Some More Figure Work

So, I thought I would tackle the other Spanish article, the one about the anatomy of cholesterol plaques (Badimón et al), and modify the news program to be a scientific-news program.  I enjoy the mental exercise of trying to figure out something visual, like a figure, so I implemented a section in the program that calls up pictures derived from the figures with labels selectively replaced by question marks.  So, beginning with the second figure in the paper, the program can quiz on the terminal emulator, launching a figure with a question mark by calling viewnior, and otherwise proceed interactively through the terminal emulator.  Yes, it’s UNIX, and it requires a desktop environment.  Not a big deal with puppy LINUX.  So, the figure is modified in mtPaint to contain question marks at the appropriate places and labeled 1.jpg, 2.jpg, 3.jpg … according to the corresponding question in the file.

cholesterol

In doing this first exercise, a few questions arose as to the difference between HDL and LDL.  They really don’t seem that fundamentally different from the picture.  (Fig. 2)  Why is one of them supposed to be that much better for you?  Is it really?

So, here’s the experiment that I came up with.  Take some mice or rats who are genetically predisposed to high cholesterol.  Feed them a healthy diet, put them on cholesterol lowering drugs, and then try to shift the concentration of cholesterol from LDL to HDL.  Let them live out their natural lives in a healthy, well cared for, and exercised, and mentally challenged environment, and take blood samples from them to monitor their cholesterol levels.  When they die of natural causes, do some pathology on their arteries.

Instead of doing control experiments, where one simply does nothing for the animals,  one could have a contest where several different groups try to compete in a contest to see whose rats and mice can live the longest.

Some questions:

1.  Can one change the HDL/LDL balance simply by upregulating Apo-A1 or downregulating ApoB-100?

2. Is it possible to engineer another molecule – say Apo-X, that would have even better properties?

3. Can increasing the levels of antioxidants (like vitamin C) improve the outcome by reducing foam cells?

Some other articles:

ApoA1 and heart failure

According to table 1 in this paper, the level of ApoA1 is related to HDL, according to the following ratio: 132.4/44.4, so with my reported HDL level of 67, this would in principle mean a probable ApoA1 level of 201 (assuming a ratio for a relationship which may be questionable), putting me in the highest tertile of the above study.

“Patients with baseline apoA1 levels in the highest tertile had one-third the rate of the primary end point of death, transplantation, or LV-assist-device (LVAD) implantation compared with the lowest tertile over a mean follow-up of about 2.7 years. The events included 29 deaths, six heart transplantations, and three LVAD implantations.”

Kinetics of Apo B-100 and Apo A-1

From the kinetics paper, assuming that table 1 is reporting levels (?) and not time (really not sure about this in a quick read), everything grossly seems to double after menopause.

From what I gather, the longer LDL stays in the blood, the more of a chance it has of being chemically modified, and recognized by receptors on macrophages.  Chemically modified LDL can also act directly on the vessel endothelium to cause damage, and therefore inflammation.  When the macrophages become loaded with cholesterol, they are called foam cells, and these foam cells are characteristic of the plaque that builds up in the arteries.  So, changing the activity of the foam cells might be another strategy.

I guess, short of research, prevention involves not cooking food too much, and not eating food with a lot of chemical additives that might interact with cholesterol to oxidize it.

The 2nd pass at a first figure file (I think that I will eventually add fill in the blank statements, either from the article that use the words, or other sources):

