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Vacuole formation

Experiments on the physiological and biochemical mechanisms of action suggest that bromethalin uncouples oxidative phosphorylation in central nervous system mitocondria(19). This could lead to a decreased production of ATP, a diminished activity of Na /K ATPase, and a subsequent fluid build up manifested by fluid-filled vacuoles between the myelin sheaths. This vacuole formation in turn leads to an increased cerebrospinal fluid pressure and increased pressure on the nerve axons, yielding a decrease in nerve impulse, paralysis, and death. [Pg.56]

These authors suggest that the multivalency of the lectins is an important factor in vacuole formation in these cells. However, we have seen that two of those lectins most active in the macrophage system, namely concanavalin A and wheat germ agglutinin, are unable to induce lysosomes in cultured fibroblasts. We are presently studying the properties of the lectins and the cells in order to more coiqpletely understand the mechanism of lectin induced accumulation of lysosomes in animal cells. [Pg.64]

Verhey, J.G.P. 1972. Vacuole formation in spray powder particles. 2. Location and prevention... [Pg.464]

Studies in rats have suggested that after pinocytosis by renal tubular cells, sucrose is incorporated into phagolysosomes (32). The intracellular accumulation of sucrose leads to vacuole formation and cellular swelling. On withdrawal, renal insufficiency resolves in most cases. However, sometimes hemodialysis is necessary (69,89). [Pg.1723]

Apoptosis is delayed and may be maximal at 24-48 h after an insult. However, apoptotic cells can be seen even within 6 h of an insult, but are not common. Apoptosis involves condensation of the nucleus. Condensation of the cytoplasm occurs with large vacuole formation. Some mitochondria may condense. Very uncommonly, some mitochondria swell in apoptosis. The cell splits up into membrane-bound apoptotic bodies that can be seen in the limit areas surrounding the core of an infarction. Apoptosis is a programmed form of cell death that occurs following a small but sufficient amount of damage to a cell. This initiates a program that eventually kills the cell. [Pg.676]

The Influence of Vacuole Formation and Growth on the Mechanical Behavior of Polymers... [Pg.233]

Vacuole dilatation information itself is not simply interpreted. The data instead are best understood through models of microstruetural failure (1). Assuming a single size of spherical filler particles encompassed by elliptically shaped voids that form arbitrarily in strain, and once formed grow at a constant rate with further deformation, then one can readily separate vacuole growth from vacuole formation. Models such as the one described above have been substantiated by microscopic studies. The solution of such models (1) indicates that the first derivative of vacuole dilatation with respect to strain c, is directly proportional to the cumulative number of vacuoles per unit volume,n, that exist at any strain. The second derivative is then directly proportional to the instantaneous frequency distribution of vacuole formation. These two results can be expressed mathematically... [Pg.237]

Verhey JGP. 1972a. Vacuole formation in spray-dried powder particles. 1. Air incorporation and bubble expansion. Netherlands Milk and Dairy Journal 26 186-202. [Pg.40]

Joiner, K. A. (1991) Rhoptry lipids and parasitophorous vacuole formation — a slippery issue. Parasitol. Today 7 226-227. [Pg.142]

Cobalt has been demonstrated to induce seminiferous tubule damage and degeneration (vacuole formation, sloughing of cells, giant cell formation) in the testes of mice following exposure for 13 weeks (Anderson et al. 1993). Coadministration of cobalt and zinc chloride in the drinking water resulted in complete or partial protection in 90% of the animals. The sites of competitive interaction between zinc an cobalt were not established in the study however, the authors postulated that the mechanism(s) may be similar to those involved in prevention of cadmium toxicity by zinc. [Pg.85]

The same phenomena (vacuolation, formation of flakes) occur also in cooling a suspension of coacervate drops in their equilibrium liquid. See p. 449, Fig. 16. [Pg.382]

VACUOLELESSl is an essential gene required for vacuole formation and morphogenesis in Arabidopsis. Dev. CeU, 1, 303-310. [Pg.294]

The decisive new property responsible for the damage to nerve tissue is, however, the acquisition of partial resistance to proteases, since the refolded protein cannot be completely degraded. This leads to protein deposits in the form of amyloid plaques in the nerve cells and finally to cell death through apoptosis and other processes. The amyloid plaques are also called scrapie-associated fibrils (SAP). As a result, the brains of damaged individuals show focal and diffuse degeneration and vacuole formation, which are responsible for the typical spongiform appearance of the TSE brain. [Pg.3846]


See other pages where Vacuole formation is mentioned: [Pg.142]    [Pg.16]    [Pg.253]    [Pg.253]    [Pg.307]    [Pg.116]    [Pg.85]    [Pg.274]    [Pg.144]    [Pg.148]    [Pg.360]    [Pg.234]    [Pg.441]    [Pg.742]    [Pg.218]    [Pg.572]    [Pg.633]    [Pg.233]    [Pg.234]    [Pg.237]    [Pg.134]    [Pg.310]    [Pg.515]    [Pg.516]    [Pg.91]    [Pg.152]    [Pg.94]    [Pg.332]    [Pg.282]    [Pg.9]    [Pg.348]   
See also in sourсe #XX -- [ Pg.308 ]

See also in sourсe #XX -- [ Pg.347 , Pg.351 , Pg.377 ]




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