Cellular collapse

Finally, we conclude that toxic reactions in plant cells injured by ozone probably take place in the following sequence sulfhydryl oxidation, lipid hydrolysis, cellular leaking, lipid peroxidation, and then cellular collapse. 

To the extent that these studies are revealing, they demonstrate that there is no simple and universal scheme that links integrity of the cytoskeleton with storage and release of mediators. This may not be a surprising finding. Even if the cytoskeleton did play a simple and direct role in mediator release, the indirect consequences of producing cellular collapse would probably cause many other outcomes that would complicate interpretation of results. This intuitively obvious matter may lead to what are the most important conclusions that can be drawn from studies with C2 toxin ... 

Fig. 15.3 The major pathways of apoptosis. The extrinsic pathway uses extracellular death ligands (Fas ligand, tumor necrosis factor (TNF)) to activate death receptors which pass the apoptotic signal to initiator caspases (e. g. capsase 8) and to the executioner caspases (e. g. caspase 3 caspase 7). In the execution phase of apoptosis, various cellular substrates are degraded leading to cellular collapse. The intrinsic pathway uses the mitochondria as a central component for activation of apoptosis. In this pathway, a multitude of intracellular signals including various stresses, DNA damage and inappropriate cell signaling lead to activation of the pro-apoptotic protein Bax which induces release of cytochrome c from mitochindria, formation of the apoptosome and activation of the initiator caspase 9. Finally, the executioner caspases are activated and cells are destructed by proteolysis. Apoptosis via this pathway can be controlled by various antiapoptotic proteins including the Bcl-2 protein and inhibitors of apoptosis.

Large amounts of a high molecular weight chemical are introduced into the cell lumina and permanent voids (Figure 12) to improve the physical properties of the object and to prevent cellular collapse of very decayed wood cells. This treatment must form a solid in the cell lumina and voids as water is removed. 

Microscopic examinations provide a record of the amount of cellular collapse that takes place during treatment. A preliminary examination of the wood can prevent confusion as to how well the treatment actually worked. In waterlogged wood and damp wood, cellular collapse is often present before treatment begins. If this fact is known, collapse observed after treatment will not be attributed to poor stabilization. 

The conservation of waterlogged wood involves removal of water, as well as improving mechanical properties. The simplest drying technique is to remove the object from water and allow it to dry. This technique will usually result in unacceptable amounts of dimensional change (i.e., a combination of cell wall shrinkage and cellular collapse). Some type of chemical pretreatment is usually applied before drying to improve the dimensional stability of the waterlogged wood. For damp woods, pretreatments may not be required. 

This method has not, however, worked well. Solvent drying does not stop all cellular collapse. In addition, it does nothing to reduce cell wall shrinkage. Even if it is successful, there is a real possibility that the shape of the object will not be representative of its original dimensions (16). Solvent drying alone has apparently never been applied successfully. 

Low temperature stability problems are caused by the pressure differential created by condensation of the cellular gases. This pressure differential across the foam membranes can cause deformation and, for lighter materials, extensive cellular collapse. Figure 14 shows volume change as a function of density under three common aging conditions. ... 

When the set of cells of a CW complex is given by means of a combinatorial enumeration, and the cell attachment maps are not too complicated, for instance if the CW complex in question is regular, it is natural to attempt to use the standard notion of cellular collapse to simplify the considered topological space, while preserving its homotopy t3rpe. 

Intuitively, a cellular collapse is a strong deformation retract that pushes the interior of a maximal cell in, using one of its free boundary cells as the starting point, much like compressing a body made of clay. The cellular collapses can be defined for arbitrary CW complexes. 

The simplicial collapse defined in Section 6.4 is a special case of Definition 11.12. We are now ready to formulate the central result of this section. For technical convenience, we restrict ourselves to considering cellular collapses in the setting of polyhedral complexes only. 

Proof of (a). Clearly, the linear extension can be chosen so that all the critical cells come first. Hence, if read in decreasing order, L gives a sequence of cellular collapses leading from 4 to 4c. 

Clearly, removing the pair (d(a),a) is a cellular collapse in particular, there exists a homotopy equivalence f A A. On the other hand, by the induction assumption, there exist a CW complex Ac with Cj t-dimensional cells and a homotopy equivalence f A Ac- Hence, setting Ac = Ac, we have obtained the desired homotopy equivalence f o f A Ac-... 

