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- Belli, LS, et al.
(författare)
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COVID-19 in liver transplant candidates: pretransplant and post-transplant outcomes - an ELITA/ELTR multicentre cohort study
- 2021
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Ingår i: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 70:10, s. 1914-
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Tidskriftsartikel (refereegranskat)abstract
- Explore the impact of COVID-19 on patients on the waiting list for liver transplantation (LT) and on their post-LT course.DesignData from consecutive adult LT candidates with COVID-19 were collected across Europe in a dedicated registry and were analysed.ResultsFrom 21 February to 20 November 2020, 136 adult cases with laboratory-confirmed SARS-CoV-2 infection from 33 centres in 11 European countries were collected, with 113 having COVID-19. Thirty-seven (37/113, 32.7%) patients died after a median of 18 (10–30) days, with respiratory failure being the major cause (33/37, 89.2%). The 60-day mortality risk did not significantly change between first (35.3%, 95% CI 23.9% to 50.0%) and second (26.0%, 95% CI 16.2% to 40.2%) waves. Multivariable Cox regression analysis showed Laboratory Model for End-stage Liver Disease (Lab-MELD) score of ≥15 (Model for End-stage Liver Disease (MELD) score 15–19, HR 5.46, 95% CI 1.81 to 16.50; MELD score≥20, HR 5.24, 95% CI 1.77 to 15.55) and dyspnoea on presentation (HR 3.89, 95% CI 2.02 to 7.51) being the two negative independent factors for mortality. Twenty-six patients underwent an LT after a median time of 78.5 (IQR 44–102) days, and 25 (96%) were alive after a median follow-up of 118 days (IQR 31–170).ConclusionsIncreased mortality in LT candidates with COVID-19 (32.7%), reaching 45% in those with decompensated cirrhosis (DC) and Lab-MELD score of ≥15, was observed, with no significant difference between first and second waves of the pandemic. Respiratory failure was the major cause of death. The dismal prognosis of patients with DC supports the adoption of strict preventative measures and the urgent testing of vaccination efficacy in this population. Prior SARS-CoV-2 symptomatic infection did not affect early post-transplant survival (96%).
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- Alemani, Mattia, et al.
(författare)
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Dry sliding of a low steel friction material against cast iron at different loads : Characterization of the friction layer and wear debris
- 2017
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Ingår i: Wear. - : Elsevier. - 0043-1648 .- 1873-2577. ; 376-377, s. 1450-1459
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Tidskriftsartikel (refereegranskat)abstract
- Pin-on-disc testing was used to investigate the sliding behavior and the wear products of a low-steel friction material against a cast iron disc at different applied loads, to investigate the effect of the temperature rise induced by frictional heating. The testing rig was operated in a clean chamber with a purified incoming air flux. The outgoing flux carries the wear particles to an impactor that counted and sorted them by average diameter and weight. At increasing applied loads, corresponding to a proportional increase of the pin-disc contact temperature, the coverage of both the pin and disc surface by a friction layer was found to increase too. The relevant X-Ray diffraction patterns revealed the presence of a large amount of graphite and different compounds originating from the friction material and from the counterface disc, mainly iron oxides, as concerns this latter. After the test at the lowest investigated load, i.e., 1 kg, the disc worn surface exhibited abrasive grooves and a discontinuous friction layer mainly made of compacted iron oxide particles. After the test at higher loads, i.e., 5 and 7 kg, the disc surface was covered by a compact friction layer. As concerns the friction layer on the pins, most of the ingredients from the friction material were detected, in association with the iron oxides from the disc. These results can be interpreted in terms of the temperature stability range of the phenolic resin used as a binder of the friction material. The characterization of the collected airborne wear debris showed that the particles produced by the low temperature (i.e., low load) test were mostly equiaxed; whereas those produced by the high temperature (i.e., high loads) tests, predominantly displayed a plate-like morphology. The mechanisms of their formation in relation to the characteristics of the friction layers are illustrated and discussed.
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- Carreca, AP, et al.
(författare)
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Galectin-9 and Interferon-Gamma Are Released by Natural Killer Cells upon Activation with Interferon-Alpha and Orchestrate the Suppression of Hepatitis C Virus Infection
- 2022
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Ingår i: Viruses. - : MDPI AG. - 1999-4915. ; 14:7
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Tidskriftsartikel (refereegranskat)abstract
- Natural killer (NK) cells mount an immune response against hepatitis C virus (HCV) infection and can be activated by several cytokines, including interleukin-2 (IL-2), IL-15, and interferon-alpha (IFN-α). By exploiting the Huh7.5 hepatoma cell line infected with the HCV JFH1 genome, we provide novel insights into the antiviral effector functions of human primary NK cells after cytokine stimulation. NK cells activated with IFN-α (IFNα-NKs) had enhanced contact-dependent and -independent responses as compared with NK cells activated with IL-2/IL-15 (IL2/IL15-NKs) and could inhibit HCV replication both in vitro and in vivo. Importantly, IFN-α, but not IL-2/IL-15, protected NK cells from the functional inhibition exerted by HCV. By performing flow cytometry, multiplex cytokine profiling, and mass-spectrometry-based proteomics, we discovered that IFNα-NKs secreted high levels of galectin-9 and interferon-gamma (IFN-γ), and by conducting neutralization assays, we confirmed the major role of these molecules in HCV suppression. We speculated that galectin-9 might act extracellularly to inhibit HCV binding to host cells and downstream infection. In silico approaches predicted the binding of HCV envelope protein E2 to galectin-9 carbohydrate-recognition domains, and co-immunoprecipitation assays confirmed physical interaction. IFN-γ, on the other hand, triggered the intracellular expressions of two antiviral gate-keepers in target cells, namely, myxovirus-1 (MX1) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1). Collectively, our data add more complexity to the antiviral innate response mediated by NK cells and highlight galectin-9 as a key molecule that might be exploited to neutralize productive viral infection.
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- Matějka, V., et al.
(författare)
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On the running-in of brake pads and discs for dyno bench tests
- 2017
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Ingår i: Tribology International. - : Elsevier Ltd. - 0301-679X .- 1879-2464. ; 115, s. 424-431
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Tidskriftsartikel (refereegranskat)abstract
- Running-in process of low metallic brake pads and cast iron discs are investigated using full scale inertia brake dynamometer designed for particle emission studies. The airborne particles are measured using ELPI+ and collected on filters. The pads and disc contact surfaces are studied using microscopy techniques. It is observed that the particle emissions from the new pads and discs are significantly higher compared with the used ones and indicates importance of proper running-in of the pads and disc for wear particle emission tests. The results also indicate that pads and disc pairs which are able to stabilize friction behavior faster will produce less particle emissions which could influence the strategies of brake material formulations or steps during their production.
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- Reddington, James P, et al.
(författare)
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Redistribution of H3K27me3 upon DNA hypomethylation results in de-repression of Polycomb target genes
- 2013
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Ingår i: Genome Biology. - : Springer Science and Business Media LLC. - 1465-6906 .- 1474-760X. ; 14:3, s. R25-
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: DNA methylation and the Polycomb repression system are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear.RESULTS: By genome-wide mapping of the Polycomb Repressive Complex 2-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and Polycomb Repressive Complex 2 from Polycomb target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression.CONCLUSIONS: An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining Polycomb Repressive Complex 2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease.
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