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Extravasation cells

A study in which B16M-F1 melanoma cells were injected intraportally found that >80% of the injected cells survived and had extravasated by day 3. However, few extravasated cells began to grow with only 1 in 40 forming micrometastases (4-16 cells) by day 3. Furthermore, few micrometastases continued to grow, with only 1 in 100 progressing to form macroscopic tumors by day 13 (Luzzi et al. 1998). Surprisingly, 36% of injected cells remained by day 13 as solitary cancer cells. [Pg.197]

The neurointerventionalist should limit the number of microcatheter injections performed during the exam, as there is growing evidence that this may increase the chances of hemorrhagic transformation of the infarcted tissue. Direct injection of contrast into stagnant vessels, which contains injured glial cells and thus breakdown of the blood-brain barrier, allows for contrast extravasation. Contrast is readily visualized on the immediate post-thrombolysis CT as an area of high attenuation in the parenchyma. In some instances, MRI with susceptibility-weighted sequences may be useful to differentiate contrast extravasation from Such a distinction... [Pg.74]

The activation of a chemokine receptor is more complex than the traditional agonist-receptor paradigm. For example, chemokine activity is mediated by GAGs (heparin, heparan, and heparin sulfate chondroitin sulfate and dermatan sulfate) at various sites during the chemotactic process. Chemokines released by tissue injury, infection, or inflammation activate adjacent endothelial cells and induce rolling and extravasation of leukocytes. These interactions between... [Pg.23]

Hieshima K, Kawasaki Y, Hanamoto H, et al. CC chemokine ligands 25 and 28 play essential roles in intestinal extravasation of IgA antibody-secreting cells. J Immunol 2004 173 3668-3675. [Pg.117]

Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel. Fig. 11.1. Atherogenesis is a persistent inflammatory response that occurs in response to conditions that cause endothelial damage (e.g., hypercholesterolemia and oxLDL). After endothelial cells are activated, they elaborate cytokines, chemokines, and other mediators that recruit mononuclear cells (monocytes and T lymphocytes) to extravasate into the vessel wall where they are activated and release additional proinflammatory factors. Macrophages are able to take up oxLDL via scavenger receptors causing them to differentiate into foam cells and form a fatty streak that progresses to an atheroma with a necrotic lipid core and a fibrous cap. Chemokines can lead to weakening of the fibrous cap and eventual plaque rupture leading to thrombosis and occlusion of the involved vessel.
The endothelium has many diverse functions that enable it to participate in in-flammatoiy reactions (H27). These include modulation of vascular tone, and hence control of local blood flow changes in structure that allow leakage of fluids and plasma proteins into extravascular tissues local accumulation and subsequent extravasation into tissues of leukocytes and synthesis of surface molecules and soluble factors involved in leukocyte activation (B43). The endothelial cells themselves can modulate vascular tone by the release of vasoactive substances such as prostacyclin, nitric oxide (NO), ET. Endothelium-derived vasoactive substances... [Pg.69]

Streptozocin -alkylating agent cell cycle independent -nephrotoxicity—can be dose-limiting -nausea and vomiting—may get progressively worse with continued administration -mucocutaneous effects (mucositis, stomatitis, diarrhea) -bone marrow suppression -irritant if extravasated (not vesicant) -delirium or depression -risk of secondary leukemias... [Pg.178]

Nanoparticles such as those of the heavy metals, like cadmium selenide, cadmium sulfide, lead sulfide, and cadmium telluride are potentially toxic [14,15]. The possible mechanisms by which nanoparticles cause toxicity inside cells are schematically shown in Fig. 2. They need to be coated or capped with low toxicity or nontoxic organic molecules or polymers (e.g., PEG) or with inorganic layers (e.g., ZnS and silica) for most of the biomedical applications. In fact, many biomedical imaging and detection applications of QDs encapsulated by complex molecules do not exhibit noticeable toxic effects [16]. One report shows that the tumor cells labeled with QDs survived in circulation and extravasated into tissues... [Pg.236]

Apart from inducing vascular damage via infiltration and degranulation of various blood cells, PAF and TNF exert also direct effects in the endothelium. In vitro, both substances cause contraction of endothelial cells, which may partially account for the increased vascular permeability and plasma extravasation observed in many species following PAF or TNF administration [311]. While it has been known for some time that endothelial cells produce PAF when stimulated with various agonists such as thrombin, it has recently been established that TNF and IL-1 also induce cultured endothelial cells to synthesize PAF, the majority of which remains associated with the cells [317]. [Pg.364]

Extravasation of tumor cells through blood vessel wall into secondary organ, and... [Pg.136]


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See also in sourсe #XX -- [ Pg.41 , Pg.42 ]




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