Endothelial Activation Lab Report

A sufficient coronary artery blood flow is essential to supply oxygen for normal cardiac activities (Craft, 2014, p. 599). Atherosclerosis is a common form of CHD. It is an inflammation disease when plasma cholesterol is high. Risk factors such as hypertension, high cholesterol, smoking and diabetes increase the risk of endothelium injuries, contributing to the increase in oxidated lipid-lipoprotein (LDL). Foam cell is produced by the increase in the number of macrophages signalled by oxidated LDL. Next, the accumulation of foam cells will cause the formation of fatty streak lesions on arteries walls. Over time, fatty streak lesions migrate to the site and form fibrous plaque due to the increase in smooth muscles and collagen. The thickening and hardening initiated by an accumulation in calcified fibrous plaque caused the blood vessels to narrow. As a result, a decrease in tissue perfusion contributing to the development of myocardial ischemia (Craft, 2014, p. 599; McCance & Huether, 2014, pp. 1145-1147).

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

Tumour necrosis factor (TNF) is responsible for the disruption of the tight junction between endothelial cells which results in an increased permeability to plasma proteins and fluid, which worsens fluid accumulation in the alveoli further impairing gas exchanged (Bersten & Soni, 2009:709). TNF comprises of two different molecules, firstly TNFa which leads to programmed cell death in target cells, and when combined with IL-1 which acts on the central nervous system causing lethargy (Marieb, 2004). TNFB stimulates granulocyte activity and B cell proliferation which shows an increase in neutrophil count (Jean- Baptise, 2007:63).

The purpose of this experiment was to identify how open and closed circulatory systems respond to chemical stimulants. During this experiment a ghost shrimp represented the open circulatory system, while the black worm represented the closed circulatory system. For each organism there resting heart rates were recorded by count the number of pulsations the organism had under a microscope. First, the shrimp and the worm were treated with caffeine, and then their heart rate was recorded after the organisms were exposed to the treatment for three minutes. The organisms were removed from the caffeine, and were given time to return back to their resting heart rates. The shrimp and the worm were then exposed to ethanol, and there hear rates were recorded again.

One source of great mortality and morbidity in Europe and North America is the cardiovascular disease, Atherosclerosis. It is recognized as a chronic inflammatory disease of the intermediate and large arteries characterized by the thickening of the arterial wall and is the primary cause of coronary and cerebrovascular heart disease (Wilson, 2005). It accounts for 4.35 million deaths in Europe and 35% death in the UK each year. Mortality rate are generally higher in men than pre-menopausal woman. Past the menopause, a woman’s risk is similar to a man’s (George and Johnston, 2010). Clinical trials have confirmed that lipid accumulation, endothelial dysfunction, cell proliferation, inflammation matrix alteration and foam cell formation are

Atherosclerosis is a lipid storage disease where too much of lipid is deposited in endothelial of arteries causing narrowing to prevent blood to flow. It is triggered by daily diet of consuming highly saturated fat, hypertension and smoking. In healthy endothelial cells, leukocytes do not stick on to the endothelial cells. During early phases of inflammation in endothelial cells, the leukocytes attach to the arteries cell wall with the help of vascular cell adhesion-1 (VCAM-1) and penentrate into the endothelial layer. VCAM-1 binds monocytes and T lymphocytes, the types of leukocytes found in early atherosclerotic plaques. ( Libby P., 2006:456S) Atherosclerosis lesion is a foam cells whereby macrophages engulf lipid particles. The lesion secretes cytokines and growth factors to promote proliferation of smooth muscle. The increased of inflammatory markers like interleukin 6 (IL-6) and interleukin 1 (IL-1) accumulated in the endothelial cells accerlate the progess of

An atherothrombotic event result in infiltration of the vessel wall caused by high levels of fibrongen, increased blood viscosity, increased platelet aggregation and thrombus formation. A pivotal role is played by inflammation in all phases of atherosclerosis. There are several characteristics of atherosclerotic plaques including the expression of cellular adhesion molecules (CAM), blunted vascular reactivity, and a prothrombotic state. Recent studies suggest that in atherosclerotic plaques PPAR- gamma (Peroxisome proliferator activated receptor gamma) is highly expressed and dugs that mimic PPAR gamma may have inhibitory effects on inflammatory process resulting in improvement of endothelial dysfunction and can modify major transcription factor

