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Rapid Death (rapid + death)
Selected AbstractsAltered immune response to CNS viral infection in mice with a conditional knock-down of macrophage-lineage cellsGLIA, Issue 2 2006Jessica Carmen Abstract Neuroadapted Sindbis Virus (NSV) is a neuronotropic virus that causes hindlimb paralysis in susceptible mice and rats. The authors and others have demonstrated that though death of infected motor neurons occurs, bystander death of uninfected neurons also occurs and both contribute to the paralysis that ensues following infection. The authors have previously shown that the treatment of NSV-infected mice with minocycline, an inhibitor that has many functions within the central nervous system (CNS), including inhibiting microglial activation, protects mice from paralysis and death. The authors, therefore, proposed that microglial activation may contribute to bystander death of motor neurons following NSV infection. Here, the authors tested the hypothesis using a conditional knock-out of activated macrophage-lineage cells, including endogenous CNS macrophage cells. Surprisingly, ablation of these cells resulted in more rapid death and similar weakness in the hind limbs of NSV-infected animals compared with that of control animals. Several key chemokines including IL-12 and monocyte chemoattractant protein-1 (MCP-1) did not become elevated in these animals, resulting in decreased infiltration of T lymphocytes into the CNS of the knock-down animals. Either because of the decreased macrophage activation directly or because of the reduced immune cell influx, viral replication persisted longer within the nervous system in knock-down mice than in wild type mice. The authors, therefore, conclude that although macrophage-lineage cells in the CNS may contribute to neurodegeneration in certain situations, they also serve a protective role, such as control of viral replication. © 2006 Wiley-Liss, Inc. [source] Effect of trehalose on survival of Bradyrhizobium japonicum during desiccationJOURNAL OF APPLIED MICROBIOLOGY, Issue 3 2003J.G. Streeter Abstract Aims: A major reason for the ineffectiveness of legume inoculants in the field is the rapid death of rhizobia because of desiccation. The major purpose of this study was to identify conditions under which ,,, -trehalose would improve survival of Bradyrhizobium japonicum during desiccation. Methods and Results: Trehalose was added to cultures just prior to desiccation or was supplied to bacteria during the 6-day growth period. A wide variety of trehalose concentrations was tested. Trehalose added to cultures at the time of desiccation improved survival slightly, but trehalose loading during growth was much more effective in protection against desiccation. Growth of bacteria with 3 mmol l,1 trehalose increased trehalose concentration in cells by about threefold and increased survival of cells placed on soya bean [Glycine max (L.) Merr.] seeds by two- to four-fold after 2 or 24 h. Average of overall results indicate that growth of bacteria with trehalose in the medium resulted in a 294% increase in survival after 24 h of desiccation. The concentration of trehalose in cells was very highly correlated with survival of bacteria. When trehalose-loaded cells were suspended in buffer or water, 60,85% of cellular trehalose was lost in about 1 h and, in spite of these losses, survival during desiccation was not reduced. Conclusions: Accumulation of trehalose in the cytoplasm is critical to the survival of B. japonicum during desiccation. Increasing the periplasmic concentration of trehalose is also beneficial but is not so critical as the concentration of trehalose in the cytoplasm. Because B. japonicum cannot utilize trehalose as a carbon source, cells can be loaded with trehalose by providing the disaccharide during the growth period. Significance and Impact of the Study: Although it may not be practical to use trehalose as a carbon source in inoculant production, it may be possible to engineer greater trehalose accumulation in rhizobia. Trehalose concentration in cells should be a useful predictor of survival during desiccation. [source] 3-Ketosteroid 9,-hydroxylase is an essential factor in the pathogenesis of Mycobacterium tuberculosisMOLECULAR MICROBIOLOGY, Issue 1 2010Yanmin Hu Summary Mycobacterium tuberculosis H37Rv contains the kshA (Rv3526) and kshB (Rv3571) genes, encoding 3-ketosteroid 9,-hydroxylase (KSH). Consistent with their predicted roles, the ,kshA and ,kshB deletion mutants of M. tuberculosis H37Rv were unable to use cholesterol