16 research outputs found

    The Roman aqueduct of Brigetio

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    The aim of the present study is to examine the literary sources and the archaeological material regarding the aqueduct of Brigetio. Based on the available information the paper examines the problem of the localization of the source which supplied the aqueduct. The catalogue includes the descriptions of the lead and terracotta water pipes from Brigetio now in the Roman collection of the Hungarian National Museum. The results are presented with regards to the construction of the urban water distribution system

    New data on the capacity of the Roman aqueduct of Brigetio

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    New excavation of the Roman Age settlement at Budapest dist. XVII, PĂ©celi Ăşt (15127) site

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    In autumn 2019 the staff of the Institute of Archaeological Sciences conducted a rescue excavation in the suburbs of Budapest, on the territory of Pécel. Based on the long research history of the investigated site (Budapest dist. XVII, Péceli út) a settlement of the Imperial Period was expected. The excavation confirmed the expectations and two buildings, several ditches, an outdoor oven and numerous refuse pits were unearthed from the 3rd–4th century AD. The features contained many Samian ware fragments, which shed light on the Roman-Barbarian trade relations during the middle Imperial Period

    Excavations in Brigetio in 2020

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    In 2020, excavations were carried out simultaneously at several locations both in the territory of the legionary fortress and the military town of Brigetio. As a result, new information was gained regarding the structure of the legionary fortress and a number of late Roman period graves were also identified. The most significant result of the campaign was the excavation of an almost intact cellar in the western zone of the canabae

    Diversity of vertebrate splicing factor U2AF35 : identification of alternatively spliced U2AF1 mRNAS

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    © 2004 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. This is an Open Access article under the CC BY license.U2 small nuclear ribonucleoprotein auxiliary factor small subunit (U2AF(35)) is encoded by a conserved gene designated U2AF1. Here we provide evidence for the existence of alternative vertebrate transcripts encoding different U2AF(35) isoforms. Three mRNA isoforms (termed U2AF(35)a-c) were produced by alternative splicing of the human U2AF1 gene. U2AF(35)c contains a premature stop codon that targets the resulting mRNA to nonsense-mediated mRNA decay. U2AF(35)b differs from the previously described U2AF(35)a isoform in 7 amino acids located at the atypical RNA Recognition Motif involved in dimerization with U2AF(65). Biochemical experiments indicate that isoform U2AF(35)b, which has been highly conserved from fish to man, maintains the ability to interact with U2AF(65), stimulates U2AF(65) binding to a pre-mRNA, and promotes U2AF splicing activity in vitro. Real time, quantitative PCR analysis indicates that U2AF(35)a is the most abundant isoform expressed in murine tissues, although the ratio between U2AF(35)a and U2AF(35)b varies from 10-fold in the brain to 20-fold in skeletal muscle. We propose that post-transcriptional regulation of U2AF1 gene expression may provide a mechanism by which the relative cellular concentration and availability of U2AF(35) protein isoforms are modulated, thus contributing to the finely tuned control of splicing events in different tissues.This work was supported in part by Grant POCTI/MGI/36547/2000 from Fundação para a Ciência e Tecnologia, Portugal, and by Grant RG0300/2000-M from the Human Frontier Science Program Organization. Supported by Fundação para a Ciência e Tecnologia Fellowship PRAXIS XXI/BD/18044/98. Supported by Fundação para a Ciência e Tecnologia Fellowship POCTI SFRH/BPD/9388/2002. Supported by Fundação para a Ciência e Tecnologia Fellowship PRAXIS XXI SFRH/BD/2914/2000.info:eu-repo/semantics/publishedVersio

    Identification of novel follicular dendritic cell sarcoma markers, FDCSP and SRGN, by whole transcriptome sequencing

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    Follicular dendritic cell (FDC)-sarcoma is a rare neoplasm with morphologic and phenotypic features of FDCs. It shows an extremely heterogeneous morphology, therefore, its diagnosis relys on the phenotype of tumor cells. Aim of the present study was the identification of new specific markers for FDC-sarcoma by whole transcriptome sequencing (WTS). Candidate markers were selected based on gene expression level and biological function. Immunohistochemistry was performed on reactive tonsils, on 22 cases of FDC-sarcomas and 214 control cases including 114 carcinomas, 87 soft tissue tumors, 5 melanomas, 5 thymomas and 3 interdigitating dendritic cell sarcomas. FDC secreted protein (FDCSP) and Serglycin (SRGN) proved to be specific markers of FDC and related tumor. They showed better specificity and sensitivity values than some well known markers used in FDC sarcoma diagnosis (specificity: 98.6%, and 100%, respectively; sensitivity: 72.73% and 68.18%, respectively). In our cohorts CXCL13, CD21, CD35, FDCSP and SRGN were the best markers for FDC-sarcoma diagnosis and could discriminate 21/22 FDC sarcomas from other mesenchymal tumors by linear discriminant analysis. In summary, by WTS we identified two novel FDC markers and by the analysis of a wide cohort of cases and controls we propose an efficient marker panel for the diagnosis of this rare and enigmatic tumor

    Understanding the Effectiveness of Incarceration on Juvenile Offending through A Systematic Review and Meta-Analysis: Do the "Get Tough" Policies work?

