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Strain Dependent (strain + dependent)
Selected AbstractsImmune-related mechanisms participating in resistance and susceptibility to glutamate toxicityEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2002Hadas Schori Abstract Glutamate is an essential neurotransmitter in the CNS. However, at abnormally high concentrations it becomes cytotoxic. Recent studies in our laboratory showed that glutamate evokes T cell-mediated protective mechanisms. The aim of the present study was to examine the nature of the glutamate receptors and signalling pathways that participate in immune protection against glutamate toxicity. We show, using the mouse visual system, that glutamate-induced toxicity is strain dependent, not only with respect to the amount of neuronal loss it causes, but also in the pathways it activates. In strains that are genetically endowed with the ability to manifest a T cell-dependent neuroprotective response to glutamate insult, neuronal losses due to glutamate toxicity were relatively small, and treatment with NMDA-receptor antagonist worsened the outcome of exposure to glutamate. In contrast, in mice devoid of T cell-dependent endogenous protection, NMDA receptor antagonist reduced the glutamate-induced neuronal loss. In all strains, blockage of the AMPA/KA receptor was beneficial. Pharmacological (with ,2 -adrenoceptor agonist) or molecular intervention (using either mice overexpressing Bcl-2, or DAP-kinase knockout mice) protected retinal ganglion cells from glutamate toxicity but not from the toxicity of NMDA. The results suggest that glutamate-induced neuronal toxicity involves multiple glutamate receptors, the types and relative contributions of which, vary among strains. We suggest that a multifactorial protection, based on an immune mechanism independent of the specific pathway through which glutamate exerts its toxicity, is likely to be a safer, more comprehensive, and hence more effective strategy for neuroprotection. It might suggest that, because of individual differences, the pharmacological use of NMDA-antagonist for neuroprotective purposes might have an adverse effect, even if the affinity is low. [source] Cardiac and coronary function in the Langendorff-perfused mouse heart modelEXPERIMENTAL PHYSIOLOGY, Issue 1 2009Melissa E. Reichelt The Langendorff mouse heart model is widely employed in studies of myocardial function and responses to injury (e.g. ischaemia). Nonetheless, marked variability exists in its preparation and functional properties. We examined the impact of early growth (8, 16, 20 and 24 weeks), sex, perfusion fluid [Ca2+] and pacing rate on contractile function and responses to 20 min ischaemia followed by 45 min reperfusion. We also assessed the impact of strain, and tested the utility of the model in studying coronary function. Under normoxic conditions, hearts from 8-week-old male C57BL/6 mice (2 mm free perfusate [Ca2+], 420 beats min,1) exhibited 145 ± 2 mmHg left ventricular developed pressure (LVDP). Force development declined by ,15% (126 ± 5 mmHg) with a reduction in free [Ca2+] to 1.35 mm, and by 25% (108 ± 3 mmHg) with increased pacing to 600 beats min,1. While elevated heart rate failed to modify ischaemic outcome, the lower [Ca2+] significantly improved contractile recovery (by >30%). We detected minimal sex-dependent differences in normoxic function between 8 and 24 weeks, although age modified contractile function in males (increased LVDP at 24 versus 8 weeks) but not females. Both male and female hearts exhibited age-related reductions in ischaemic tolerance, with a significant decline in recovery evident at 16 weeks in males and later, at 20,24 weeks, in females (versus recoveries in hearts at 8 weeks). Strain also modified tolerance to ischaemia, with similar responses in hearts from C57BL/6, 129/sv, Quackenbush Swiss and FVBN mice, but substantially greater tolerance in BALB/c hearts. In terms of vascular function, baseline coronary flow (20,25 ml min,1 g,1) was 50,60% of maximally dilated flows, and coronary reactive and functional hyperaemic responses were pronounced (up to 4-fold elevations in flow in hearts lacking ventricular balloons). These data indicate that attention to age (and sex) of mice will reduce variability in contractile function and ischaemic responses. Even small differences in perfusion fluid [Ca2+] also significantly modify tolerance to ischaemia (whereas modest shifts in heart rate do not impact). Ischaemic responses are additionally strain dependent, with BALB/c hearts displaying greatest intrinsic tolerance. Finally, the model is applicable to the study of vascular reactivity, providing large responses and excellent reproducibility. [source] Physiological