128 research outputs found
Flow boiling heat transfer in a helically coiled steam generator for nuclear power applications
Forced convection boiling of water was experimentally investigated in a 24 mlong full-scale helically coiled steam generator tube, prototypical of the steam generators with in-tube boiling used in small modular nuclear reactor systems. Overall, 1575 axially local and peripherally averaged heat transfer coefficient measurements were taken, covering operating pressures in the range of 2–6 MPa, mass fluxes from 200 to 800 kg m-2 s-1 and heat fluxes from 40 to 230 kW m-2. The heat transfer coefficient was found to depend on the mass flux and on the heat flux, indicating that both nucleate boiling and convection are contributing
to the heat transfer process. Seven widely quoted flow boiling correlations for straight tubes fitted the present helical coil databank with a mean absolute percentage error within 15–20%, which was comparable with the experimental uncertainty of the measured heat transfer coefficient values, thus indicating that curvature effects on flow boiling are small and negligible in practical applications
European Economies in the First Epoch of Imperialism and Mercantilism. 1415-1846.
The costs and benefits of European Imperialism from the conquest of Ceuta, 1415, to the Treaty of Lusaka, 1974.Twelfth International Economic History Congress. Madrid, 1998.Patrick K. O'Brien and Leandro Prados de la Escosura (eds.)Editada en la Fundación Empresa PúblicaJorge M. Pedreira. «To Have and To Have not». The Economic Consequences of Empire: Portugal (1415-1822).-- Bartolomé Yun-Casalilla. The American Empire and the Spanish Economy: An Institutional and Regional Perspective.-- Pieter C. Emmer. The Economic Impact of the Dutch Expansion Overseas, 1570-1870.-- Paul Butel and François Crouzet. Empire and Economic Growth: the Case of 18th Century France.-- Stanley L. Engerman. British Imperialism in a Mercantilist Age, 1492-1849: Conceptual Issues and Empirical Problems.Publicad
Pre-incubation of cell-free HIV-1 group M isolates with non-nucleoside reverse transcriptase inhibitors blocks subsequent viral replication in co-cultures of dendritic cells and T cells.
In order to study the inhibitory effect of various reverse transcriptase inhibitors (RTIs) on cell-free HIV, we adapted a recently described in vitro system, based on co-cultures of dendritic cells and resting CD4 T cells, modelling early target cells during sexual transmission. The compounds tested included the second-generation non-nucleoside RTI (NNRTI) TMC-120 (R147681, dapivirine) and TMC-125 (R165335, travertine), as well as the reference nucleoside RTI AZT (zidovudine), the nucleotide RTI PMPA (tenofovir) and the NNRTI UC-781. The virus strains included the reference strain HIV-1Ba-L and six primary isolates, representative of the HIV-1 group M pandemic. They all display the non-syncytium-inducing and CCR5 receptor-using (NSI/R5) phenotype, important in transmission. Cell-free virus was immobilized on a poly-L-lysine (PLL)-treated microwell plate and incubated with compound for 1 h. Afterwards, the compound was thoroughly washed away; target cells were added and cultured for 2 weeks, followed by an extended culture with highly susceptible mitogen-activated T cells. Viral production in the cultures was measured on supernatant with HIV antigen ELISA. Negative results were confirmed by showing absence of proviral DNA in the cells. TMC-120 and TMC-125 inhibited replication of HIV-1Ba-L with average EC50 values of 38 nM and 117 nM, respectively, whereas the EC50 of UC-781 was 517 nM. Complete suppression of virus and provirus was observed at compound concentrations of 100, 300 and 1000 nM, respectively. Inhibition of all primary isolates followed the same pattern as HIV-1Ba-L. In contrast, pre-treating the virus with the nucleotide RTI PMPA and AZT failed to inhibit infection even at a concentration of 100000 nM. These data clearly suggest that NNRTIs inactivate RT enzymatic activity of different viral clades (predominant in the epidemic) and might be proposed for further testing as a sterilizing microbicide worldwide
Transformation of B Lymphocytes by SV40, a small DNA tumor virus
For decades we have assessed the risk to humans by the monkey virus SV40, through studies in animal models and humans.
