Revisió de la família Nolidae (Insecta, Lepidoptera) de la col·lecció del Museu de Zoologia de Barcelona

Abstract not availabl

Revisió dels Thyatirinae i els Axiidae als Països Catalans

In this article, the 10 species of Axiidae and Thyatirinae of the lberian peninsula are reviewed, giving the flying time with another interesting data. By this work, the total number of species of Thyatirinae knovvn from the lberian peninsula is increased from 8 to 9. Tetheella fluctuosa is the new record (also a new genus for the peninsu la). The Distribution in the catalan countries (Eastern part of the lberian península) is given based on bibliographical data and specially on new data from different col lections and captures, moreover, maps of the area (U.T.M.) of the 7 rarest species and a colour picture vvith the 10 species are included.En el presente artículo se revisan las 10 especies ibéricas de los grupos Axiidae y Thyatirinae, señalando las épocas de vuelo y otros datos de interés. Con este trabajo, el número de los Thyatirinae conocidos en la península Ibérica se aumenta de 8 a 9. La especie nueva es Tetheella fluctuosa (género también nuevo). En base a la bibliografía, y, sobre todo, a datos inéditos obtenidos de la consulta de diversas colecciones y las nuevas capturas, se da la distribución en los Países Catalanes (zona oriental de la península Ibérica). Finalmente, se incluyen mapas UTM de la zona, de las 7 especies más raras, y una fotografía de color de las 10 especies tratadas

Cysteine cathepsins control hepatic NF-κB-dependent inflammation via sirtuin-1 regulation

Sirtuin-1 (SIRT1) regulates hepatic metabolism but its contribution to NF-κB-dependent inflammation has been overlooked. Cysteine cathepsins (Cathepsin B or S, CTSB/S) execute specific functions in physiological processes, such as protein degradation, having SIRT1 as a substrate. We investigated the roles of CTSB/S and SIRT1 in the regulation of hepatic inflammation using primary parenchymal and non-parenchymal hepatic cell types and cell lines. In all cells analyzed, CTSB/S inhibition reduces nuclear p65-NF-κB and κB-dependent gene expression after LPS or TNF through enhanced SIRT1 expression. Accordingly, SIRT1 silencing was sufficient to enhance inflammatory gene expression. Importantly, in a dietary mouse model of non-alcoholic steatohepatitis, or in healthy and fibrotic mice after LPS challenge, cathepsins as well as NF-κB-dependent gene expression are activated. Consistent with the prominent role of cathepsin/SIRT1, cysteine cathepsin inhibition limits NF-κB-dependent hepatic inflammation through the regulation of SIRT1 in all in vivo settings, providing a novel anti-inflammatory therapeutic target in liver disease.This study was supported by grants from the Instituto de Salud Carlos III (PI13/00374 to MM), Ministerio de Economía y Competitividad (SAF2015-69944-R to JFC, SAF2013-47246-R to AC, SAF2015-66515-R to AM) and co-funded by FEDER (Fondo Europeo de Desarrollo Regional, Unión Europea. “Una manera de hacer Europa”); center grant P50-AA-11999 from Research Center for Liver and Pancreatic Diseases (US-NIAAA to JFC); and by CIBERehd. AT is a recipient of a FPU fellowship recipient from the Ministerio de Educación, Cultura y Deporte.Peer Reviewe

AXL inhibition prevents NAFLD progression in mice with soluble AXL as marker of the NAFLD to NASH transition

