yields, with DE providing the highest yield (8.05 g/100 g of CBS), compared to others (5.13-5.92 g/100 g of CBS). The phenolic content (3.57-38.2 mg/kg of lipid extract) varied depending on the solvent used, with protocatechuic acid being the most abundant compound (up to 32.2 mg/kg of lipid extract obtained with EE). Brassicasterol was detected in all the extracts (337-520 mg/kg of lipid extract), confirming the presence of valuable phytosterols. Additionally, 115 VOCs were quantified across all samples, with great variation between solvents (23.4-116.5 mg/kg of lipid extract). This study highlights CBS as a valuable source of bioactive lipids and supports their valorisation for the recovery of high-value compounds. These results pave the way for the development of natural ingredients applicable in functional foods, nutraceuticals, and cosmetics, contributing to agro-industrial waste reduction and promoting circular economy strategies
Measurement of correlations among net-charge, net-proton, and net-kaon multiplicity distributions in Pb-Pb collisions at sqrt(sNN) = 5.02 TeV
Correlations among conserved quantum numbers, such as the net-electric charge,
the net-baryon, and the net-strangeness in heavy-ion collisions, are crucial for exploring the
QCD phase diagram. In this paper, these correlations are investigated using net-proton
number (as a proxy for the net-baryon), net-kaon number (for the net-strangeness), and
net-charged particle number in Pb-Pb collisions at √
sNN = 5.02TeV with the ALICE detector.
The observed correlations deviate from the Poissonian baseline, with a more pronounced
deviation at LHC energies than at RHIC. Theoretical calculations of the Thermal-FIST
hadron resonance gas model, HIJING, and EPOS LHC event generators are compared with
experimental results, where a significant impact of resonance decays is observed. Thermal-
FIST calculations under the grand canonical and canonical ensembles highlight significant
differences, underscoring the role of local charge conservation in explaining the data. Recent
lattice QCD studies have demonstrated that the magnetic field generated by spectator protons
in heavy-ion collisions affects susceptibility ratios, in particular those related to the net-electric
charge and the net-baryon numbers. The experimental findings are in qualitative agreement
with the expectations of lattice QCD
Convergent evolution of the G3BP1-binding motif in betacoronavirus nucleocapsid proteins
Betacoronaviruses (β-CoVs) display divergent mechanisms to evade host antiviral responses, yet the evolutionary origin and functional relevance of their strategies remain unclear. Stress granules (SGs), central to host defenses, are disrupted by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleocapsid (N) protein via its interaction with G3BP1 mediated by an 15ITFG18 motif. This interaction inhibits SG assembly, enhancing viral replication and immune evasion. Here, we analyzed 179 N protein sequences across β-CoVs subgenera and identified the ITFG motif in sarbecoviruses but not in MERS-CoV or embecoviruses. Among tested CoVs, only SARS-CoV-2 N showed robust G3BP1 binding in vitro and in infected cells. Phylogenetic analyses revealed that the ΦxFG motif emerged independently in sarbecoviruses and a bat-infecting merbecovirus clade. The VGTF motif in these merbecoviruses also binds to G3BP1, suggesting convergent evolution in viral evasion strategies. The emergence of this motif was unrelated to 4a protein inactivation, another viral protein that inhibits SG formation
Changing clinical and laboratory characteristics of Progressive Multifocal Leukoencephalopathy: a retrospective national cohort study
Background: Progressive Multifocal Leukoencephalopathy (PML) is a severe demyelinating disease caused by JC polyomavirus (JCV), affecting immunocompromised individuals. We describe PML demographic, clinical, radiological and laboratory characteristics and survival over time and according to underlying condition in a large retrospective patient cohort. Methods: This is a retrospective cohort including Italian PML patients observed between 1987 and 2024, with known year of diagnosis and underlying disease. Results: We included 456 cases with either a definite (n=376, 82.4%) or clinico-radiological (n=80, 17.6%) PML diagnosis. The relative frequency of HIV-associated cases decreased through four time periods (1987-1996; 1997-2004; 2005-2012; 2013-2024) from 99% to 43%, in parallel with increasing age (p<0.0001), proportion of women (p<0.001) and CD4+ counts (p<0.001), but not cerebrospinal fluid (CSF) or plasma JCV-DNA levels at diagnosis. One-year survival probability increased from 23.8% in 1987-1996 to 59.2% in 2013-2024, with highest values in natalizumab-treated multiple sclerosis (93.8%), followed by combination antiretroviral treatment (cART)-treated HIV infection (55%), hematological malignancies (50.8%), primary immunodeficiencies (41.3%) and cART-untreated HIV infection (11.9%). At multivariate analysis excluding cART-untreated people with HIV, JCV-DNA levels in both CSF and plasma were independently associated with an increased mortality risk of 2.9% and 7.2%, respectively, for each Log increase in JCV-DNA. Conclusions: This observational study showed a changing epidemiological context over 37 years. Although survival improved over time, it remained poor even in the last decade, with a one-year survival probability of 59.2%
