Proliferation Extracellular release

Angiotensin-II AT, Human cDNA Artherosderosis, cardiac hypertrophy, congestive heart failure, hypertension, myocardial infarction, renal disease, cancer, diabetes, obesity, glaucoma, cystic fibrosis, Alzheimer s disease, Parkinson s disease Smooth muscle contraction, cell proliferation and migration, aldosterone and ADH release, central and peripheral sympathetic stimulation, extracellular matrix formation, tubular sodium retention, neuroprotection... 

Figure 21.18 Exit of tumour cells from a tumour into the bloodstream and entry into a new tissue for formation of a new tumour. Exit depends on lack of adhesion between tumour cells and release of proteolytic enzymes to destroy extracellular stroma. Cells travel to new tissue via the blood on lymph. They secrete proteolytic enzymes and bore a hole in the extracellular stroma of new tissue and then infiltrate and proliferate.

Figure 4.2. Diagram outlining the pathogenesis of liver fibrosis. Injury to parenchymal cells (PC) results in the activation of Kupffer cells (KC) and sinusoidal endothelial cells (SEC) and the recruitment of inflammatory cells (IC). These cells release cytokines, growth factors and reactive oxygen species that induce activation and proliferation of hepatic stellate cells (HSC). HSCs gradually transform into myofibroblasts (MF), the major producers of extracellular matrix (ECM) proteins.

Many microbial infections and toxins are spread by biofilms. Biofilm formation occurs on virtually every surface, starting with the adhesion of planctonic cells or small dispersed biofilm fragments. Proliferation of the cells is accompanied by the expression of an extracellular polysaccharide-based matrix [6], The cells embedded in this matrix are well protected and up to 1000 times less susceptible to antibiotics [7], Once a biofilm is formed, it is extremely difficult to remove this contamination. Thus, all antimicrobial surfaces should prevent the primary attack [8], One class of antimicrobial surfaces prevents the primary attack by creating surfaces that are not sticky to microbial cells, i.e., they do not allow adhesion of these cells. The other major class of antimicrobial surfaces is based on the killing of approaching microbes (see Fig. 2). Interestingly, both approaches can be achieved either by permanent surface modifications or by releasing bioactive compounds. 

Thyroid orbitopathy is an inflammatory disease of the orbital tissues. This inflammation is mediated through cytokine release, proliferation of fibroblasts, increased deposition of extracellular matrix, and adipocyte differentiation and proliferation. These cellular changes result in enlargement of the extraocular muscles and increased volume of orbital soft tissues, which presents clinically as exophthalmos and optic nerve compression. Edema, inflammation, and late fibrosis account for the decreased function of the extraocular muscles despite relative preservation of the muscle fibers themselves. 

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