583:, I see that the former is a "major component" of the latter, but that still doesn't really explain why lowering triglycerides would necessarily lower VLDL, let alone LDL. (From all the reading I've done – only a tiny fraction of what's known – on these health-related biochemical articles, one thing I've learned is that one cannot assume that lowering molecule A that's a building block of molecule B doesn't necessarily lower B, as there seem to be many ways to assemble any given molecule B, even assuming metabolism doesn't shift to accommodate the change.) Could someone knowledgeable add a brief, explicit connection? Thanks. ~
264:— The dietary portion presently reads: "Dietary Insulin induces HMG-CoA reductase activity, whereas glucagon downregulates it. While glucagon production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate. The rise of insulin is, in general, determined by the unfolding of carbohydrates into glucose during the process of digestion. Glucagon levels are very low when insulin levels are high." Upregulates? Downregulates? Unfolds? Does this just mean increase or decrease? I have a doctorate (not in medicine) and I
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the actual claim is of an increase in vasodilation and a decrease in serum oxidizability. I can't see where either of these directly supports the claim of lowering LDL. Vasodilation refers to increasing the diameter of the vessel, not a reduction in something that might be blocking it. Lastly, the abstract/summary of the paper does not mention how long (if at all) the effect persisted after the consumption of the tea extract.
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decrease the rise in glucose level as insulin controls its level.Orally taken insulin is degraded in stomach and is of no use so artificially synthesized insulin is used for it.When carbohydrates breaks down in our body to simpler molecule eg. glucose for easy digestion, insulin is secreted from pancreas.
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in the introduction, it is written"A single LDL particle is about 260-300 nm in diameter (submicroscopic )..." further down, the diameter of LDL is given as 22 nm, which according to the given reference should be correct. I guess the first value is actually in
Angstrom. As 10 A = 1 nm, 220A = 22nm.
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While I was at it I looked at the citation regarding green tea and removed that from the section as well (now there is no section on Plant
Remedies). The citation was based on a study of FIVE women (way too small of a sample) who were given some extract of the tea (not the tea itself) and even then
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Health is a very emotive subject - with multiple schools of scientific thought, it is not bad to recognise this complexity in the text. It is important though that the text remains focused on LDL not on what inputs, outputs and diets effect LDL, those other focuses are for other articles where those
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This table underscores that "average" does not mean "healthy," as well as the sharp rise of risks with age. Even before age 30, average male levels are already borderline unhealthy, and LDL levels and risks rise sharply afterward. The rising trend in men is followed 10 or 20 years later by women
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I was listening to Audio Digest (an audio CME for healthcare professionals) the other day and it has been suggested that ldl levels below 80 mg/dl can arrest atherosclerosis, while levels below 70 mg/dl can even reverse it. I don't have enough time to find documentation for this, but if anyone is
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that the dietary part is especially useless to the layman... maybe add some examples of food which would upregulate or downregulate LDL synthesis, or which foods may contain high levels of B3 (niacin). I also recall learning that moderate alcohol consumption may help regulate LDL (by means of HDL
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particles. About half of the IDL particles are taken up and destroyed by the liver. The other half continue to deliver their contents to the cells. After that the (now even smaller) IDL remnants are called LDL particles. They are small enough to sneak into the spaces between the cells lining the
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the above lines tells the relation between insulin and glucagon .These are hormones which oppose each other.Insulin anticipates HMG-coA reductase activity whereas glucagon decreases.Dietry carbohydrate is what we take from food ie.orally.when there is low production of insulin in body we need to
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It is licensed
Creative Commons Attribution, so there is no obvious reason not to use one or two of the TIFFs or MPEGs (I lack the skill to do it myself). Of interest is the fact that the ApoB100 protein molecule is 1/6 of the total mass, and almost surrounds the lipid core. The thing is almost
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These recommended levels are extraordinary. The current (Nov 2009) recommended level in Europe is "no more than 160 mg/dl". It might be pointed out that even this is regarded in many quarters as suspect, i.e. ratcheted down by the pharmaceutical industry, and that a figure of 180 might be more
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I'm not even going to attempt to flesh this page out, since I'm not able to follow most of the links I can find on the subject, certainly not at the end of a work day (I'm a marine biologist dang it18:40, 27 December 2016 (UTC)18:40, 27 December 2016 (UTC)18:40, 27 December 2016 (UTC)18:40, 27
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The whole concept of "good" and "bad" cholesterol is completely flawed and has been refuted endlessly in recent years, so I'm not sure why it is still sat atop the wikpedia page for LDL. Hopefully an editor can go about rectifying this. One source of many:
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As with all things chemistry and health related, there are those exclaiming science, and those exclaiming myth. I don't presume to judge this particular topic, but this article seems well written, and the source sited by above does not exist.