It is easy to see that the proof of Theorem 11.13(b) actually works in greater generality one can take arbitrary CW complexes, at the same time replacing cellular collapses by arbitrary homotopy equivalences. More precisely, we have the following result. 

C. It is secreted along with noradrenaline by the adrenal medulla, from which it may be obtained. It may be synthesized from catechol. It is used as the acid tartrate in the treatment of allergic reactions and circulatory collapse. It is included in some local anaesthetic injections in order to constrict blood vessels locally and slow the disappearance of anaesthetic from the site of injection. Ultimately it induces cellular activation of phosphorylase which promotes catabolism of glycogen to glucose. 

Cellular materials can collapse by another mechanism. If the cell-wall material is plastic (as many polymers are) then the foam as a whole shows plastic behaviour. The stress-strain curve still looks like Fig. 25.9, but now the plateau is caused by plastic collapse. Plastic collapse occurs when the moment exerted on the cell walls exceeds its fully plastic moment, creating plastic hinges as shown in Fig. 25.12. Then the collapse stress (7 1 of the foam is related to the yield strength Gy of the wall by... 

The cellular cytoskeleton, primarily composed of microfilaments, microtubules, and intermediate filaments, provides structural support and enables cell motility. The cytoskeleton is composed of biological polymers and is not static. Rather, it is capable of dynamic reassembly in less than a minute [136], The cytoskeleton is built from three key components, the actin filaments, the intermediate filaments, and the microtubules. The filaments are primarily responsible for maintaining cell shape, whereas the microtubules can be seen as the load-bearing elements that prevent a cell from collapsing [136], The cytoskeleton protects cellular structures and connects mechanotransductive pathways. Along with mechanical support, the cytoskeleton plays a critical role in many biological processes. 

On the other hand stable cavitation (bubbles that oscillate in a regular fashion for many acoustic cycles) induce microstreaming in the surrounding liquid which can also induce stress in any microbiological species present [5]. This type of cavitation may well be important in a range of applications of ultrasound to biotechnology [6]. An important consequence of the fluid micro-convection induced by bubble collapse is a sharp increase in the mass transfer at liquid-solid interfaces. In microbiology there are two zones where this ultrasonic enhancement of mass transfer will be important. The first is at the membrane and/or cellular wall and the second is in the cytosol i. e. the liquid present inside the cell. 

As with caspase-3, these hits were converted into potent, soluble inhibitors by replacing the disulfide linkage with a simple alkyl linkage (Fig. 9.10). As in the case of caspase-3, rigidifying the linker could improve affinity, as could introducing a hydrophobic moiety at the S2 position. Several of these molecules demonstrated activity in cellular assays and selectivity for caspase-1 over the closely related caspase-5. Crystallography of several of these molecules in complex with caspase-1 revealed that they bind in an extended conformation as expected, but that the S2 pocket that collapses in caspase-3 remains open in caspase-1. 

In severely damaged cells the cell contents were collapsed into an aggregated mass (Fig. 9). Few cellular membranes were evident except for the internal membrane system of the chloro-plasts (Fig. 9G). The crystalline arrays were distributed throughout the aggregated mass (Fig. 9C) and accumulations of electron-dense material occurred generally in association with the periphery of the aggregated mass (Fig. 9, arrows). 

The result of this is that the pH difference and therefore potential difference across the membrane collapses, and there is no energy to drive the ATP synthesis. However, electrons can still flow through the chain, which drives the citric acid cycle to produce them, and so cellular metabolism still continues, and indeed, without the constraint of ATP synthesis, the electron flow is more rapid and so other metabolic rates also increase in rate. Oxygen can still be reduced to water, and so this will be used up also and require replacement. 

While unaffected by water, styrofoam is dissolved by many organic solvents and is unsuitable for high-temperature applications because its heat-distortion temperature is around 77°C. Molded styrofoam objects are produced commercially from expandable polystyrene beads, but this process does not appear attractive for laboratory applications because polyurethane foams are much easier to foam in place. However, extruded polystyrene foam is available in slabs and boards which may be sawed, carved, or sanded into desired shapes and may be cemented. It is generally undesirable to join expanded polystyrene parts with cements that contain solvents which will dissolve the plastic and thus cause collapse of the cellular structure. This excludes from use a large number of cements which contain volatile aromatic hydrocarbons, ketones, or esters. Some suitable cements are room-temperature-vulcanizing silicone rubber (see below) and solvent-free epoxy cements. When a strong bond is not necessary, polyvinyl-acetate emulsion (Elmer s Glue-All) will work. 

---