136 research outputs found

    Ontogenetic shift in the trophic role of the invasive killer shrimp Dikerogammarus villosus: a stable isotope study

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    none5noThe introduction of the amphipod Dikerogammarus villosus in European fresh waters is to date recognized as a threat to the integrity of invaded communities. Predation by D. villosus on native benthic invertebrates is assumed as the key determinant of its ecological impact, yet available information describe the species as a primary consumer as well as a carnivore depending on local conditions. Here, we assessed the trophic position (TP) of D. villosus in Lake Trasimeno, a recently invaded lentic system in central Italy, using the CN isotopic signatures of individuals captured in winter spanning two orders of magnitude in body size. TP estimations were compared with those characterizing the native amphipod Echinogammarus veneris and other representative invertebrate predators. On average, D. villosus showed a trophic position higher than E. veneris, and comparable with that of odonate nymphs. An in-depth analysis revealed that large-sized individuals had a trophic position of 3.07, higher than odonates and close to that of the hirudinean predator Erpobdella octoculata, while small-sized specimens had a trophic position of 2.57, similar to that of E. veneris (2.41). These findings indicate that size-related ontogenetic shifts in dietary habits may per se vary the nature of the interaction between Dikerogammarus villosus and native invertebrates from competition to predation. Information collated from published isotopic studies corroborated the generality of our results. We conclude that intra-specific trophic flexibility may potentially amplify and make more multifaceted the impact of the species on other invertebrate species in invaded food webs.openMancini F.; De Giorgi R.; Ludovisi A.; Vizzini S.; Mancinelli G.Mancini, F.; De Giorgi, R.; Ludovisi, A.; Vizzini, S.; Mancinelli, G

    Ultrasound diagnosis of serous surface papillary borderline ovarian tumor: A case series with a review of the literature

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    Serous surface papillary borderline ovarian tumors (SSPBOTs) are a rare morphologic variant of serous ovarian tumors that are typically confined to the ovarian surface, while the ovaries themselves tend to appear normal in size and shape. In this report, we describe the findings from five premenopausal women diagnosed with SSPBOTs, in whom ultrasound showed grossly normal ovaries that were partially or wholly covered with irregular solid tumors. In all five cases, histologic examination showed evidence of borderline serous tumors. These findings demonstrate that SSPBOTs can be diagnosed on a preoperative sonographic examination, which could facilitate conservative, fertility-sparing surgery in young women affected by this condition. © 2015 Wiley Periodicals, Inc. J Clin Ultrasound, 2015

    On Rationality

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    Rationality is an enduring topic of interest across the disciplines and has become even more so, given the current crises that are unfolding in our society. The four books reviewed here, which are written by academics working in economics, political science, political theory and philosophy, provide an interdisciplinary engagement with the idea of rationality and the way it has shaped the institutional frameworks and global political economy of our time. Rational choice theory has certainly proved to be a useful analytic tool in certain contexts, and instrumental reason has been a key tenet of human progress in several periods of history, including the industrial revolution and the modernity that emerged in the nineteenth century. Given the complexity of our current challenges, however, is it time to ask whether this paradigm might be better complemented by more holistic and heterodox approaches? Hindmoor A and Taylor TY (2015) Rational Choice (Political Analysis), 2nd edn. London; New York: Palgrave Macmillan. Massumi (2015) The Power at the End of the Economy. Durham: Duke University Press. Brown (2015) Undoing the Demos: Neoliberalism’s Stealth Revolution. New York: Zone Books. Ludovisi SG (ed.) (2015) Critical Theory and the Challenge of Praxis: Beyond Reification. Farnham; Burlington, VT: Ashgate

    Enhanced B-cell differentiation and reduced proliferative capacity in chronic hepatitis C and chronic hepatitis B virus infections

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    BACKGROUND & AIMS: Chronic microial infections aare frequently associated with B-cell activation and polyclonal proliferation, potentially leading to autoimmunity and lymphoproliferative disorders. We assessed B-cell phenotype and function in chronic hepatitis B (HBV) and chronic hepatitis C (HCV) virus infection. METHODS: We studied 70 patients with chronic HCV infection, 34 with chronic HBV infection and 54 healthy controls, B-cell phenotype was assessed by flow cytometry using monoclonal antibodies specific for CD27, the CD69, CD71, and CD86 activation markers and the chemokine receptor CXCR3. Differentiation into immunoglobulin-producing cells (IPC) was analysed by ELISpot upon stimulation and with CD40 ligand+IL-10 as surrogate bystander T-cell help or CpG oligodeoxynucleotide+IL-2, as innate immunity signal. Proliferation was examined by cytometry using carboxyfluorescein diacetate succinimidyl ester (CFSE) after stimulation with CpG. RESULTS: A significantly higher proportion of B cells from both HCV-and HBV-infected patients expressed activation markers compared with controls and a positive correlation was found between CXCR3(+) B cells and HCV RNA values. Memory B cells from patients with chronic HCV and HBV infections showed enhanced differentiation into IPC compared with controls, although this was restricted to IgG and at a lower level in HCV-compared with HBV-infected patients. Moreover, patients' activated B cells displayed significantly lower proliferative ability compared to healthy donors despite low expression of the FcRL4 exhaustin marker. CONCLUSIONS: B-cell activation, but not exhaustion, is common in chronic viral hepatitis. However, enhanced B-cell differentiation and deficient proliferative capacity were not associated with commitment to terminal differentiation

    A metastable equilibrium model for the relative abundances of microbial phyla in a hot spring

