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Medicine science fair project:
Creating a simple diagnostic tool for earlier detection of cardiac disease




Science Fair Project Information
Title: Creating a simple diagnostic tool for earlier detection of cardiac disease
Subject: Medicine
Subcategory: Heart Disease
Grade level: High School - Grades 9-12
Academic Level: Ordinary
Project Type: Building / Engineering
Cost: Medium
Awards: Google Science Fair Finalist
Affiliation: Google Science Fair
Year: 2015
Materials and Techniques: Electrochemical sensor, cholesterol biomarkers, functionalized carbon nanotube (fCNT), Native LDL, , electrochemical sensor, colorimetric sensor, voltammetry measurements, enzyme Ink
Concepts: Oxidized-LDL, atherosclerosis
Description: Cardiac Disease's pathogenesis is largely attributed to cholesterol, predominantly carried by low-density lipoproteins (LDL). However, recent research has found that oxidized-LDL is significantly more potent in the initiation and development of atherosclerosis. This research aims to produce an on-site, ultra-low cost, rapid diagnostic with ox-LDL and cholesterol biomarkers. The cholesterol sensor was fabricated by depositing enzymes using a retrofitted consumer inkjet printer. Cholesterol levels were successfully quantified by the inkjet-printed sensors utilizing a smartphone camera for image capture. Two Ox-LDL sensors were developed. An electrochemical sensor, with a functionalized carbon nanotube (fCNT) electrode and a portable potentiostat, and a paper-based colorimetric sensor. The latter, utilizing an iodometric reaction to detect lipid peroxides of Ox-LDL, is the first paper-based ox-LDL test. The fCNT sensor detected ox-LDL at levels found in blood. The iodometric sensor differentiated color for the high and low ox-LDL concentrations.
Link: https://www.googlesciencefair.com/projects/en/2015/8a
Short Background

Oxidized-LDL Role in Atherosclerosis


CC 3.0 - GNU 1.2
The progression of atherosclerosis (narrowing exaggerated)

Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form of arteriosclerosis in which an artery-wall thickens as a result of invasion and accumulation of white blood cells (WBCs) (foam cell) and proliferation of intimal-smooth-muscle cell creating a fibrofatty plaque.

The chronic endothelial injury hypothesis is one of two major mechanisms postulated to explain the underlying cause of atherosclerosis and coronary heart disease (CHD), the other being the lipid hypothesis. Although an ongoing debate involving connection between dietary lipids and CHD sometimes portrays the two hypotheses as being opposed, they are in no way mutually exclusive. Moreover, since the discovery of the role of LDL cholesterol (LDL-C) in the pathogenesis of atherosclerosis, the two hypotheses have become tightly linked by a number of molecular and cellular processes.

Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized. This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.

Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium. Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis.

Once inside the vessel wall, LDL particles can become more prone to oxidation. Endothelial cells respond by attracting monocyte white blood cells, causing them to leave the blood stream, penetrate into the arterial walls and transform into macrophages. The macrophages' ingestion of oxidized LDL particles triggers a cascade of immune responses which over time can produce an atheroma if HDL removal of fats from the macrophages does not keep up. The immune system's specialized white blood cells (macrophages) absorb the oxidized LDL, forming specialized foam cells. If these foam cells are not able to process the oxidized LDL and recruit HDL particles to remove the fats, they grow and eventually rupture, leaving behind cellular membrane remnants, oxidized materials, and fats (including cholesterol) in the artery wall. This attracts more white blood cells, resulting in a snowballing progression that continues the cycle, inflaming the artery. The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial lining thickens, increasing the separation between the plaque and lumen. This somewhat offsets the narrowing caused by the growth of the plaque, but it causes the wall to stiffen and become less compliant to stretching with each heart beat.

Foam cells are fat-laden macrophages seen in atherosclerosis. They are an indication of plaque build-up, or atherosclerosis, which is commonly associated with increased risk of heart attack and stroke.

In chronic hyperlipidemia, lipoproteins aggregate within the intima of blood vessels and become oxidized by the action of oxygen free radicals generated either by macrophages or endothelial cells. The macrophages engulf oxidized low-density lipoproteins (LDLs) by endocytosis via scavenger receptors, which are distinct from LDL receptors. The oxidized LDL accumulates in the macrophages and other phagocytes, which are then known as foam cells. Foam cells form the fatty streaks of the plaques of atheroma in the tunica intima of arteries.

See also:
https://en.wikipedia.org/wiki/Atherosclerosis
https://en.wikipedia.org/wiki/Chronic_endothelial_injury_hypothesis
https://en.wikipedia.org/wiki/Foam_cell

Source: Wikipedia (All text is available under the terms of the GNU Free Documentation License and Creative Commons Attribution-ShareAlike License.)

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