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Membrane stretching

This is the definition of the surface tension according to the Gibbs surface model [1], According to this definition, the surface tension is related to an interface, which behaves mechanically as a membrane stretched uniformly and isotropically by a force which is the same at all points and in all directions. The surface tension is given in J m-2. It should be noted that the volumes of both phases involved are defined by the Gibbs dividing surface X that is located at the position which makes the contribution from the curvatures negligible. [Pg.163]

The surface tension defined above was related to an interface that behaved mechanically as a membrane stretched uniformly and isotropically by a force which is the same at all points on the surface. A surface property defined this way is not always applicable to the surfaces of solids and the surface energy of planar surfaces is defined to take anisotropy into account. The surface energy is often in the literature interchanged with surface tension without further notice. Although this may be useful in practice, it is strictly not correct. [Pg.164]

Homologs of VR1 with a high threshold (> 52°C) for activation by noxious heat, or sensitivity to membrane stretch, provisionally termed vanilloid receptor-like protein (VRL-1) (Caterina et al., 1999) and stretch-inactivated channel (SIC) (Suzuki et al., 1999), respectively, have been identified. Neither channel is activated by vanilloid agonists (Caterina et al., 1999 Suzuki et al., 1999). A mouse ortholog of VRL-1 acts as a growth factor regulated channel (GRC) permeable to Ca2+ ions (Kanzaki et al., 1999). A splice variant of VR1 (VR.5 sv) that lacks the majority of the intracellular N-terminal domain is refractory to activation by vanilloid agonists, protons or noxious... [Pg.508]

Various other physical processes lead in their mathematical description to equations of the same form as Flq (2). especially in its steady-state form, Such processes include the conduction of electricity in a conductor, or the shape of a thin membrane stretched over a curved boundary. This situation has led to the development of analogies (electric analogy, soap film analogy) to heal conduction processes, which are useful because they often offer the advantages of simpler experimentation. [Pg.759]

Osteoblast intracellular calcium is regulated by membrane stretch or shear stress and by other mechanisms (Kamioka et al., 2006). Further, the absence of stretch causes atrophy. This effect is important, with acute and severe bone loss caused by disuse or unweighting (Bikle and Halloran, 1999). Stretch-induced calcium... [Pg.544]

Davidson RM. 1993. Membrane stretch activates a high-conductance K+ channel in G292 osteoblastic-like cells. J Membr Biol 131 81-92. [Pg.555]

With viscoelastic models used by an increasing number of researchers, time and temperature dependence, as well as strain hardening and nonisotropic properties of the deformed parison can, in principle, be accounted for. Kouba and Vlachopoulos (97) used the K-BKZ viscoelastic constitutive equation to model both thermoforming and parison membrane stretching using two-dimensional plate elements in three-dimensional space. Debbaut et al. (98,99) performed nonisothermal simulations using the Giesekus constitutive equation. [Pg.854]

Different mechanisms are involved in the opening of volume-regulatory ion channels they are cell type-dependent and involve direct channel activation by membrane stretch, alterations in intracellular free [Ca2+] or activation of membrane-bound signaling systems. For example, swelling of hepatocytes apparently opens stretch-activated nonselective cation channels, which allow passage of Ca2+into the cell (Bear, 1990). Swelling in turn stimulates phospholipase C to produce inositol-1,4,5-trisphosphate, which in turn mobilizes Ca2+ from intracellular stores. The resulting increase in [Ca2+] may then activate Ca2+-sensitive K+ channels, thus... [Pg.190]

Bear, C.E. (1990). A nonselective cation channel in rat liver cells is activated by membrane stretch. Am. J. Physiol. 258, C421-C428. [Pg.206]

