946,364 research outputs found
BARR-C:2018 and MISRA C:2012: Synergy Between the Two Most Widely Used C Coding Standards
The Barr Group’s Embedded C Coding Standard (BARR-C:2018, which originates from the 2009 Netrino’s Embedded C Coding Standard) is, for coding standards used by the embedded system industry, second only in popularity to MISRA C. However, the choice between MISRA C:2012 and BARR-C:2018 needs not be a hard decision since they are complementary in two quite different ways. On the one hand, BARR-C:2018 has removed all the incompatibilities with respect to MISRA C:2012 that were present in the previous edition (BARR-C:2013). As a result, disregarding programming style, BARR-C:2018 defines a subset of C that, while preventing a significant number of programming errors, is larger than the one defined by MISRA C:2012. On the other hand, concerning programming style, whereas MISRA C leaves this to individual organizations, BARR-C:2018 defines a programming style aimed primarily at minimizing programming errors. As a result, BARR-C:2018 can be seen as a first, dramatically useful step to C language subsetting that is suitable for all kinds of projects; critical projects can then evolve toward MISRA C:2012 compliance smoothly while maintaining the BARR-C programming style. In this paper, we introduce BARR-C:2018, we describe its relationship with MISRA C:2012, and we discuss the parallel and serial adoption of the two coding standards
BARR-C:2018 and MISRA C:2012 (with Amendment 2): Synergy Between the Two Most Widely Used C Coding Standards
The Barr Group's Embedded C Coding Standard (BARR-C:2018, which originates from the 2009 Netrino's Embedded C Coding Standard) is, for coding standards used by the embedded system industry, second only in popularity to MISRA C. However, the choice between MISRA C:2012 and BARR-C:2018 needs not be a hard decision since they are complementary in two quite different ways. On the one hand, BARR-C:2018 has removed all the incompatibilities with respect to MISRA C:2012 that were present in the previous edition (BARR-C:2013). As a result, disregarding programming style, BARR-C:2018 defines a subset of C that, while preventing a significant number of programming errors, is larger than the one defined by MISRA C:2012. On the other hand, concerning programming style, whereas MISRA C leaves this to individual organizations, BARR-C:2018 defines a programming style aimed primarily at minimizing programming errors. As a result, BARR-C:2018 can be seen as a first, dramatically useful step to C language subsetting that is suitable for all kinds of projects; critical projects can then evolve toward MISRA C:2012 compliance smoothly while maintaining the BARR-C programming style. In this paper, we introduce BARR-C:2018, we describe its relationship with MISRA C:2012, and we discuss the parallel and serial adoption of the two coding standards
Clonal origin of Epstein-Barr virus-infected T/NK-cell subpopulations in chronic active Epstein-Barr virus infection
Clonal expansion of Epstein-Barr virus (EBV) infected B-cells occasionally occurs in immunocompromized subjects. EBV-infected T/natural killer (NK)-cells proliferate in patients with chronic active EBV infection (CAEBV) that is a rare mononucleosis syndrome. It is classified into either T-cell type or NK-cell type according to the primary target of infection, while the pathogenesis remains unclear. To search the clonal origin of EBV-infected T/NK-cells, virus distribution and clonotype were assessed by using highly purified cell fractions obtained from 6 patients. Patient 1 had a monoclonal proliferation of EBV-infected T-cell receptor Vδ2/Vγ9-expressing cells, and carried lower copy number of EBV in αβT-cells. Patients 2 and 3 had a clonal expansion of EBV-infected CD4+T-cells, and lower EBV load in CD56+cells. Patients 4, 5 and 6 had an expansion of CD56+cells with higher EBV load than CD3+cells. EBV-terminal repeats were determined as clonal bands in the minor targeted populations of 5 patients. The size of terminal repeats indicated the same clonotype in minor subsets as in major subsets of 4 patients. However, EBV was not detected in bone marrow-derived lineage negative CD34+cells of patients. These results suggested that EBV could infect T/NK-cells at differentiation stage, but spared bone marrow CD34+hematopoietic stem cells in CAEBV patients
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Charles B. Moore Family papers, 1832-1917
Transcript of a letter sent to Charles B. Moore from J. C. Barr discussing oil drilling in Jersey County, the health of acquaintances, railroad construction, farming, weather, as well as other family and local news. The third page of the letter is a segment added by Mary A. Barr discussing family life including visiting and gardening
Charles B. Moore Family papers, 1832-1917
Transcript of a letter sent to Charles B. Moore from J. C. Barr discussing oil drilling in Jersey County, the health of acquaintances, railroad construction, farming, weather, as well as other family and local news. The third page of the letter is a segment added by Mary A. Barr discussing family life including visiting and gardening
Sam Barr Interview, 1973
Sam Barr was born in a boxcar in Forsythe, Montana on May 19, 1914 to Samuel Arthur Barr, an itinerant line man with a power company and his wife Julia Cecelia (Weber) Barr. The family returned to Ortonville when Sam was six months old. Sam was educated in Ortonville until illness took him out of school before graduating high school. In the early 1950s Sam became involved in politics. He served 12 years as a representative in the Minnesota State Legislature.