and 4-androstene-3,17-dione as primary carbon and energy sources. Interestingly, ,kshA and ,kshB mutants were also unable to metabolize the steroid substrate 5,-androstane-3,17-dione, whereas wild-type M. tuberculosis H37Rv could. The deletion of either of these genes lead to rapid death of the microorganism in murine infection models and in macrophages, showing that kshA and kshB are essential factors for M. tuberculosis pathogenesis. Penta-acylated trehalose (PAT) biosynthesis was altered in the ,kshB mutant, but not the ,kshA mutant. The ,kshB mutant synthesizes all other types of lipids. The ,kshB mutant had a thickened outer layer in its cell wall. KshB thus appears to be involved in multiple processes, probably as a reductase of different oxygenases. We conclude that an impaired 3-ketosteroid 9,-hydroxylase activity is the cause of the highly attenuated phenotype of our M. tuberculosis H37Rv mutants. [source] Phytophthora pinifolia sp. nov. associated with a serious needle disease of Pinus radiata in ChilePLANT PATHOLOGY, Issue 4 2008A. Durán During the course of the past three years, a new disease of Pinus radiata, referred to as ,Daño Foliar del Pino' (DFP) has appeared in the Arauco province of Chile and subsequently spread to other areas. The disease is typified by needle infections, exudation of resin at the bases of the needle brachyblasts and, in younger trees, necrotic lesions in the cambium, which eventually girdle the branches. The disease causes the death of young seedlings and mature trees can also succumb after a few years of successive infection, probably hastened by opportunistic fungi such as Diplodia pinea. Isolations on selective medium for Phytophthora spp. led to the consistent isolation of a Phytophthora sp. from needle tissue. DNA sequence comparisons for the ITS rDNA and cox II gene regions, and morphological observation showed that this oomycete represents a previously undescribed species for which the name Phytophthora pinifolia sp. nov. is provided. This new species is characterized by unbranched sporangiophores, and non-papillate, sub-globose to ovoid sporangia that are occasionally free from the sporangiophore with medium length pedicels. Despite using a number of oospore inducing techniques, oogonia/antheridia were not observed in isolates of P. pinifolia. Pathogenicity trials with P. pinifolia showed that it is pathogenic to P. radiata and causes rapid death of the succulent apical parts of young plants. Phytophthora pinifolia is the first Phytophthora known to be associated with needles and shoots of a Pinus sp. and its aerial habit is well matched with the occurrence and symptoms of DFP in Chile. [source] Prolactin Levels in Sudden Unexpected Death in EpilepsyEPILEPSIA, Issue 1 2000K. Opeskin Summary: Purpose: To assess serum prolactin levels in sudden unexpected death in epilepsy (SUDEP) and control groups to test the hypothesis that if seizures occur routinely as a terminal event in SUDEP, then raised prolactin levels may be an indicator of terminal seizure. Methods: Blood was taken for measurement of prolactin levels from subjects with SUDEP and three control groups. The control groups were those with epilepsy dying from causes other than epilepsy (e.g., ischemic heart disease or injuries), physiologically stressed individuals without epilepsy (they were admitted to the hospital after an acute illness and died after several hours to 3 days), and nonepileptic rapid deaths (these people collapsed suddenly and died at the scene). In the SUDEP group, evidence for terminal seizure was considered to be at least one of the following: body found half on, half off the bed, or urinary incontinence at the scene, or bitten lips or tongue at autopsy. Results: There was evidence for terminal seizure at the scene or at autopsy in four of the 10 SUDEP cases. Serum prolactin levels were not significantly increased in the SUDEP group compared with the controls. None of the SUDEP subjects, including those with clinical evidence of a terminal seizure, had high prolactin levels characteristic of those observed after seizures in living subjects. Conclusions: Prolactin levels are not raised in SUDEP, even if there is evidence of terminal seizure. As prolactin takes 15,20 min to peak after a seizure in life, there may be insufficient time for a prolactin increase to occur in SUDEP. Thus prolactin levels cannot be used to determine if a deceased individual with epilepsy had a seizure or to answer the broad question whether SUDEP is always associated with a terminal seizure. [source] | ||||||||||