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Pore Properties (pore + property)
Selected AbstractsPore properties as indicators of breakdown mechanisms in experimentally weathered limestonesEARTH SURFACE PROCESSES AND LANDFORMS, Issue 8 2001Dawn T. Nicholson Abstract The results are reported of four experimental weathering tests , freeze , thaw, wetting and drying, slake durability and salt weathering , on five different types of limestone. Effective porosity, mercury intrusion porosimetry and scanning electron microscopy were used to evaluate changes in pore properties, while weight loss and fracture density were used to assess deterioration severity. A primary aim was to observe modifications in porosity due to weathering and to draw inferences about the internal rock deterioration mechanisms taking place. It is concluded that the five limestones not only show a wide range of resistance to weathering in general but considerable difference in resistance to particular weathering processes. Consequently, when assessing durability it is essential to consider rock properties in the context of the weathering process to which the rock is subject. The type of deterioration indicator used is also important in interpretation of durability. A variety of pore modification mechanisms operate, including changes in pore connectivity, pore infilling, and the introduction of additional void space. There are indications that changes to the internal pore structure of rocks due to weathering may be a precursor to more substantial macrodeterioration. Copyright © 2001 John Wiley & Sons, Ltd. [source] Effect of amyloid ,-peptide on permeability transition pore: A comparative studyJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2002Paula I. Moreira Abstract A potentially central factor in neurodegeneration is the permeability transition pore (PTP). Because of the tissue-specific differences in pore properties, we directly compared isolated brain and liver mitochondria responses to the neurotoxic A, peptides. For this purpose, the following parameters were examined: mitochondrial membrane potential (,,m), respiration, swelling, ultrastructural morphology, and content of cytochrome c. Both peptides, A,25,35 (50 ,M) and A,1,40 (2 ,M), had a similar toxicity, exacerbating the effects of Ca2+, although, per se, they did not induce (PTP). In liver mitochondria, A, led to a drop in ,,m and potentiated matrix swelling and disruption induced by Ca2+. In contrast, brain mitochondria, exposed to the same conditions, demonstrated a higher capacity to accumulate Ca2+ before the ,,m drop and a slight increase of mitochondrial swelling compared with liver mitochondria. Furthermore, mitochondrial respiratory state 3 was depressed in the presence of A,, whereas state 4 was unaltered, resulting in an uncoupling of respiration. In both types of mitochondria, A, did not affect the content of cytochrome c. The ,,m drop was reversed when Ca2+ was removed by EGTA or when ADP plus oligomycin was present. Pretreatment with cyclosporin A or ADP plus oligomycin prevented the deleterious effects promoted by A, and/or Ca2+. It can be concluded that brain and liver mitochondria show a different susceptibility to the deleterious effect of A, peptide, brain mitochondria being more resistant to the potentiation by A, of Ca2+ -induced PTP. © 2002 Wiley-Liss, Inc. [source] Noradrenaline inhibits exocytosis via the G protein ,, subunit and refilling of the readily releasable granule pool via the ,i1/2 subunitTHE JOURNAL OF PHYSIOLOGY, Issue 18 2010Ying Zhao The molecular mechanisms responsible for the ,distal' effect by which noradrenaline (NA) blocks exocytosis in the ,-cell were examined by whole-cell and cell-attached patch clamp capacitance measurements in INS 832/13 ,-cells. NA inhibited Ca2+ -evoked exocytosis by reducing the number of exocytotic events, without modifying vesicle size. Fusion pore properties also were unaffected. NA-induced inhibition of exocytosis was abolished by a high level of Ca2+ influx, by intracellular application of antibodies against the G protein subunit G, and was mimicked by the myristoylated ,,-binding/activating peptide mSIRK. NA-induced inhibition was also abolished by treatment with BoNT/A, which cleaves the C-terminal nine amino acids of SNAP-25, and also by a SNAP-25 C-terminal-blocking peptide containing the BoNT/A cleavage site. These data indicate that inhibition of exocytosis by NA is downstream of increased [Ca2+]i and is mediated by an interaction between G,, and the C-terminus of SNAP-25, as is the case for inhibition of neurotransmitter release. Remarkably, in the course of this work, a novel effect of NA was discovered. NA induced a marked retardation of the rate of refilling of the readily releasable pool (RRP) of secretory granules. This retardation was specifically abolished by a G,i1/2 blocking peptide demonstrating that the effect is mediated via activation of G,i1 and/or G,i2. [source] | ||||||||||