Download Entry slip hypercholesterolemia names Meuwese, M.C., Mooij, H. et

Entry slip hypercholesterolemia names ____________________________
Meuwese, M.C., Mooij, H. et al (2009). Partial recovery of the endothelial glycocalyx upon rousuvastatin therapy in
patients with heterozygous familial hypercholesterolemia. J. Lipid Research 50, 148-153.
1. Authors: Where are these authors located?
2. From the Abstract:
* What is the endothelial glycocalyx? And of what macromolecules is it composed (see also introduction; presenters
should provide detailed structure/ diagrams, indicating macromolecular components)
What is the proposed function of the endothelial glycocalyx?
Therefore why were they testing patients with familial hypercholesterolemia?
What was their hypothesis?
Why did they use heterozygous FH patients? (vs. homozygous??)
What did they measure in the patients?
What drug had the patients been taking to lower lipids?
How did they calcuolate VG and what was found for FH, FH + drug, normal?
What is atherogenic vulnerability, and why do FH patients have it?
3. Introduction: What is the cause of familial hypercholesterolemia? And what inheritance pattern?
What gene is typically affected? (not given in the article; see review or your books) and why the problem for people?
** Presenters: show clear diagrams or structures of glycocalyx and explain its function.
[ Show clear diagrams of endothelial wall and explain movement of different cell types through wall
All students: what arey leukocytes and thrombocytes and why do they move through endothelial wall?
The authors note that they have a novel way to measure glycocalyx volume, and found less glycocalyx in patients with
hyperglycemia (type 1 diabetes); they also found less glycocalyx in patients with several other conditions, including:
__________________
4. Methods. What patients did they enroll, how many? What were the controls?
Why did they not have placebo controls?
They measured VG by ‘subtracting plasma volume from the intravascular distribution of a glycocalyx permeable
tracer’. How did they determine the circulating blood volume?
What are autologous erythrocytes, and why use them? and what is sodium fluorescein used for?
They used Dextran-40 to estimate intravascular volume plus glycocalyx. What is Dextran 40? What size, how many
glucose monomers (not given in the article)?
5. Results:
Why did the FH patients discontinue statin drugs for 4 weeks before beginning the study?
Table 1. ** What is LDL cholesterol and what does it do (see textbook or review – not explained in article)
What result did they observe for the LDL cholesterol of the FH patients vs. controls?
What result did they see for the LDL cholesterol after 8 weeks treatment with the drug?
Fig. 1. What did they find for system glycocalyx volume in the different groups?
Why did they do OPS imaging of capillaries, and what did they find about the thickness of glycocalyx? Treated vs.
untreated.
Fig. 2.What is vascular permeability and how did they measure that? Why inject dextran, how detect dextran in the
blood?
What does it mean if the curve has a steeper slope?
Discussion/ Conclusions
What is the main problem with people with FH? What is the effect of statins?
What are the authors main conclusions, and what are their intentions for future work?
What are some some study limitations they mention?
What are some questions you have about these experiments?