nouns 06 spanish-news.txt from largely from Badimón et al edited 5-8-2013
c: ?  ENG: superficie polar  SENT:
c: ?  ENG: fosfolípidos  SENT:  Las lipoproteínas son estructuras compuestas de proteínas y ___________ que facilitan el transporte de lípidos en el torrente circulatorio.
c: ?  ENG: ApoA-II  SENT:
c: ?  ENG: triglicéridos  SENT: Las LDL consisten en un núcleo apolar que contiene __________ y ésteres de colesterol y una cubíerta hidrófila formada por fosfolipidos, colesterol libre y proteínas, predóminantemente la apolipoproteńa B-100, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: colesterol libre  SENT: Las LDL consisten en un núcleo apolar que contiene triglicéridos y ésteres de colesterol y una cubíerta hidrófila formada por fosfolipidos, ________ ______ y proteínas, predóminantemente la apolipoproteńa B-100, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: apolipoproteína C-III  SENT: Los genes que codifícan la apolipoproteína A-I, la ___________ ______, y la apolipoproteína A-IV están situados próximamente en el cromosoma 11q23, formando el denominado “cluster A-I/C-III/…” Nogueras y Lafuente Av Diabetol 2002; 18: 199-202.
c: ?  ENG: apolipoproteína C-I  SENT: Las HDL o liproteínas de alta densidad no tienen apolipoproteína B, pero poseen apolipoproteína A-I, apolipoproteína A-II, apolipoproteína A-IV, apolipoproteína E, __________ __, apolipoproteína C-II, y apolipoproteína C-III. Nogueras y Lafuente Av Diabetol 2002; 18: 199-202.
c: ?  ENG: núcleo apolar  SENT: Las LDL consisten en un _______ _______ que contiene triglicéridos y ésteres de colesterol y una cubíerta hidrófila formada por fosfolipidos, colesterol libre y proteínas, predóminantemente la apolipoproteńa B-100, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: apolipoproteína A-IV  SENT: Los genes que codifícan la apolipoproteína A-I, la apolipoproteína C-III, y la ____________ ___ están situados próximamente en el cromosoma 11q23, formando el denominado “cluster A-I/C-III/…” Nogueras y Lafuente Av Diabetol 2002; 18: 199-202.
c: ?  ENG: ésteres de colesterol  SENT: Las LDL consisten en un núcleo apolar que contiene triglicéridos y ______ __ _______ y una cubíerta hidrófila formada por fosfolipidos, colesterol libre y proteínas, predóminantemente la apolipoproteína B-100, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: apolipoproteína A-V  SENT: El polimorfismo SNP3 de __________ ___ se asocia positivamente con polimorfismos en apolipoproteína C-III, y negativemente con el polimorfísmo apolipoproteínas A-IV T347S y de la zona intergénica apoliporteína A-IV/VT>C. Nogueras y Lafuente Av Diabetol 2002; 18: 199-202.
c: ?  ENG: apolipoprorteína A-1  SENT:  En general, a medida que aumentan los niveles de HDL, aumentan los valores de _________ ___.
c: ?  ENG: H  SENT: La Apolipoproteína A (Apo A) es el principal componente polipeptídico de las ___DL.
c: ?  ENG: L  SENT: Las ___DL consisten en un núcleo hidrófugo que contiene triglicéridos y ésteres de colesterol y una cubíerta hidrófila formada por fosfolipidos, colesterol libre y proteínas, predóminantemente la apolipoproteńa B-100, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: apolipoproteína C-II  SENT: Las HDL o liproteínas de alta densidad no tienen apolipoproteína B, pero poseen apolipoproteína A-I, apolipoproteína A-II, apolipoproteína A-IV, apolipoproteína E, apolipoproteína C-I, __________ ____, y apolipoproteína C-III. Nogueras y Lafuente Av Diabetol 2002; 18: 199-202.
c: ?  ENG: apolipoproteína B-100  SENT: Las LDL consisten en un núcleo apolar que contiene triglicéridos y ésteres de colesterol y una cubíerta hidrófila formada por fosfolipidos, colesterol libre y proteínas, predóminantemente la _________ _____, que actúa de ligando con receptores de la membrana celular.
c: ?  ENG: apolipoproteína E SENT: La ___________ __ paricipa en la unión de las lipoproteínas con los proeoglucagones y es reconocida por los receptores de LDL y por la proteína relacionada con el receptor de LDL (LRP).

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