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    Many studies link the compositions of microbial communities to their environments, but the energetics of organism-specific biomass synthesis as a function of geochemical variables has rarely been assessed. We describe a thermodynamic model that integrates geochemical and metagenomic data for biofilms sampled at five sites along a thermal and chemical gradient in the outflow channel of the hot spring known as ‘‘Bison Pool’’ in Yellowstone National Park. The relative abundances of major phyla in individual communities sampled along the outflow channel are modeled by computing metastable equilibrium among model proteins with amino acid compositions derived from metagenomic sequences. Geochemical conditions are represented by temperature and activities of basis species, including pH and oxidation-reduction potential quantified as the activity of dissolved hydrogen. By adjusting the activity of hydrogen, the model can be tuned to closely approximate the relative abundances of the phyla observed in the community profiles generated from BLAST assignments. The findings reveal an inverse relationship between the energy demand to form the proteins at equal thermodynamic activities and the abundance of phyla in the community.Although the metabolisms used by many members of these communities are driven by chemical disequilibria, the results support the possibility that higher-level patterns of chemotrophic microbial ecosystems are shaped by metastable equilibrium states that depend on both the composition of biomass and the environmental conditions

    Employing a systematic approach to biobanking and analyzing clinical and genetic data for advancing COVID-19 research

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    Association of Toll-like receptor 7 variants with life-threatening COVID-19 disease in males: findings from a nested case-control study

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    Background: Recently, loss-of-function variants in TLR7 were identified in two families in which COVID-19 segregates like an X-linked recessive disorder environmentally conditioned by SARS-CoV-2. We investigated whether the two families represent the tip of the iceberg of a subset of COVID-19 male patients.Methods: This is a nested case-control study in which we compared male participants with extreme phenotype selected from the Italian GEN-COVID cohort of SARS-CoV-2-infected participants (<60y, 79 severe cases versus 77 control cases). We applied the LASSO Logistic Regression analysis, considering only rare variants on young male subsets with extreme phenotype, picking up TLR7 as the most important susceptibility gene.Results: Overall, we found TLR7 deleterious variants in 2.1% of severely affected males and in none of the asymptomatic participants. The functional gene expression profile analysis demonstrated a reduction in TLR7-related gene expression in patients compared with controls demonstrating an impairment in type I and II IFN responses.Conclusion: Young males with TLR7 loss-of-function variants and severe COVID-19 represent a subset of male patients contributing to disease susceptibility in up to 2% of severe COVID-19

    Ultra-rare RTEL1 gene variants associate with acute severity of COVID-19 and evolution to pulmonary fibrosis as a specific long COVID disorder

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    Background: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a novel coronavirus that caused an ongoing pandemic of a pathology termed Coronavirus Disease 19 (COVID-19). Several studies reported that both COVID-19 and RTEL1 variants are associated with shorter telomere length, but a direct association between the two is not generally acknowledged. Here we demonstrate that up to 8.6% of severe COVID-19 patients bear RTEL1 ultra-rare variants, and show how this subgroup can be recognized. Methods: A cohort of 2246 SARS-CoV-2-positive subjects, collected within the GEN-COVID Multicenter study, was used in this work. Whole exome sequencing analysis was performed using the NovaSeq6000 System, and machine learning methods were used for candidate gene selection of severity. A nested study, comparing severely affected patients bearing or not variants in the selected gene, was used for the characterisation of specific clinical features connected to variants in both acute and post-acute phases. Results: Our GEN-COVID cohort revealed a total of 151 patients carrying at least one RTEL1 ultra-rare variant, which was selected as a specific acute severity feature. From a clinical point of view, these patients showed higher liver function indices, as well as increased CRP and inflammatory markers, such as IL-6. Moreover, compared to control subjects, they present autoimmune disorders more frequently. Finally, their decreased diffusion lung capacity for carbon monoxide after six months of COVID-19 suggests that RTEL1 variants can contribute to the development of SARS-CoV-2-elicited lung fibrosis. Conclusion: RTEL1 ultra-rare variants can be considered as a predictive marker of COVID-19 severity, as well as a marker of pathological evolution in pulmonary fibrosis in the post-COVID phase. This notion can be used for a rapid screening in hospitalized infected people, for vaccine prioritization, and appropriate follow-up assessment for subjects at risk. Trial Registration NCT04549831 (www.clinicaltrial.org

    An explainable model of host genetic interactions linked to COVID-19 severity

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    We employed a multifaceted computational strategy to identify the genetic factors contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing (WES) dataset of a cohort of 2000 Italian patients. We coupled a stratified k-fold screening, to rank variants more associated with severity, with the training of multiple supervised classifiers, to predict severity based on screened features. Feature importance analysis from tree-based models allowed us to identify 16 variants with the highest support which, together with age and gender covariates, were found to be most predictive of COVID-19 severity. When tested on a follow-up cohort, our ensemble of models predicted severity with high accuracy (ACC = 81.88%; AUCROC = 96%; MCC = 61.55%). Our model recapitulated a vast literature of emerging molecular mechanisms and genetic factors linked to COVID-19 response and extends previous landmark Genome-Wide Association Studies (GWAS). It revealed a network of interplaying genetic signatures converging on established immune system and inflammatory processes linked to viral infection response. It also identified additional processes cross-talking with immune pathways, such as GPCR signaling, which might offer additional opportunities for therapeutic intervention and patient stratification. Publicly available PheWAS datasets revealed that several variants were significantly associated with phenotypic traits such as “Respiratory or thoracic disease”, supporting their link with COVID-19 severity outcome
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