Trabajo presentado en el The Digital International Liver Congress, celebrado del 27 al 29 de agosto de 2020Background and Aims: TYRO3, AXL and MERTK are receptor tyrosine kinases activated by the ligand GAS6. AXL signalling is increased in NASH patients, promotes fibrosis in hepatic stellate cells and inflammation in Kupffer cells, while GAS6 protects hepatocytes against lipotoxicity via MERTK. Recent data has shown that the AXL kinase inhibitor bemcentinib, by blocking AXL signalling and increasing GAS6 levels, reduces experimental NASH. However, AXL's role in the NAFLD/NASH transition has not been addressed. Identifying mechanisms responsible for NAFLD progression into NASH could provide early markers and novel therapeutic targets. Method: Mice were fed a high-fat methionine-restricted choline deficient (HFCD) diet for 2 and 4 weeks, and a high-fat diet with fructose (HFF) for 4 months to induce different degrees of NAFLD/NASH. Mouse Gas6, soluble levels of Axl (sAXL) and Mertk were measured by ELISA. Human GAS6, sAXL and MERTK were measured by ELISA in control and patient serum, and compared with biochemical and histological data. Transaminases and triglycerides were measured at the Hospital Clinic Core. The collagen content was measured by staining with Sirius Red and quantified by imaging software. H&E staining was performed and NAS score evaluated. Transcriptomic analysis of genes related to liver inflammation and fibrosis were measured in commercial microarrays and by qPCR. Results: After 4 weeks feeding with HFCD diet, early NASH was detected featuring liver steatosis, liver inflammation, hepatocellular ballooning and fibrosis. AXL inhibition with bemcentinib for 2 weeks reduced all these hepatic anomalies, including triglyceride serums levels and liver steatosis, preventing NAFLD progression. After 2 weeks of HFCD diet, mice presented fatty liver without fibrosis; however, transcriptomic analysis evidenced strong upregulation of pro-fibrotic and pro-inflammatory genes, while soluble Axl levels were already increased. Of note, one week bemcentinib administration not only reduced specific inflammatory and fibrotic genes such as Ccr2 or Col1a1, but also hepatic steatosis and NAS score. In contrast,in HFF-fed mice only liver steatosis was observed, without evidence of fibrosis or inflammation nor changes in sAxl levels. Interestingly, previous and on-going clinical data show significant sAXL increase in clinical patients with only diagnosed liver steatosis, showing no histological signs of inflammation or fibrosis. These results justify further transcriptomic patient evaluation and possible evolution depending on sAXL levels. Conclusion: sAXL levels reveals as a potential NAFLD-NASH transition marker, indicative of the initiation of liver inflammation and fibrosis before histological detection. Early treatment with bemcentinib prevented experimental NASH appearance, pointing to AXL antagonism as possible strategy for future clinical trials

Malignancy following heart transplantation: differences in incidence and prognosis between sexes – a multicenter cohort study

[Abstract] Male patients are at increased risk for developing malignancy postheart transplantation (HT); however, real incidence and prognosis in both genders remain unknown. The aim of this study was to assess differences in incidence and mortality related to malignancy between genders in a large cohort of HT patients. Incidence and mortality rates were calculated for all tumors, skin cancers (SCs), lymphoma, and nonskin solid cancers (NSSCs) as well as survival since first diagnosis of neoplasia. 5865 patients (81.6% male) were included. Total incidence rates for all tumors, SCs, and NSSCs were lower in females [all tumors: 25.7 vs. 44.8 per 1000 person‐years; rate ratio (RR) 0.68, (0.60–0.78), P < 0.001]. Mortality rates were also lower in females for all tumors [94.0 (77.3–114.3) vs. 129.6 (120.9–138.9) per 1000 person‐years; RR 0.76, (0.62–0.94), P = 0.01] and for NSSCs [125.0 (95.2–164.0) vs 234.7 (214.0–257.5) per 1000 person‐years; RR 0.60 (0.44–0.80), P = 0.001], albeit not for SCs or lymphoma. Female sex was associated with a better survival after diagnosis of malignancy [log‐rank p test = 0.0037; HR 0.74 (0.60–0.91), P = 0.004]. In conclusion, incidence of malignancies post‐HT is higher in males than in females, especially for SCs and NSSCs. Prognosis after cancer diagnosis is also worse in males

Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector

This paper presents measurements of the $W^+ \rightarrow \mu^+\nu$ and $W^- \rightarrow \mu^-\nu$ cross-sections and the associated charge asymmetry as a function of the absolute pseudorapidity of the decay muon. The data were collected in proton--proton collisions at a centre-of-mass energy of 8 TeV with the ATLAS experiment at the LHC and correspond to a total integrated luminosity of 20.2~\mbox{fb^{-1}}. The precision of the cross-section measurements varies between 0.8% to 1.5% as a function of the pseudorapidity, excluding the 1.9% uncertainty on the integrated luminosity. The charge asymmetry is measured with an uncertainty between 0.002 and 0.003. The results are compared with predictions based on next-to-next-to-leading-order calculations with various parton distribution functions and have the sensitivity to discriminate between them.Comment: 38 pages in total, author list starting page 22, 5 figures, 4 tables, submitted to EPJC. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2017-13