Endothelial Migration Rate

The cardiovascular system is a network of the heart, blood vessels and the blood. It circulates blood throughout the blood vessels in our body in order to provide individual cells with oxygen and nutrients, and help to dispose of metabolic waste. Capillaries, which are the smallest blood vessels, have extremely thin walls. This is so diffusion can happen more efficiently. Every cell has capillaries passing through very close so there is a shorter distance for diffusion to occur. During my experiment, it showed that the larger the agar cube, the more of remaining agar which was left to be diffused. It also showed that the smaller the agar cube, the less remaining agar was left to be diffused. The findings from my experiment prove that the smaller

Atrioventricular (AV) node: the area of the heart conduction system responsible for receiving impulses from the SA node via intermodal pathways and stimulate the ventricles to contract

While inflammation is often viewed in a negative connotation, inflammation is actually an essential component of the healing process. Inflammation is commonly associated with pain, swelling, and redness; however, these effects are the body’s natural response to injury as blood and white blood cells move into the tissue and stimulate the repair process.2, 29 Therefore it is important to understand that even though certain molecular signals are traditionally identified as pro-inflammatory molecules, they are also critical molecules to support tissue regeneration through stimulation of reparative cells. Only when inflammation persists, as in chronic wounds, can it lead to tissue damage and prevent progression through the healing process. Therefore,

“The process by which tissue repair takes place is termed wound healing and is comprised of a continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore a semblance of their usual discipline and having done so resume their normal function”. ("The Cellular Biology of Wound Healing" 2016)

Adheres to human intestinal epithelial cells at “the apical brush boarder of the enterocytic Caco-2 cells” and binds to the muscus produced “by the HT29-MTX musuc secreting cells” (1). This was all mediated by a proteinaceous adhesion-promoting factor that is species specific.

- Leukocyte activation, adhesion, and chemotaxis. C5a activates leukocyte, thereby increasing adhesion to endothelium. It is also a potent chemotactic agent for neutrophils, monocytes, basophils and eosinophils.

Outward remodeling is initiated with increased shear stress caused by high flow. The shear stress signals endothelial cell proliferation and production of nitric oxide by endothelial cells (17, 20). Nitric oxide induces metalloproteinases, degradation of extracellular matrix, inhibit proliferation of smooth muscle cells and promote apoptosis of smooth muscle cells (20). Normal endothelium is resistant to adhesion by monocytes; however, when exposed to shear stress, monocytes can attach to endothelium (10). The recruited monocytes or macrophages, the mature form of monocytes, also play a key role in remodeling by producing matrix-metalloproteinases (MMPs) among other tissues that produce MMPs (10, 20). At least 13 different MMPs have been identified and MMP-2 and MMP-9 are noted to cleave elastin (1). The matrix proteolytic activity or the breakdown of extracellular matrix is necessary as it provides additional space for enlarging vessel (20) and also fragments of elastin allows for smooth muscle proliferation (10). The outward remodeling is reversible if the shear stress is decreased for a prolonged period

The factors limiting the growth of malignant neoplasm include the basal membrane and various components of the surrounding stroma, increased interstitial pressure, limited oxygen supply to tumor cells and the formation of active oxygen forms, hypoxia conditions, and permanent exposure to immune system cells. Given the intra-tumoral heterogeneity, in the struggle for survival, some tumor cells may be subjected to regression and death, while other cells, which resist powerful, counteracting micro-environmental factors, gain an aggressive phenotype and the ability of metastatic progression. Invasive tumor growth is enabled by the detachment of malignant cells from the tumor mass due to a reduction in or complete loss of intercellular adhesion molecules, and, therefore, the cells gain the ability of anomalously high motility enabling penetration through the stiff structural elements of the surrouss means the ability to thrust aside adjacent tissues, and also to actively invade and, therefore, destroy these

by three steps: attachment, uptake, and membrane fusion (7). GP1 is involved in adhesion of the

In vitro evidence suggested that modulation of integrin αIIbβ3–mediated functions was influenced by engagement of the PECAM-1 group, so the next stage involved testing if a fundamental integrin αIIbβ3 platelet

Hallmark of acute inflammation is increased vascular permeability leading to the escape of a protein-rich fluid (exudate) into the extravascular tissue.

Epithelial cells (ECs) are the structural unit of epithelium, a tissue type that is responsible for lining the inner and outer surfaces of the body, as well as formation of many glands [1]. ECs are polarized, with the apical surface facing the lumen and the basal surface anchoring to a specialized extracellular matrix (ECM) layer, known as the basal lamina or basement membrane which separates epithelial cells from underlying tissues (Fig. 1). To maintain the physical and functional integrity of the epithelium, ECs are also laterally linked to one another through cell-to-cell adhesion molecules (CAM), most importantly, members of the cadherin family [2]. As a result, ECs within an ordinary epithelium have very limited mobility. Nevertheless, non-pathological epithelial plasticity does occur, for example, in neurulation – an important morphogenetic movement during embryogenesis [3]. Under these circumstances, ECs tend to move in concert and the integrity of the whole epithelium is not compromised [4].

Reduction in macrophage infiltration, lead to concomitant decrease in circulating cancer cells. In addition, the EGF–CSF paracrine loop is also important for intravasation, as blocking either signaling pathway lead to a significant reduction in the number of blood-borne cancer cells. Cancer cells and macrophages also use collagen fibres as tram lines to rapidly travel through the stroma. Many of these fibres are tethered to blood vessels, resulting in cancer cells accumulating at these vessels. The density of these fibres is regulated by macrophages, at least during development. (Joyce & Pollard, 2009), (Hanahan & Weinberg, 2011)

An antibody induced complement mediated process results in epithelial detachment. Passive transfer studies in newborn mice have shown that antibodies to BPAg2 induce subepidermal blisters by an inflammatory mechanism. This interaction triggers immunologic events that result in the expression of inflammatory mediators that induce migration of lymphocytes, eosinophils, neutrophils, and mast cells to the BMZ. The separation of epithelium from the underlying tissue within the BMZ results from either direct cytotoxic action or the effect of lysosomal proteolytic enzymes. Passive transfer studies of antibodies against laminin 5 induce noninflammatory subepidermal blisters which indicate that antilaminin 5 IgG is pathogenic, although the mechanism is not clear. Anti α6 Antibody produced separation of epithelium from basement membrane. Fibroblasts also are activated secondary to the

Cells are independent units of life. However, when a cell becomes part of an organism, it becomes part of a tissue and organ system. Cells in a tissue are joined to each other and to the extracellular matrix (ECM) by cell junctions. There are three kinds of cell junctions: Occluding junctions, anchoring junctions and communication junctions. Occluding junctions occur in the epithelium where the adjacent cells are so tightly sealed together that even small molecules cannot pass. Communicating junctions allow the exchange of chemical and electrical signals between cells. Anchoring junctions are the ones which attach a cell either to its neighbor or to the extracellular matrix. Formation of an anchoring junction requires the cells to stick to each other. Various molecules mediate adhesion between cells following which the cytoskeleton forms a structure around them. The anchoring junctions thus formed can be of four types- desmosomes, hemidesmosomes, focal adhesions and adherens junctions. In order for a proper tissue to form, it is important for the cells of the tissue to bind together. It is equally important to prevent the invasion and binding of other cells. Thus, cell adhesion has to be specific. This is where the cell adhesion molecules come into play (Alberts et al. 2002).