The purpose of this experiment was to observe the effect of hazardous chemicals on the human circulatory system causing cardiovascular disease. It was suggested that there are problems in circulatory system due to imbalance in the body by environmental factors and food consumed. To observe this 180 males who worked in factories who were exposed to harmful chemicals were selected as the experimental group and 135 males who were not exposed to any chemicals were taken as the control group. All of the subjects were asked basic questions about their work and personal habits. In order to measure risk for cardiovascular disease their physical tests were performed along with blood tests to record lipoprotein cholesterol, glucose and triglyceride in

NF-kB, a key transcriptional factor which have been found to be activated in a variety of inflammatory disorders such as cardiovascular, cancer and neurodegenration. Various research groups have reported the down-regulation of NF-kB by of Ganoderma in LPS induced immunological models [64,

The ACT, or Activated Clotting Time, can be used int he clinic to evaluate and diagnose secondary hemostasis from conditions such as rodenticide toxicosis and other disorders that cause a decrease in clotting factors. This test is performed by adding a blood sample to a special ACT tube containing a substance such as diatomaceous earth that activates the coagulation factors. A severe decrease, less than 5% of normal activity, in these clotting factors or a severe decrease in platelet numbers will lead to an increase in the length of time it takes the blood to clot after it has been added to the ACT tube. The ACT is not very sensitive to milder decreases in clotting factors.

IκB kinase and NF-κB (IKK/NF-κB) activation are commonly implicated in myocarditis, heart failure, and inflammation-related cardiovascular diseases. However, much of their significance remains unclear. Recent studies involving mice, whose genes have been altered, have assisted in

PCI causes mechanical damage, induces immune response and cascade inflammatory response, stimulates the proliferation of vascular smooth muscle cells and deposition of extracellular matrix, leading to neointimal thickening and restenosis. platelets, neutrophils, and monocytes play a central role in the initial inflammatory response after PCI，studies showed that Mac-1 and platelet mediated leukocyte adhesion play an important role in vascular inflammation and restenosis after coronary stent implantation. Platelets and fibrin are deposited on the vascular walls of the endothelium, and by a series of cell adhesion molecules they collect white blood cells into the damaged blood vessels. The initial platelet leukocyte binding and rolling through leukocyte receptor P- selectin glycoprotein ligand -1 (PSGL-1) and P- protein binding to platelet mediated, when the leukocyte integrin Mac-1 (CD11b / CD18) combined with platelet glycoprotein Ib alpha 53 or platelet glycoprotein IIb / IIIa binding protein fiber the original, leukocyte rolling stop and firmly attached to the adherent

Coronary endothelial dysfunction is associated with various pathological impairments, such as the disruption of cardiovascular homeostasis, poor blood circulation, myocardial injury, the accumulation and adhesion of platelets and monocytes, the increase in vasoconstriction, increased expression of inflammatory factors, and impairment in vascular regeneration which increase the risk of atherosclerosis.

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

This different expression of cell cycle regulatory proteins may be responsible for apoptosis of vascular smooth muscle cell and plaque destabilization [171]. Rao et al studied the mechanism of plaque rupture in carotids and proposed the mechanism by which EGFR activation induced MMP-1 and MMP-9 decreases the interstitial collagen causing plaque instability and increased vulnerability of plaque rupture, paving a future direction for translational approach of this concept for the prevention of myocardial infarction. It was also proposed that for plaque stabilization, selective blockade of EGFR and MMP-9 may be a promising strategy [172]. Identification of specific markers indicating a plaque prone to rupture and risk predictors for plaque rupture is an interesting area for further research. Currently we are working on the role of HMGB-1, RAGE, ENRAGE, TLR-4, TREM-1, TREM-2, MMP-1 and MMP-9 in plaque stability and destabilization in carotid artery.