and oenological traits of different Dekkera/Brettanomyces bruxellensis strains under wine-model conditionsFEMS YEAST RESEARCH, Issue 7 2008Ileana Vigentini Abstract Contamination of wine by Dekkera/Brettanomyces bruxellensis is mostly due to the production of off-flavours identified as vinyl- and especially ethyl-phenols, but these yeasts can also produce several other spoiling metabolites, such as acetic acid and biogenic amines. Little information is available about the correlation between growth, viability and off-flavour and biogenic amine production. In the present work, five strains of Dekkera bruxellensis isolated from wine were analysed over 3 months in wine-like environment for growth, cell survival, carbon source utilization and production of volatile phenols and biogenic amines. Our data indicate that the wine spoilage potential of D. bruxellensis is strain dependent, being strictly associated with the ability to grow under oenological conditions. 4-Ethyl-phenol and 4-ethyl-guaiacol production ranged between 0 and 2.7 and 2 mg L,1, respectively, depending on the growth conditions. Putrescine, cadaverine and spermidine were the biogenic amines found. [source] Relative viscosity models and their application to capillary flow data of highly filled hard-metal carbide powder compoundsPOLYMER COMPOSITES, Issue 1 2005Tomas Honek The rheological behavior of highly filled polymer systems used in powder injection molding (PIM) technology strongly influences the final properties of the products. In this study, the capillary flow data of multi-component polymer binders,based on polyethylene, paraffin, ethylene-based copolymers, and polyethylene glycol,compounded with three various hard-metal carbide powders were employed. The rheology of such highly filled (up to 50 vol%) multiphase systems is necessarily a complex phenomenon characterized by strain dependent, non-Newtonian properties complicated by flow instabilities and yield. Over 15 mathematical models proposed for highly filled systems were tested, some of them calculating the maximum filler loading. Due to the complex structure of the filler (irregular shape, particle size distribution) and a multi-component character of the binder, the applicability of these models varied with the powder-binder systems studied. However, the particular values of maximum loadings are in good accordance with the predictions based on powder characteristics. Simple modification of Frankel-Acrivos model to the systems containing unimodal hard-metal carbide powders with particles of an irregular shape and broad particle size distribution gave precise agreement between experimental data and model prediction. POLYM. COMPOS., 26:29,36, 2005. © 2004 Society of Plastics Engineers. [source] Interferon-, treatment of female (NZW × BXSB)F1 mice mimics some but not all features associated with the Yaa mutationARTHRITIS & RHEUMATISM, Issue 4 2009Meera Ramanujam Objective Male (NZW × BXSB)F1 mice develop antiphospholipid syndrome (APS) and proliferative glomerulonephritis that is markedly accelerated by the Yaa locus encoding an extra copy of Tlr7. Female (NZW × BXSB)F1 mice with only 1 active copy of Tlr7 develop late-onset glomerulonephritis but not APS. Because a major function of Toll-like receptor 7 is to induce type I interferons (IFNs), our goal was to determine whether IFN, can induce or accelerate the manifestations of systemic lupus erythematosus (SLE) in female (NZW × BXSB)F1 mice. Methods Eight-week-old female (NZW × BXSB)F1 mice were injected with a single dose of adenovirus expressing IFN,. Mice were monitored for the development of thrombocytopenia and proteinuria. Sera were tested for anticardiolipin and anti-Sm/RNP antibodies. Mice were killed at 17 or 22 weeks of age, and their kidneys and hearts were examined histologically and by immunohistochemistry. Spleen cells were phenotyped, and enzyme-linked immunospot assays for autoantibody-producing B cells were performed. Results IFN, markedly accelerated nephritis and death in female (NZW × BXSB)F1 mice. A significant increase in spleen cell numbers associated with a striking increase in the number of activated B and T cells was observed. Marginal-zone B cells were retained. IFN,-induced increased titers of autoantibodies were observed, but thrombocytopenia was not observed. Cardiac damage was milder than that in male mice. Conclusion IFN, accelerates the development of renal inflammatory disease in female (NZW × BXSB)F1 mice but induces only mild APS and does not induce thrombocytopenia. The effect of IFN, on SLE disease manifestations is strain dependent. These findings are relevant to our understanding of the physiologic significance of the IFN signature. [source] | ||||||||||