While there is increase in the accumulation of opinions over its DNA sequence prevalence in certain human cancers, especially non-Hodgkin’s lymphoma, only few works have been addressed towards SV40 presence in human blood of healthy subject.
In this work, experiment one, detected SV40 DNA sequences in 10/60 (17%) buffy coats of normal human blood donor of Aviano, Italy.
In other to have insight if SV40 plays a role in lymphomagenesis, experiment two and three observed it’s in vitro interaction with normal human lymphocytes using infected and transfected purified T and B cells with SV40 virus and plasmid pSV3Neo.
SV40 DNA sequences was detected with PCR analysis for 100 days post-infection (d.p.i) in both infected and transfected T and B cells respectively. Indirect immunoflourescence techniques detected VP1 protein for 50-d.p.i in infected cells and Tag protein in both infected and transfected throughout the d.p.i in culture, suggesting proper integration of SV40 into the cells. RT-PCR experiment also detected mRNA Tag for 30 and 20-d.p.i in infected T and B cells respectively.
Trypan blue analysis and alamar blue assays revealed an increase of infected/transfected cells number and successively, a drastic and constant reduction in cell numbers in culture.
Effective production of progeny was revealed with C.P.E and plaque assay with different titers in infected cells using CV-1 monolayer cells. Structure distortion was observed in both cell lines from early d.p.i using TEM.
Presence of SV40 DNA sequence in normal blood donors suggested the human PBMCs to be a reservoir for SV40 virus.
Furthermore, in this study, it has proved such as T cells and B are experimentally susceptible to infection by SV40. Further research will deepen and will focus on assessing the role of SV40 as a co-factor in the genesis of lymphoma
Cytotoxic T Lymphocyte Recognition Sequences as Markers for Distinguishing Among Tumour Antigens Encoded by SV40, BKV and JCV
Simian virus 40 (SV40) has been shown to be associated with a number of human tumours. Two other human papova viruses, BKV and JCV, infect humans at a relatively high frequency and are activated upon immune suppression. The T antigens of both of these viruses share considerable homologies with the transforming protein T antigen of SV40. We have used SV40 T antigen specific cytotoxic T lymphocyte (CTL) clones to discriminate among the T antigens of SV40, BKV and JCV. These CTL clones directed to four distinct CTL epitopes serve as specific probes and can differentiate subtle alterations or deletions in the CTL epitopes relative to SV40 T antigen. Using this strategy, we have been able to authenticate three SV40 viruses isolated from humans as all four distinct CTL epitopes in the T antigens encoded by these three SV40 human isolates (SVCPC, SVMEN, and SVPML-1) were found to be identical to prototype SV40. We have further identified a 198 amino acid deletion T antigen variant of SVCPC. The finding of a deletion mutant in the SVCPC virus population suggests that the cellular immune response may play a role in the selection of antigenic loss variants
SV40 large T antigen directed by regulatory elements of the human alpha-1-antitrypsin gene. A transgenic mouse system that exhibits stages in liver carcinogenesis
SV40 large T antigen (T-ag) is a potent oncogene able to transform many cell types. The human alpha-1-antitrypsin (AAT) gene encodes the major serine protease inhibitor in plasma. The 5\u27 flanking sequence of the AAT gene contains cis-acting elements that specify the expression of reporter genes in transgenic mice. Although the AAT gene is expressed primarily in the liver, it also is expressed in epithelial cells of the stomach, kidney, intestine and pancreas. A fusion gene with the 5\u27 flanking region of AAT driving the SV40 large T-ag gene was used to generate transgenic mice. Between 2 and 6 months of age, 6 of 7 founder mice developed hepatic neoplasms. Kidney hyperplasia (3/7) and carcinomas of the stomach (4/7) and pancreas (1/7) also were observed. Tumor cells in the different sites expressed T-ag that was detectable by immunohistochemical staining. A transgenic mouse line (1812) was established; liver tumors develop reproducibly in all offspring. Cellular changes progressing to liver tumor