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    The juvenile system is no longer perceived as a social welfare model, but has become more punitive approximating a crime control model. Juveniles are not responsible for the majority of crime in the United States and are not the most serious and violent demographic; however, they are incarcerated at a higher rate than adults. Incarceration is an element of deterrence currently used by the juvenile justice system without a clear conclusion of whether or not it works to reduce juvenile crime. The goal of this research was to first conduct a systematic review of prior studies on the effectiveness of incarceration on recidivism rates for juvenile offenders. A meta-analysis design was used on selected studies that met the inclusion criteria to determine if a relationship exists. This study compared and reviewed the recidivism rates of juvenile offenders sentenced to incarceration with a comparison group as identified in each study. The method for statistical measurement to test the research questions focused on analyzing effect sizes with a mean effect size through a meta-analysis. Moderators were analyzed across groups on their effect on recidivism. The length of the sentences for juveniles were examined and the results showed an association between longer sentences and reduced recidivism. Additionally, the effect sizes comparing recidivism between incarceration with non-incarceration resulted in negative relationship. Incarcerating juveniles is not a deterrent for criminal behavior, rather incarceration increased recidivism. It is time for policy makers to adhere to the evidence that incarceration does not deter crime and accept that imprisoning juveniles does not fulfill the promises of reducing crime and increasing public safety

    Three Empirical Essays on Informality

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    [eng] Informality is a very complex subject, with the informal workers we see on the streets as only the surface of larger and more complicated issues. The word "informality," when applied to labour, has negative associations. However, it is necessary to identify the economic agents that make up this sector. In this way, studying informality from different perspectives is one of the most important objectives of this thesis. The thesis focuses its analysis on informal labour and economic units, placing the informality of firms at the centre of the study in two chapters. In this way, two main aspects of informality are studied here: labour informality and business informality. Labour informality is analysed in a macroeconomic context and its relationship with investments. Firm informality is analysed from a micro-firm perspective, which has been largely ignored in the literature, with the measurement of micro-firm informality on a per-state basis within a developing country, Mexico, as another objective. A further objective is to ascertain whether there are differences in efficiency between formal and informal micro-firms. The particular objectives and results are as follows: Chapter 2 examines how informal labor markets affect the flows of FDI, and also whether this effect is similar in developed and developing countries. It highlights for the period of study (1996-2009), and the use of panel econometric models in this kind of researches. The sample is made up 65 countries. In addition, this paper uses a dynamic model as an extension of the analysis to establish whether such an effect exists and what its indicators and significance may be. While the results shows that informal labor markets are significant and do positively affect the flow of FDI, these effects are felt up to a certain level of informality, above which the effect becomes negative. The results are similar for developed and developing countries and are robust to several checks. Chapter 3 analyzes the determinants of micro-firms informality in Mexican states inasmuch as the research for micro firms in a developing country has been less noticeable. In this paper, Mexico is taken as case of study by its high level of micro firm informality and the heterogeneity among Mexican states, but also due to data availability. Panel econometric models are estimated for a sample of 32 states over the period 2008-2012. In addition, this paper uses different definitions of informality to check the robustness of the results. The obtained empirical evidence allows us to conclude that, although, economic factors are the main causes of informality variables such as corruption and education have important role to play. Chapter 4 separates formal and informal micro firms in order to test whether there are efficiency differences between them, and to explain these differences. One of the novelties of the study is the use of the Oaxaca-Blinder decomposition method, which enables an analysis of the differences between both groups of firms after controlling for their different allocation of factors. The empirical evidence suggests that output differences can be explained by endowment characteristics, while efficiency differences are explained by endowment returns. The main variables to explain the gap between the groups are the owner’s level of education, the firm’s age, the owner’s motivations, and financing as well

    Siglec-H-Deficient Mice Show Enhanced Type I IFN Responses, but Do Not Develop Autoimmunity After Influenza or LCMV Infections

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    Siglec-H is a DAP12-associated receptor on plasmacytoid dendritic cells (pDCs) and microglia. Siglec-H inhibits TLR9-induced IFN-α production by pDCs. Previously, it was found that Siglec-H-deficient mice develop a lupus-like severe autoimmune disease after persistent murine cytomegalovirus (mCMV) infection. This was due to enhanced type I interferon responses, including IFN-α. Here we examined, whether other virus infections can also induce autoimmunity in Siglec-H-deficient mice. To this end we infected Siglec-H-deficient mice with influenza virus or with Lymphocytic Choriomeningitis virus (LCMV) clone 13. With both types of viruses we did not observe induction of autoimmune disease in Siglec-H-deficient mice. This can be explained by the fact that both types of viruses are ssRNA viruses that engage TLR7, rather than TLR9. Also, Influenza causes an acute infection that is rapidly cleared and the chronicity of LCMV clone 13 may not be sufficient and may rather suppress pDC functions. Siglec-H inhibited exclusively TLR-9 driven type I interferon responses, but did not affect type II or type III interferon production by pDCs. Siglec-H-deficient pDCs showed impaired Hck expression, which is a Src-family kinase expressed in myeloid cells, and downmodulation of the chemokine receptor CCR9, that has important functions for pDCs. Accordingly, Siglec-H-deficient pDCs showed impaired migration towards the CCR9 ligand CCL25. Furthermore, autoimmune-related genes such as Klk1 and DNase1l3 are downregulated in Siglec-H-deficient pDCs as well. From these findings we conclude that Siglec-H controls TLR-9-dependent, but not TLR-7 dependent inflammatory responses after virus infections and regulates chemokine responsiveness of pDCs.</p
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