To install click the Add extension button. That's it.
The source code for the WIKI 2 extension is being checked by specialists of the Mozilla Foundation, Google, and Apple. You could also do it yourself at any point in time.
How to transfigure the Wikipedia
Would you like Wikipedia to always look as professional and up-to-date? We have created a browser extension. It will enhance any encyclopedic page you visit with the magic of the WIKI 2 technology.
Try it — you can delete it anytime.
Install in 5 seconds
Yep, but later
4,5
Kelly Slayton
Congratulations on this excellent venture… what a great idea!
Alexander Grigorievskiy
I use WIKI 2 every day and almost forgot how the original Wikipedia looks like.
LP PLA 2 TEST - INFLAMMATION TESTING **ROAD TO BETTER HEALTH** (OAG)
"Phospholipase A2 – New Information on the Possible Root Cause"
What is a Phospholipase A2 Test?
Dr. Ron Krauss - Human Lipoprotein Responses and Cardiovascular Risk
Transcription
Function
In the blood Lp-PLA2 travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density lipoprotein HDL. Several lines of evidence suggest that HDL-associated Lp-PLA2 may substantially contribute to the HDL antiatherogenic activities.[8] It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL.
Lp-PLA2 is platelet-activating factor (PAF) acetylhydrolase (EC 3.1.1.47), a secreted enzyme that catalyzes the degradation of PAF to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate.[9]
Clinical significance
Lp-PLA2 is involved in the development of atherosclerosis,[7] an observation that has prompted interest as a possible therapeutic target (see, e.g. the investigational drug Darapladib). In human atherosclerotic lesions, 2 main sources of Lp-PLA2 can be identified, including that which is brought into the intima bound to LDL (from the circulation), and that which is synthesized de novo by plaque inflammatory cells (macrophages, T cells, mast cells)."
A meta-analysis involving a total of 79,036 participants in 32 prospective studies found that Lp-PLA2 levels are positively correlated with increased risk of developing coronary heart disease and stroke.[11]
^Tew DG, Southan C, Rice SQ, Lawrence MP, Li H, Boyd HF, et al. (April 1996). "Purification, properties, sequencing, and cloning of a lipoprotein-associated, serine-dependent phospholipase involved in the oxidative modification of low-density lipoproteins". Arteriosclerosis, Thrombosis, and Vascular Biology. 16 (4): 591–9. doi:10.1161/01.ATV.16.4.591. PMID8624782.
^Tellis CC, Tselepis AD (May 2009). "The role of lipoprotein-associated phospholipase A2 in atherosclerosis may depend on its lipoprotein carrier in plasma". Biochimica et Biophysica Acta. 1791 (5): 327–38. doi:10.1016/j.bbalip.2009.02.015. PMID19272461.
^Mohler ER, Ballantyne CM, Davidson MH, Hanefeld M, Ruilope LM, Johnson JL, Zalewski A (April 2008). "The effect of darapladib on plasma lipoprotein-associated phospholipase A2 activity and cardiovascular biomarkers in patients with stable coronary heart disease or coronary heart disease risk equivalent: the results of a multicenter, randomized, double-blind, placebo-controlled study". Journal of the American College of Cardiology. 51 (17): 1632–41. doi:10.1016/j.jacc.2007.11.079. PMID18436114.
Yamada Y, Yokota M (July 1997). "Loss of activity of plasma platelet-activating factor acetylhydrolase due to a novel Gln281-->Arg mutation". Biochemical and Biophysical Research Communications. 236 (3): 772–5. doi:10.1006/bbrc.1997.7047. PMID9245731.
Hiramoto M, Yoshida H, Imaizumi T, Yoshimizu N, Satoh K (December 1997). "A mutation in plasma platelet-activating factor acetylhydrolase (Val279-->Phe) is a genetic risk factor for stroke". Stroke. 28 (12): 2417–20. doi:10.1161/01.str.28.12.2417. PMID9412624.
Yamada Y, Ichihara S, Fujimura T, Yokota M (February 1998). "Identification of the G994--> T missense in exon 9 of the plasma platelet-activating factor acetylhydrolase gene as an independent risk factor for coronary artery disease in Japanese men". Metabolism. 47 (2): 177–81. doi:10.1016/S0026-0495(98)90216-5. PMID9472966.
Yoshida H, Imaizumi T, Fujimoto K, Itaya H, Hiramoto M, Yoshimizu N, et al. (September 1998). "A mutation in plasma platelet-activating factor acetylhydrolase (Val279Phe) is a genetic risk factor for cerebral hemorrhage but not for hypertension". Thrombosis and Haemostasis. 80 (3): 372–5. doi:10.1055/s-0037-1615214. PMID9759612. S2CID23924021.