102,406 research outputs found
carman
No full textcar nThis morning a carman with a load of lumber, in trying to take a short cut from Water Street through a small lane, experience a complete breakdown. T he slide w ent to pieces under the load. [antedates DNE 1978 citePRINTED ITEM DNE SupG.M. Story [check] WKOCT. 5 1987Used I and SupUsed I and SupUsed Supcart, LONG CAR(T), ~boy, car-driver, ~ manChecked by Cathy Wiseman on Fri 03 Apr 201
carman
No full textcar nA carman pleaded guilty to having no bells on his horse or slide. Sentence was suspended.DNE Sup G.M. StoryFEB.8 1990Used I and SupUsed I and SupUsed Supcart, LONG CAR(T), ~boy, car-driver, ~ manChecked by Cathy Wiseman on Fri 03 Apr 201
carman
No full textcar nA carman driving with horse and cart along Duckworth St, at 10:30 Wednesday night, was thrown out of the vehicle, opposite Dr McKenzie's surgery. [antedates DNE car n 3, 1978 cite]PRINTED ITEM DNE SupG.M. Story MAR.7 1988[check] WKUsed I and SupUsed I and SupNot usedcart, LONG CAR(T), ~boy, car-driver, ~ manChecked by Cathy Wiseman on Fri 03 Apr 2015; Card marked DNE Sup, but not used
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Direct evidence that naturally occurring mutations within hepatitis B core epitope alter CD4+ T-cell reactivity.
No full textExacerbations of chronic hepatitis B have been associated with accumulation of mutations in the HBV core gene, with amino acid (aa) substitutions clustering between aa 50 and 69. This region of the nucleocapsid protein is known as an immunodominant epitope for CD4+ T-lymphocytes, however the impact of these mutations on T-cell reactivity has not been investigated. For this purpose, we undertook fine mapping of the reactivity of peripheral blood lymphocytes, isolated from patients with acute (n = 8) or chronic hepatitis B (n = 10), against a panel of branched synthetic peptides. The peptide aa sequences corresponded to the wild type HBV (aa 50-69), or contained 1-3 aa changes derived on the basis of naturally occurring mutations. In four of eight patients with acute hepatitis B the wild type peptide 50-69, which corresponded to the core gene sequence of HBV present in these patients, induced a strong T-cell proliferative response. In the same cases, the T-cell response to the mutant peptides was altered at various degrees, depending on the number and the position of aa changes. The most pronounced inhibition of CD4+ T-cell response (between 44 and 92%) was caused by a peptide ligand with two aa substitutions at positions 64 and 67. These results demonstrate that mutations within immunodominant epitopes of the HBV nucleocapsid can affect the CD4+ T-lymphocyte reactivity, which may have a role for the accumulation of certain HBV strains after hepatitis flares during the course of chronic HBV infection
New hydraulic insights into rapid sand filter bed backwashing using the Carman–Kozeny model
No full textFluid flow through a bed of solid particles is an important process that occurs in full-scale water treatment operations. The Carman–Kozeny model remains highly popular for estimating the resistance across the bed. It is common practice to use particle shape factors in fixed bed state to match the predicted drag coefficient with experimentally obtained drag coefficients. In fluidised state, however, where the same particles are considered, this particle shape factor is usually simply omitted from the model without providing appropriate reasoning. In this research, it is shown that a shape factor is not a constant particle property but is dependent on the fluid properties as well. This dynamic shape factor for irregularly shaped grains increases from approximately 0.6 to 1.0 in fluidised state.We found that unstable packed beds in moderate up-flow conditions are pseudo-fixed and in a setting state. This results in a decreasing bed voidage and simultaneously in a decreasing drag coefficient, which seems quite contradictory. This can be explained by the collapse of local channels in the bed, leading to a more uniform flow distribution through the bed and improving the available surface for flow-through. Our experimental measurements show that the drag coefficient decreases considerably in the laminar and transition regions. This is most likely caused by particle orientation, realignment and rearrangement in particles’ packing position.A thorough hydraulic analysis shows that up-flow filtration in rapid sand filters under backwash conditions causes the particle bed to collapse almost imperceptibly. In addition, an improved expression of the drag coefficient demonstrated that the Carman–Kozeny model constant, however often assumed to be constant, is in fact not constant for increasing flow rates. Furthermore, we propose a new pseudo-3D image analysis for particles with an irregular shape. In this way, we can explain the successful method using optimisation of the extended terminal sub-fluidisation wash (ETSW) filter backwashing procedure, in which turbidity and peaks in the number of particles are reduced with a positive effect on water quality.Complex Fluid ProcessingSanitary Engineerin
Core protein evolution after selection of hepatitis B precore mutants and correlation with disease severity
No full textIn chronic hepatitis B virus (HBV) infection seroconversion from hepatitis B e antigen (HBeAg) to hepatitis B e antibody (HBeAb) may be followed either by remission of the disease with low-level viraemia, or by continuing inflammation with high-level viraemia. In both situations the virus may acquire a mutation in the precore sequence which prevents it from encoding HBeAg. We now show that the number of amino acid substitutions in the HBV core is low in viral sequences from patients with HBeAg positive chronic liver disease and HBeAg negative HBeAb positive patients in remission, but the frequency of substitutions is high in HBeAg, negative HBeAb positive patients with active liver disease. Furthermore we show that these substitutions cluster in the promiscuous CD4+ T-helper-cell epitope and in HBV core/e antibody binding determinants, but are not found in regions recognized by major histocompatability complex (MHC) restricted cytotoxic T lymphocytes. Sequential viral sequences from patients before and after HBeAg/HbeAb seroconversion shows that core mutations arise either at the same time or after the precore stop mutation which prevents the virus from encoding HBeAg. These results are consistent with the hypothesis that after clearance of HBeAg, mutations in regions of the virus recognized by CD4+ helper T cells and B cells allow persistence of the HBe negative virus in HBeAb positive patients with viraemia and active hepatitis
Handwritten biographical information on Paulina T. McClung Merritt
No full textA handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
No full textIFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
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