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I suggest there be a section explaining the terms "LDL cholesterol" and "HDL cholesterol". Since LDL and HDL are lipoproteins, they cannot be cholesterol. I guess that in this case, LDL and HDL are used as adjectives: "LDL cholesterol" -:
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There was an introductory paragraph explaining that LDL-C is not necessarily the "bad" cholesterol and is important for regular functioning, etc. There were no citations and it did not have a neutral tone--I removed it for that reason.
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The most commonly used predictors of adverse health outcomes are both LDL-C and Total
Cholesterol. Presumably LDL-C is more specific and targeted, and has greater predictive value than Total Cholesterol? The article should address this
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In the part (Recommended range; changing targets) I have added request for citation; there is mentioned scientific research in general instead of direct citation or reference and this creates false appearence that it has valid source.
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Some pretty snazzy illustrations appeared in this article a few years ago: "Three-Dimensional cryoEM Reconstruction of Native LDL Particles to 16Å Resolution at
Physiological Body Temperature" by a Finnish group, published on-line at
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Just rewrote the introduction so that first paragraph a. explain what lipoproteins do - for people who want a one sentance answer b. where LDL stands in relation to other lipoproteins c. recognises that their are two types of LDL
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I agree that LDL and LDL-C need to be differentiated in the article. Of course, LDL does contain cholesterol and triglycerides. Blood tests actually report HDL-C and LDL-C: the amount of cholesterol (C) in each of the fractions.
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Under "lowering cholesterol" what is meant by the unfolding of carbohydrates to glucose. Isn't this language a little bit confusing. Does he mean the break down of carbohydrates. "unfolding is not a very good word.
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And phrases like 'as opposed to HDL, which is frequently referred to as "good cholesterol" or "healthy cholesterol"', which appears in the first paragraph of the article, should be avoided as they are nonsense.
611:(Actually, Knowledge is much clearer and more detailed on lipoproteins now than it was 5 years ago when heart troubles first impelled me to these pages. I don't mean to diss you if it was not so clear in 2009.)
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This table suggests a benefit to consideration of a lifelong primary coronary prevention lifestyle, and heightened vigilance to check and respond to cholesterol rise after age 30 for men and age 40 for women.
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particles are produced in the liver in order to deliver newly made triglycerides and cholesterol to the cells that need them. After delivering part of their load, the (now smaller) VLDL remnants are called
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Ravnskov U, de
Lorgeril M, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, Hynes N, Kendrick M, Langsjoen PH, Mascitelli L, McCully KS, Okuyama H, Rosch PJ, Schersten T, Sultan S, Sundberg R (2018).
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interested, it would be useful to have this in the article. It would seem that the current guidelines for LDL are out of date given new information and research into realistically healthy levels.
1223:. No major clinical organization, regulatory agency, or scientific consensus on systematic reviews or meta-analyses concludes that the LDL evidence as a risk factor is "inaccurate" or "flawed".
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I agree and removed the mention. The WP page supports no such claim and the citation is just a supplement maker's product page (i.e., not a credible source for this sort of claim).
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92:, not a doctor.. or whatever ;). However, if someone could kindly point out what the 'it' in the stub means that might help a \bit (I kind of assume cholesterol, but not sure).
