Answer:
Thanks for you question. Your hypothesis suggests a linear relationship between serum Cholesterol levels and MI. This hypothesis seems to ignore the difference in the prevalence and effectiveness of LDL receptors in the FH patient.
FH patients who have inherited the mutation from both parents have very few LDL receptors in their blood and therefore almost no ability to pass the unused Cholesterol through the liver. FH patients who are heterozygous will have more LDL receptors although both will find Cholesterol removal problematic without the addition of a PCSK9 inhibitor.
In short, your hypothesis need to account for other factors that are in play.
Explanation:
Consider my case. I am a 64 year old male who has Heterozygous Familial Hypercholesterolemia. Before treatment at age 12 my Total cholesterol was 510 mg/dl. My genetic testing shows two mutations to the LDL Receptor gene with only one mutation being pathogenic. My first heart attack was at 47 and first stroke at 62. My current LDL is too low to detect with the use of a PCSK9 inhibitor (Repatha®).
Answer:
C
Explanation:
A, B, and D are done by other things, but acid can also be used to get rid of unneeded/wanted bacteria or organisms.
Hopefully this quizlet an help you.
<span>https://quizlet.com/35658769/chapter-12-flash-cards/</span>
Answer:
A
Explanation:
insulin is released from pancreas when blood sugar level rises