formation occur in discrete stages with predictable kinetics in animals of the 1812 line: (i) embryonal/fetal stage, no major histological changes; (ii) newborn to 2 weeks of age, hyperplastic livers with minor cellular changes; (iii) mice between 3 and 8 weeks of age, diffuse liver cell dysplasia without observable tumor nodules; (iv) mice 8 weeks of age and older, hepatocellular carcinomas and hepatoblastomas in a background of liver dysplasia. There was uniform expression of T-ag in the majority of hepatocytes in the first two stages, whereas the dysplastic stage was characterized by variation in both the intensity of staining and the proportion of positive cells. Most tumor nodules expressed high levels of T-ag, but occasional negative and very weakly staining nodules were observed. T-ag was found complexed with the cellular p53 protein in tumor cells. This transgenic mouse system provides a practical model for the molecular analysis of defined steps in hepatocarcinogenesis
High efficiency LOW AM/PM 6W C-band MMIC power amplifier for a space radar program
This paper describes the design of a compact C-band MMIC power amplifier. Intensive non-linear and electro-magnetic simulations with accurate table-based models allowed the chips to achieve very good performance. A linear gain of 28 dB, an output power greater than 6 W with 50 % of power added efficiency and 3°/dB of AM/PM conversion at 2.5 dB gain compression have been measured over production at ambient temperature in the useful bandwidth
Business Ecosystem in Asian Context: The Challenges of Social Embeddedness. Call for papers
This is the author accepted manuscript
Specific antigen of tumor cell transformed by DNA extracted from SV-40 virus
In the immunofluorescent study it has been revealed that rabbit sera immunized with transformed cells induced by SV-40 DNA, produce circulating antibody capable of re:lcting with intranuclear antigens synthesized by SV-40 complyte virus transforming process, In addition, the result confirmed that SV-40 DNA replicates DNA-containing
viruses in the host cell and that also the genome coding for the synthesis of SV-40 tumor antigen is resposible for viral DNA.</p
Investigation into how mitotic spindle checkpoint function is compromised by Sv40 large T antigen.
The viral oncoprotein Simian virus 40 large T antigen (LT) efficiently immortalises primary rodent cells and occasionally transforms them to tumourigenicity. It has long been known that LT can cause genomic instability and induce aneuploidy, and that it disrupts the mitotic spindle checkpoint, involved in monitoring the segregation of sister chromatids. LT has recently been shown to interact with the spindle checkpoint protein Bubl. This thesis describes research into the effects of LT on spindle checkpoint function and examines the possibility that interaction of LT with Bubl is responsible. Novel monoclonal antibodies against Bubl were developed to aid this research. The interaction site of Bubl was mapped to amino acids 89-97 of LT using co-immunoprecipitation experiments in several cell lines, each expressing LT with a different mutation in the amino-terminal region. The non-Bub 1-binding (dl89-97) mutant was capable of immortalising rat embryo fibroblasts as efficiently as wild- type LT, but was defective for focus formation, perhaps suggesting a role for Bubl in the mechanism for transformation by LT. In the presence of the microtubule-depolymerising drug nocodazole, the spindle checkpoint is activated and cells arrest in mitosis. LT was shown to compromise spindle checkpoint function, allowing some cells to pass through to the next cell cycle even in the presence of nocodazole. However, without Bubl interaction, LT loses this ability and the spindle checkpoint is robust. An investigation of the checkpoint proteins and complexes present during spindle checkpoint activation in cells expressing wild-type or dl89-97 LT was initiated to analyse possible mechanisms for perturbation of the spindle checkpoint by LT. This study raises the possibility that LT induces genetic instability in mammalian cells by perturbation of spindle checkpoint function, and that this may be a critical component of the mechanism by which LT transforms cells
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