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don't understand these four sentences. Will a medical person please put this in lay terms? And make some distinction between "dietary insulin" and what, injected insulin? --
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Excerpt - "This view has been challenged as inaccurate and based on flawed research methodology. The issue remains controversial and vigorously contested in the literature."
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level regulation??). Might want to mention that too much alcohol would have the opposite effects, as metabolizing lots of EtOH would increase your triglyceride levels.
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the subsquent two paragraphs introduce aspects of the issues in research, testing and clinical use of tests that are covered in greater detail in subsquent sections.
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The most effective approach has been minimizing fat stores located inside the abdominal cavity (visceral body fat) in addition to minimizing total body fat.
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for the following statement makes no mention of LDL cholesterol, but rather, describes effective approaches to reducing abdominal visceral fat:
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Lowering the blood lipid concentration of triglycerides helps lower the amount of LDL, because VLDL gets converted in the bloodstream into LDL.
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Can someone translate that into english, please? Does that mean we should increase or decrease fructose intake to reduce LDL? Thanks. --
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blood vessels, which is how the trouble begins. I infer that anything that increases or decreases VLDL is likely to do the same for LDL.
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143:) that a low carbohydrate diet correlates with a healthy LDL distribution - there is no reference for it and it seems to be dubious.
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When you have finished reviewing my changes, you may follow the instructions on the template below to fix any issues with the URLs.
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When you have finished reviewing my changes, you may follow the instructions on the template below to fix any issues with the URLs.
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The words and table format are mine and original. The information is attributed to "Controlling
Cholesterol The Natural Way."
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because it seems to assume that readers will already know the implied connection between triglycerides and VLDL. Reading
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This article is loaded with far too many technical terms and jargon to be easily understandable for the average reader.
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416:"cholesterol, that is carried by LDL proteins". Is this correct? If yes, it should be evident in the article, as well.
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It seems like a pretty major gap in this article is a complete absence of where, why and how LDL are synthesized.
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to delete these "External links modified" talk page sections if they want to de-clutter talk pages, but see the
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to delete these "External links modified" talk page sections if they want to de-clutter talk pages, but see the
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At the same time low levels of LDL-C are associated with cancer and infectious disease in the elderly, so ..
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looks like this page may have just been flooded with ad placement. A cleanup/revert, if someone has time?
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If you have discovered URLs which were erroneously considered dead by the bot, you can report them with
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https://web.archive.org/web/20140202053506/http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04.htm
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1054:. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit
944:. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit
1207:(excerpt below) were removed because there is no prevailing clinical standard to indicate that LDL is
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Yeah, there's a lot of jargon in this article with little common-language synthesis. Compare to
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845:, it sounds pretty bogus. Also, the study it links to seems... suspect at best. Thoughts?
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If you found an error with any archives or the URLs themselves, you can fix them with
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This isn't my specialty, but according to google, it's
Friedwald, not Freidwald. -
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Best to discuss here for consensus if warranted for reinstatement in the article,
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777:(who in later life are actually more at risk for coronary events than men).
1110:. No special action is required regarding these talk page notices, other than
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http://www.nhlbi.nih.gov/health-pro/guidelines/current/cholesterol-guidelines/
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I will update this if I find a source that more directly supports it. --
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http://www.liposcience.com/userfiles/content/files/weightofevidence.pdf
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Does the bit about
Garcinia belong here? Based on the page itself,
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ones (mmol/l) but I'm sure it needs to be done (the same goes for
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Garcinia section (now including entire Plant
Remedies section)
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303:- historical reference on the heterogeneity of LDL particles.
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http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04.htm
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http://www.docsopinion.com/health-and-nutrition/lipids/ldl-p/
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Whoops, I see that its actually discussed two sections up.
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for additional information. I made the following changes:
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for additional information. I made the following changes:
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Raised LDL is strongly linked to artery calcification.