Dielectron production in central Pb-Pb collisions at sqrt(sNN) = 5.02 TeV
The first measurement of the e+e− pair production at midrapidity and low invariant mass in central Pb-Pb
collisions at √s NN = 5.02 TeV at the Large Hadron Collider is presented. The yield of e+e− pairs is compared
with a cocktail of expected hadronic decay contributions in the invariant mass (mee) and pair transverse
momentum (pT,ee) ranges mee < 3.5 GeV/c2 and pT,ee < 8 GeV/c. For 0.18 < mee < 0.5 GeV/c2 the ratio of
data to the cocktail of hadronic contributions amounts to 1.40 ± 0.11 (stat.) ± 0.23 (syst.) ± 0.16 (cocktail) and
1.42 ± 0.11 (stat.) ± 0.23 (syst.)+0.24
−0.29 (cocktail), including or not including medium effects in the estimation
of the heavy-flavor background, respectively. It is consistent with predictions from two different models for an
additional contribution of thermal e+e− pairs from the hadronic and partonic phases. In the intermediate-mass
range (1.2 < mee < 2.6 GeV/c2 ), the pair transverse impact parameter of the e+e− pairs (DCAee, where “DCA”
denotes “distance of closest approach”) is used for the first time in Pb-Pb collisions to separate displaced
dielectrons from heavy-flavor hadron decays from a possible (thermal) contribution produced at the interaction
point. The data are consistent with a suppression of e+e− pairs from cc and an additional prompt component.
Finally, the first direct-photon measurement in the 10% most central Pb-Pb collisions at √s NN = 5.02 TeV is
reported via the study of virtual direct photons in the transverse momentum range 1 < pT < 5 GeV/c. A model
including prompt photons, as well as photons from the preequilibrium and fluid-dynamic phases, can reproduce
the result, while being at the upper edge of the data uncertainties
Reply to: sodium-glucose cotransporter-2 inhibitors and the significant risk of euglycaemic keto-acidosis in cardiac surgery
The MCL elderly III trial protocol: an international, randomized, open-label phase II trial to investigate the combinations of venetoclax, ibrutinib and rituximab or bendamustine, ibrutinib and rituximab in patients with treatment naive mantle cell lymphoma not eligible for dose-intensive treatment
Background: Mantle cell lymphoma (MCL) is a rare B-cell Non-Hodgkin-lymphoma that predominantly affects elderly patients. While younger and fit patients receive an intensive first-line treatment, older or comorbid patients have limited options of chemo-immunotherapy (CIT) alone followed by anti-CD20-antibody maintenance. Targeted oral agents as Bruton`s tyrosine kinase inhibitors (BTKi, e.g. ibrutinib) - and B-cell lymphoma 2 (Bcl2) - inhibitors (e.g. venetoclax) have revolutionized the treatment especially for relapsed patients, with apparent synergistic effects. The MCL elderly III trial of the European MCL Network is an international phase II trial evaluating the efficacy of the combination of ibrutinib, venetoclax and rituximab as well as the CIT bendamustine and rituximab in combination with ibrutinib in elderly patients with untreated MCL. Methods: The primary trial objective is to evaluate efficacy in both treatment arms as measured by failure-free survival at 30 months separately in both treatment arms. Secondary endpoints include progression-free survival, response rates, overall survival, adverse events as well as quality of life and impact of frailty and sarcopenia on treatment outcome through geriatric and body composition assessments via imaging. Exploratory endpoints comprise the rate of minimal residual disease negativity and kinetics of immune reconstitution. Current status: The first patient was included in May 2023, with full site activation achieved in Q1 2025. Until May 15th 2025, 75 of 150 planned patients were enrolled in 27 German and Italian trial sites. Discussion: This is the first randomized trial to exploratively compare a BTKi-Bcl2i-anti-CD20 triplet to a BTK-CIT combination in older MCL patients. Trial registration: The trial is registered on EU Clinical Trial Register (20225018089600)