In this interview, Sam Barr discusses his early background and his first involvement in politics in the 1950s. He discusses Bill Sorenson, representative, and Barr\u27s first election to the House. He discusses major issues during his 12 years as a representative, including: sales tax issues, bills sponsored by Barr (small loan industry bill and doctor procurement for rural Minnesota bill), Barr\u27s association with UMN Morris and the establishment of UMN Morris, non-party designated legislature vs. party-type legal issue, a cloud seeding bill, the regard for the Minnesota government and representative Ed Martinson.https://digitalcommons.morris.umn.edu/mnoralhistories/1119/thumbnail.jp
Immunodominance of lytic cycle antigens in Epstein-Barr virus-specific CD4+ T cell preparations for therapy.
Epstein-Barr virus (EBV) is associated with a number of human malignancies. EBV-positive post-transplant lymphoproliferative disease in solid organ and hematopoietic stem cell transplant recipients has been successfully treated by the adoptive transfer of polyclonal EBV-specific T cell lines containing CD4+ and CD8+ T cell components. Although patients receiving T cell preparations with a higher CD4+ T cell proportion show better clinical responses, the specificity of the infused CD4+ component has remained completely unknown.
We generated LCL-stimulated T cell lines from 21 donors according to clinical protocols, and analyzed the antigen specificity of the CD4+ component in EBV-specific T cell preparations using a genetically engineered EBV mutant that is unable to enter the lytic cycle, and recombinantly expressed and purified EBV proteins. Surprisingly, CD4+ T cell lines from acutely and persistently EBV-infected donors consistently responded against EBV lytic cycle antigens and autoantigens, but barely against latent cycle antigens of EBV hitherto considered principal immunotherapeutic targets. Lytic cycle antigens were predominantly derived from structural proteins of the virus presented on MHC II via receptor-mediated uptake of released viral particles, but also included abundant infected cell proteins whose presentation involved intercellular protein transfer. Importantly, presentation of virion antigens was severely impaired by acyclovir treatment of stimulator cells, as currently performed in most clinical protocols.
These results indicate that structural antigens of EBV are the immunodominant targets of CD4+ T cells in LCL-stimulated T cell preparations. These findings add to our understanding of the immune response against this human tumor-virus and have important implications for the improvement of immunotherapeutic strategies against EBV
Upregulation of Id1 by Epstein-Barr Virus-encoded LMP1 confers resistance to TGFβ-mediated growth inhibition
Background
Epstein-Barr virus (EBV)-encoded LMP1 protein is commonly expressed in nasopharyngeal carcinoma (NPC). LMP1 is a prime candidate for driving tumourigenesis given its ability to activate multiple signalling pathways and to alter the expression and activity of variety of downstream targets. Resistance to TGFβ-mediated cytostasis is one of the growth transforming effects of LMP1. Of the downstream targets manipulated by LMP1, the induction of Id1 and inactivation of Foxo3a appear particularly relevant to LMP1-mediated effects. Id1, a HLH protein is implicated in cell transformation and plays a role in cell proliferation, whilst Foxo3a, a transcription factor controls cell integrity and homeostasis by regulating apoptosis. The mechanism(s) by which LMP1 induces these effects have not been fully characterised.
Results
In this study, we demonstrate that the ability of LMP1 to induce the phosphorylation and inactivation of Foxo3a is linked to the upregulation of Id1. Furthermore, we show that the induction of Id1 is essential for the transforming function of LMP1 as over-expression of Id1 increases cell proliferation, attenuates TGFβ-SMAD-mediated transcription and renders cells refractory to TGFβ-mediated cytostasis. Id1 silencing in LMP1-expressing epithelial cells abolishes the inhibitory effect of LMP1 on TGFβ-mediated cell growth arrest and reduces the ability of LMP1 to attenuate SMAD transcriptional activity. In response to TGFβ stimulation, LMP1 does not abolish SMAD phosphorylation but inhibits p21 protein expression. In addition, we found the induction of Id1 in LMP1-expressing cells upon stimulation by TGFβ. We provide evidence that LMP1 suppresses the transcriptional repressor ATF3, possibly leading to the TGFβ-induced Id1 upregulation.
Conclusion
The current data provide novel information regarding the mechanisms by which LMP1 suppresses TGFβ-induced cytostasis, highlighting the importance of Id1 in LMP1 mediated cell transformation
Micro RNAs of Epstein-Barr virus promote cell cycle progression and prevent apoptosis of primary human B cells.
Cellular and viral microRNAs (miRNAs) are involved in many different processes of key importance and more than 10,000 miRNAs have been identified so far. In general, relatively little is known about their biological functions in mammalian cells because their phenotypic effects are often mild and many of their targets still await identification. The recent discovery that Epstein-Barr virus (EBV) and other herpesviruses produce their own, barely conserved sets of miRNAs suggests that these viruses usurp the host RNA silencing machinery to their advantage in contrast to the antiviral roles of RNA silencing in plants and insects. We have systematically introduced mutations in EBV's precursor miRNA transcripts to prevent their subsequent processing into mature viral miRNAs. Phenotypic analyses of these mutant derivatives of EBV revealed that the viral miRNAs of the BHRF1 locus inhibit apoptosis and favor cell cycle progression and proliferation during the early phase of infected human primary B cells. Our findings also indicate that EBV's miRNAs are not needed to control the exit from latency. The phenotypes of viral miRNAs uncovered by this genetic analysis indicate that they contribute to EBV-associated cellular transformation rather than regulate viral genes of EBV's lytic phase
Charles B. Moore Family papers, 1832-1917
Letter sent to Charles B. Moore from J. C. Barr discussing oil drilling in Jersey County, the health of acquaintances, railroad construction, farming, weather, as well as other family and local news. The third page of the letter is a segment added by Mary A. Barr discussing family life including visiting and gardening
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