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Before age 30: 136 mg/dL (men) and 126 mg/dL (women)
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Age above 60: 164 mg/dL (men) and 159 mg/dL (women)
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Age 50 to 59: 165 mg/dL (men) and 159 mg/dL (women)
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Age 40 to 49: 162 mg/dL (men) and 136 mg/dL (women)
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Age 30 to 39: 149 mg/dL (men) and 129 mg/dL (women)
1114:using the archive tool instructions below. Editors
980:using the archive tool instructions below. Editors
819:LDL-P would be VERY important to add to article.
1100:This message was posted before February 2018.
966:This message was posted before February 2018.
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1283:: CS1 maint: multiple names: authors list (
843:http://en.wikipedia.org/Garcinia_gummi-gutta
181:In the section "Lowering LDL-cholesterol",
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1200:LDL and risk of cardiovascular diseases
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596:Look it up! According to Knowledge,
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1050:. Please take a moment to review
940:. Please take a moment to review
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720:spherical at body temperature.
902:dimensions of LDL inconsistent
800:focuses can be expanded upon.
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320:Blame it on small dense LDL
78:tag is missing the closing
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1131:(last update: 5 June 2024)
1043:Hello fellow Wikipedians,
997:(last update: 5 June 2024)
933:Hello fellow Wikipedians,
882:LDL-C vs Total Cholesterol
832:18:28, 8 August 2014 (UTC)
754:Average LDL levels, by age
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148:21:21, 30 March 2007 (UTC)
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455:recommended levels of ldl
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139:I removed the statement (
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555:Triglycerides & VLDL
357:high-density lipoprotein
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52:05:49, 6 June 2008 (UTC)
1217:cardiovascular diseases
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1048:Low-density lipoprotein
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938:Low-density lipoprotein
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674:I second the motion. --
1173:Introductory paragraph
788:rewriting introduction
391:No graphics or models?
135:Low carbohydrate diet
1112:regular verification
978:regular verification
1102:After February 2018
968:After February 2018
58:December 2016 (UTC)
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410:LDL cholesterol?!?
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1279:cite journal
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1180:— Preceding
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1126:source check
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581:Triglyceride
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72:Cite error:
56:
30:
27:Minor issues
1256:: 959–970.
1213:risk factor
1186:24.48.69.87
847:216.80.69.8
738:Eall Ân Ûle
689:Eall Ân Ûle
631:Eall Ân Ûle
482:realistic.
462:—Preceding
425:—Preceding
240:—Preceding
214:—Preceding
34:—Preceding
1232:References
1163:Report bug
1029:Report bug
648:Synthesis?
195:Steliotron
1146:this tool
1139:this tool
1066:dead link
1012:this tool
1005:this tool
726:Solo Owl
677:Solo Owl
619:Solo Owl
484:Escoville
270:LisaSmall
167:Citations
131:2-9-2006
84:help page
82:(see the
1271:30198808
1182:unsigned
1152:Cheers.—
1018:Cheers.—
911:unsigned
746:contribs
734:unsigned
697:contribs
685:unsigned
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639:contribs
627:unsigned
537:unsigned
464:unsigned
427:unsigned
242:unsigned
216:unsigned
159:Snellios
101:European
48:contribs
36:unsigned
1221:WP:RSUW
1070:tag to
1052:my edit
942:my edit
887:issue.-
423:- Tom
301:6827999
235:I agree
129:ganaaaa
94:Rgamble
1298:WP:CON
1062:Added
824:ee1518
802:X-mass
588:(talk)
585:Jeff Q
815:LDL-P
564:vague
520:Iglam
266:still
40:Cag66
16:<
1306:talk
1302:Zefr
1285:link
1268:PMID
1215:for
1190:talk
919:talk
893:talk
872:talk
851:talk
828:talk
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598:VLDL
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328:T@lk
310:T@lk
298:PMID
250:talk
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199:talk
145:Icek
120:T@lk
107:and
64:talk
44:talk
1258:doi
1209:not
1120:RfC
1090:to
1080:to
986:RfC
956:to
603:IDL
415:-->
323:JFW
305:JFW
153:Ads
115:JFW
111:).
105:HDL
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