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Charles B. Moore Family papers, 1832-1917
No full textTranscript 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
No full textTranscript 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
Nellie (Mrs. D. P.) Barr, died Oct 30, 1876 at Houston, Tex.
No full textPortrait of Cornelia ''Nellie'' Rose Barr, wife of photographer David Perry Barr. She is seated in a studio, leaning against the arm of a couch, with her head propped up with her arm, and looking at the camera.Recto: [notation] Died Oct 30, 1876 at Houston, Tex. Verso: [notation] Nellie (Mrs. D. B. [sic]) Barr [imprinted] Barr & Wright, Photographers, Houston, Texas
Charles B. Moore Family papers, 1832-1917
No full textLetter 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
Recommended from our members
Charles B. Moore Family papers, 1832-1917
No full textLetter 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
Lymphoid hyperplasia and lymphoma in transgenic mice expressing the small non-coding RNA, EBER1 of Epstein-Barr virus
No full textBackground. Non-coding RNAs have critical functions in diverse biological processes, particularly in gene regulation. Viruses, like their host cells, employ such functional RNAs and the human cancer associated Epstein-Barr virus (EBV) is no exception. Nearly all EBV associated tumours express the EBV small, non-coding RNAs (EBERs) 1 and 2, however their role in viral pathogenesis remains largely obscure.Methodology/Principal FindingsTo investigate the action of EBER1 in vivo, we produced ten transgenic mouse lines expressing EBER1 in the lymphoid compartment using the mouse immunoglobulin heavy chain intronic enhancer E++. Mice of several of these E++EBER1 lines developed lymphoid hyperplasia which in some cases proceeded to B cell malignancy. The hallmark of the transgenic phenotype is enlargement of the spleen and mesenteric lymph nodes and in some cases enlargement of the thymus, liver and peripheral lymph nodes. The tumours were found to be of B cell origin and showed clonal IgH rearrangements. In order to explore if EBER1 would cooperate with c-Myc (deregulated in Burkitt's lymphoma) to accelerate lymphomagenesis, a cross-breeding study was undertaken with E++EBER1 and E++Myc mice. While no significant reduction in latency to lymphoma onset was observed in bi-transgenic mice, c-Myc induction was detected in some E++EBER1 single transgenic tumours, indicative of a functional cooperation. Conclusions/SignificanceT his study is the first to describe the in vivo expression of a polymerase III, non-coding viral gene and demonstrate its oncogenic potential. The data suggest that EBER1 plays an oncogenic role in EBV associated malignant disease
Conditional immortalization of human B cells by CD40 ligation
No full textIt is generally assumed that human differentiated cells have a limited life-span and proliferation capacity in vivo, and that genetic modifications are a prerequisite for their immortalization in vitro. Here we readdress this issue, studying the long-term proliferation potential of human B cells. It was shown earlier that human B cells from peripheral blood of healthy donors can be efficiently induced to proliferate for up to ten weeks in vitro by stimulating their receptor CD40 in the presence of interleukin-4. When we applied the same stimuli under conditions of modified cell number and culture size, we were surprised to find that our treatment induced B cells to proliferate throughout an observation period of presently up to 1650 days, representing more than 370 population doublings, which suggested that these B cells were immortalized in vitro. Long-term CD40-stimulated B cell cultures could be established from most healthy adult human donors. These B cells had a constant phenotype, were free from Epstein-Barr virus, and remained dependent on CD40 ligation. They had constitutive telomerase activity and stabilized telomere length. Moreover, they were susceptible to activation by Toll-like receptor 9 ligands, and could be used to expand antigen-specific cytotoxic T cells in vitro. Our results indicate that human somatic cells can evade senescence and be conditionally immortalized by external stimulation only, without a requirement for genetic manipulation or oncoviral infection. Conditionally immortalized human B cells are a new tool for immunotherapy and studies of B cell oncogenesis, activation, and function
Micro RNAs of Epstein-Barr virus promote cell cycle progression and prevent apoptosis of primary human B cells.
No full textCellular 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
Characterization of murine gammaherpesvirus 68 glycoprotein B (gB) homolog: similarity to Epstein-Barr virus gB (gp110)
No full textMurine gammaherpesvirus 68 (MHV-68) is a natural pathogen of murid rodents and displays similar pathobiological characteristics to those of the human gammaherpesvirus Epstein-Barr virus (EBV). However, in contrast to EBV, MHV-68 will replicate in epithelial cells in vitro. It has therefore been proposed that MHV-68 may be of use as a model for the study of gammaherpesviruses, EBV in particular, both in vitro and in vivo. The EBV homolog of herpes simplex virus glycoprotein B (gB), termed gp110, is somewhat unusual compared with those of many other herpesviruses. We therefore decided to characterize the homolog of gB encoded by MHV-68 (termed MHV gB) to observe the properties of a gammaherpesvirus gB produced in epithelial cells and also to test the relatedness of MHV-68 and EBV. The MHV gB-coding sequence was determined from cloned DNA. The predicted amino acid sequence shared closest homology with gammaherpesvirus gB homologs. Biochemical analysis showed that MHV gB was a glycoprotein with a molecular weight of 105,000. However, the glycans were of the N-linked, high-mannose type, indicating retention in the endoplasmic reticulum. In line with this, MHV gB was localized to the cytoplasm and nuclear margins of infected cells but was not detected on the cell surface or in virions. Additionally, anti-MHV gB antisera were nonneutralizing. Thus, the MHV gB was unlike many other herpesvirus gBs but was extremely similar to the EBV gB. This highlights the close relationship between MHV-68 and EBV and underlines the potential of MHV-68 as a model for EBV in epithelial cells both in vitro and in vivo
Liberty and Union forever the watchword of the free [first line of chorus]
No full textstrophic with choruspiano and voiceJohns Hopkins University, Levy Sheet Music Collection, Box
088, Item 136Words by C.B. Barr. Music Composed and Arranged by J.T. Wamelink.Krebs & Bro. Lith. Pittsburg
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