Two different types of membrane-based osmosensors have been proposed for animal cells extracellular solute sensors and membrane stretch-activated sensors. The former sensors are conjectured to function by detecting changes in the concentration of specific ions, for instance, sodium ion, in the external fluids. There is some indirect evidence for sodium-specific sensors in animal cells, and sodium-gated cation channels have been proposed as candidates for this role. However, no direct evidence for their involvement as upstream osmoregulatory elements has yet been presented. [Pg.265]

Membrane stretch-activated sensors, membrane-localized proteins whose activities are modulated by mechanical forces generated in the membrane due to stress, appear to be more promising candidates for the role of... [Pg.265]

Figure 1 Physical and chemical stimuli affecting the gating of bacterial MS channels. (A) The structure of the pentameric MscL channel (left) and a channel monomer (right) from Mycobacterium tuberculosis according to the 3-D structural model of a closed channel (7). MscL is activated by membrane stretch, amphipaths (e.g., lysophopholipids, chlorpromazine, and trinitrophenol) and parabens. The channel activity is inhibited by Gd + and static magnetic fields (SMF) and is modulated by temperature and intracellular pH (3). (B) The structure of the MscS heptamer (left) and the channel monomer (right) from E. coli based on the 3-D structural model of MscS (8) most likely depicting an inactive or desensitized functional state of the channel (3). MscS is activated by membrane stretch, amphipaths, and parabens and is modulated by voltage. The activity of the channel is inhibited by Gd + and high hydrostatic pressure (HHP) (3). The arrows point at membrane structures (i.e., channel protein and/or lipid bilayer) affected by the specific stimuli. Figure 1 Physical and chemical stimuli affecting the gating of bacterial MS channels. (A) The structure of the pentameric MscL channel (left) and a channel monomer (right) from Mycobacterium tuberculosis according to the 3-D structural model of a closed channel (7). MscL is activated by membrane stretch, amphipaths (e.g., lysophopholipids, chlorpromazine, and trinitrophenol) and parabens. The channel activity is inhibited by Gd + and static magnetic fields (SMF) and is modulated by temperature and intracellular pH (3). (B) The structure of the MscS heptamer (left) and the channel monomer (right) from E. coli based on the 3-D structural model of MscS (8) most likely depicting an inactive or desensitized functional state of the channel (3). MscS is activated by membrane stretch, amphipaths, and parabens and is modulated by voltage. The activity of the channel is inhibited by Gd + and high hydrostatic pressure (HHP) (3). The arrows point at membrane structures (i.e., channel protein and/or lipid bilayer) affected by the specific stimuli.
DHPC increases the sensitivity of liposomes to ultrasound application. DHPC is a short chain lipid, which can stabilize broken edges of bilayers (15, 16) allowing the openings created by membrane stretch to remain open longer, allowing more contents to be released. [Pg.126]

From the above remarks follow applications of investigation of the states of minimal surfaces and possible changes in their shapes (catastrophes) on altering some control parameters. For example, foams may be formed at a phase boundary, thus determining the rate and character of reagent transport at the interface. Some small marine animals, such a Radiolaria, are built of skeletons covered with membranes. Thus, the structure of foam at the phase boundary or the shape of a radiolarian result from the same condition of a minimal surface area of the foam stretched at the interface or the membrane stretched on the skeleton of a radiolarian. [Pg.23]

Flow FFF. The three flow FFF systems (Flow I, II, and III) are each constructed of two Lucite blocks with inset ceramic frits, a membrane, and a spacer. The frits provide a homogeneous distribution of cross-flow over the entire channel area. A membrane stretched over one frit surface serves as the accumulation wall and retains sample inside the channel. Systems Flow I and II were assembled with the YM-30 ultrafiltration membrane (Amicon, Danvers, MA) and Flow III with the Celgard 2400 polypropylene membrane (Hoechst-Celanese, Separations Products Division, Charlotte, NC). The frit of the second Lucite block defines the opposite (depletion) wall. The spacers, consisting of Teflon (Flow I) or Mylar (Flow II, Flow III), determine the channel thickness. [Pg.309]


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