Vascular Endothelial Development

We studied the correlation between the micro-vascular density and type of cells “benign and malignant”: We noticed the higher vascularity of cases of cystitis, compared to the vascularity of malignant tumors, this could be explained by the higher vascularity of the active cells, edema, inflammatory infiltrate and vascular congestion during the inflammatory process.

Figure 2 [3]: The role of cadherin and catenin in the binding of cancer cells to the endothelium.

6. Atherosclerosis, pp.1157. is a form of arteriosclerosis in which thickening and hardening of the vessel are caused by the accumulation of lipid-laden macrophages w/I the arterial wall, which leads to the formation of a lesion called a plaque. It is not a single disease but rather a pathologic process that can affect vascular syustemns throughtout the body, resulting in ischemic syndromes that can vary widely in their severity and clinical manisfestations. It is the leading contributor to coronary artery and cerebrocascular disease. Athrosclerosis is an inflammatory disease, the lesions progress from endothelial injury and dysfunction

Discuss the different types of blood vessels. Include the different layers composing blood vessels (remember to include tissue types) in your discussion.

Atherosclerosis is a disease affecting the innermost layer of large and medium sized such as aorta and coronary arteries. It is a slow developing disease, it is complex and often starts in childhood and progresses with increasing age (Miksch, Hunter, & Papailiou, 2005). It appears as focal thickenings called fibrofatty plaques in an artery wall, these plaques are

The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.

Coronary artery disease is the most common cause of a myocardial infarction (MI). As a result of CAD, plaque builds up in the arteries, thus narrowing the coronary arteries and preventing adequate blood flow to the heart. This condition is called atherosclerosis. In 2012, Huether, S., & McCance, K. defines Atherosclerosis when it begins to occur when there has been an injury to the coronary vessel wall. When injury occurs on the vessels endothelial layer it triggers a clotting mechanism. That mechanism sends chemotaxsis signals through the body for monocytes/macrophages to come clean the open vessel wall that is leaking LDL into the blood. The macrophages attempt to digest the fatty substance but have a hard time doing so. When the cells cannot digest the LDL, cell proliferation happens and they become static. Static macrophages turn into foam cells that then begin to cover the open vessel wall. Stasis of these foam cells occurs and forms a fatty streak, beginning to slowly occlude the artery. Then with time, build up of collagen occurs on top of the

Presently, the treatment strategies used are risk factor modification, conventional pharmacology and surgical revascularization. These strategies have hitherto not been of enormous solution as the disease progression still result in recurrent symptoms. This has now led to the exploitation of advances in comprehending the vascular biology of atherogenesis to introduce novel cell and molecular-based therapies. The application of immunomodulation, lipid-lowering agents like statins, gene transfer, antisense technology and so on has resulted in new therapeutic strategies to interrupt cell proliferation and disorder of the vessel wall. In this essay, immunomudulation and lipid-lowering agent shall be discussed.

Instead the patient was given pre- and postoperative G-CSF to mobilize endothelial progenitor cells and induce MSC proliferation. Additionally during the surgery the scaffold was saturated with hrEPO, G-CSF and TGF-β prior to implantation. hrEPO functioned to increase angiogenesis to the scaffold, which was also promoted by the omental covering. TGF-β functioned to increase MSC recruitment and induce chondrocyte differentiation. These chondrocytes would then repopulate the scaffold’s cartilage rings and function as a mechanical support. Chondrogenesis was confirmed at two-year post-operative as structural rigidity was seen on bronchoscopic evaluation. Pre and postoperative treatment with these agents however was linked to an increase in leukocytes within the first postoperative week, however by day-nine the leukocyte count

This paper talks about the discovery of cancer cells, and how different doctors and physicians have tried to get a better understand of it over the centries. The causes of and treatment plans as well as trying to prevent cancer. Breast cancer, happened to be the first cancer cell discovered, so this paper is going to concentrate specifically on breast cancer. It will talk about the different treatment plans that can be considered as well as ways to prevent breast cancer.

A leading cause of death in patients with cancer, 28 thrombosis is associated with higher

In another study it was reported that miR-221 and miR-222 had antiangiogenic characteristics in endothelial cells. This study came up

Endothelial cells are those that are found in endothelium tissue. Endothelial tissue typically lines the surface of various blood and lymphatic vessels. The endothelial cells are in direct contact with the blood and lymphatic cells. More specifically, endothelial cells that come in contact with blood are called vascular endothelial cells. Sickle Cell Anemia is a blood disorder that results in an abnormality in the hemoglobin found in the red blood cells. Endothelial cells are involved with many functions of the cardiovascular system. High amounts of circulation endothelial cells have been known to be found in patients with Sickle Cell Anemia. The article examines the origin, surface phenotype, and function of circulating endothelial cells in patients with the disease.

Many of the vaso-protective function of endothelium is provide by the Nitric Oxide(NO)20.Endothelium damaged by turbulent or non-laminar blood causes decreased production of NO.Such kind of blood flow also stimulates endothelial cells to produce adhesion molecules, which recruit and bind inflammatory cells. Hypercholesterolemia seems to inactivate the normal function of NO. The net effect is endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation of a local vascular inflammatory response. Lipids in the blood, particularly low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL), also bind to endothelial cells. 18Firstly LDL is transported across the healthy intima and become trapped in intima of a vessel wall.It undergoes oxidative modification and then oxidized LDL(OxLDL) is formed5.OxLDL is mighty inducer of inflammatory molecules.It adds up to the inflamotory signaling by endothelium that activates chemotactic substances, growth factors that attracts monocytes to vessel wall21Eventually OxLDL transforms monocytes into macrophages which makes the Forms cells, which are the hallmark of atherosclerosis. Oxidized LDL impair the signal transduction between endothelial cell surface receptors and NO production, inhibit NO synthase activity and inactivates NO realese from endothelial cells.22.Once the endothelium is impaired, oxidized LDL is stored in vascular endothelium and by the process of series of mechanism, foam cells are formed and then eventually fatty plaque that occludes the vessel along with the decreased amount of NO which decreases the ability of the vessel to dilate. As the plaque grows arterial wall narrowing and thickening occurs5. This plaque and narrowing of vessel results in decreased blood flow

If the endothelium were to be considered an organ, it would be without a doubt the largest, with its 6 trillion cells, area of 5000m2, and 1kg weight. With knowledge of the endothelium stemming back to the early 1600s with William Harvey’s work on the circulation as a closed circuit with a pump and Marcello Malpighi’s observations of blood capillaries, the focus over the next 400 years was mainly on the pump itself, leading to the creation of a major clinical field – cardiology. Although scientists were aware of blood vessels and their role in circulation, it wasn’t until the early 1960s that the endothelium was able to be seen with electron microscopy and therefore be differentiated and characterized.1 The recognition of