|1.||Sékétéli, A: 10 articles (02/2007 - 03/2002)|
|2.||Noma, M: 10 articles (02/2007 - 03/2002)|
|3.||Amazigo, Uche V: 8 articles (09/2015 - 02/2007)|
|4.||Noma, Mounkaila: 6 articles (09/2015 - 01/2012)|
|5.||Howlett, Geoffrey J: 6 articles (02/2011 - 03/2007)|
|6.||Amazigo, U V: 6 articles (03/2002 - 03/2002)|
|7.||Zouré, Honorat G M: 5 articles (09/2015 - 07/2012)|
|8.||Wanji, Samuel: 5 articles (01/2015 - 02/2007)|
|9.||Rensen, Patrick C N: 5 articles (01/2011 - 02/2005)|
|10.||Berbée, Jimmy F P: 5 articles (01/2011 - 02/2005)|
07/01/2003 - "LPL activity remained in the range observed in C57/BL6J mice, and purified apoC-II transiently relieved FLS mice from hypertriglyceridemia. "
02/01/2015 - "When added to serum from a patient with apoC-II deficiency, it restored normal levels of LPL-induced lipolysis and also enhanced lipolysis in serum from patients with type IV and V hypertriglyceridemia. "
07/01/2012 - "However, there is not enough current evidence to clarify whether increased apoC-II causes hypertriglyceridemia or is an epiphenomenon reflecting hypertriglyceridemia. "
07/01/2012 - "In contrast, both an excess and a deficiency of apoC-II are associated with reduced LPL activity and hypertriglyceridemia. "
01/01/2007 - "Furthermore, the decrease of LPL activity in the heart, along with the inhibitory effects of excess apoC-II, may contribute to the hypertriglyceridemia observed in apoC-II transgenic mice."
11/01/1985 - "The tendency for decreased plasma apoC levels following alimentary lipemia confirms previous reports, and provides further data to support the concept that some apoC is cleared from plasma in association with TRL remnants. "
03/28/2000 - "Genetic deficiencies of apoC-II and overexpression of apoC-II in transgenic mice are both associated with severe hyperlipidemia, indicating a complex role for apoC-II in the regulation of blood lipid levels. "
06/01/2006 - "Endogenous apoC-I increases hyperlipidemia in apoE-knockout mice by stimulating VLDL production and inhibiting LPL."
03/01/1999 - "A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. "
01/01/1993 - "The variant may be altered in some other property, such as lipid binding, but since the distribution of apoC-IISF revealed no simple co-inheritance with lipid levels, it is unclear to what extent it plays a role in the observed hyperlipidemia. "
04/01/1985 - "We have reached the following conclusions regarding this family: (1) the common kinetic abnormality of VLDL-TG metabolism in the hypertriglyceridemic brothers was a low clearance of VLDL-TG; (2) impaired catabolism of VLDL could not be explained by the apoprotein C or E patterns; and (3) the most severe hypertriglyceridemia occurred when the decreased FCR was present in conjunction with VLDL-TG overproduction due to obesity. "
01/01/2013 - "ApoC-I and H5C levels very early in life may affect the development of dyslipidemia and obesity in childhood."
06/01/2007 - "Mice that overexpress human apolipoprotein C-I (apoC-I) homozygously (APOC1(+/+) mice) are protected against obesity and show cutaneous abnormalities. "
11/01/2012 - "WAT apoC-I secretion over 4 hours correlated with fasting total and non-high-density lipoprotein apoC-I but not with high-density lipoprotein apoC-I and was the primary predictor of 4-hour postprandial increases in TRL apoC-I. Correction for TRL apoC-I eliminated the association of WAT apoC-I with 6-hour area under the curve of plasma (13)C-triglyceride; correction for insulin sensitivity or inflammation did not. "
09/01/2014 - "Plasma apoC-I, apoC-II, apoC-III, and apoE are not associated with adiposity, insulin sensitivity, or inflammation in obese but healthy postmenopausal women. "
09/01/2014 - "At baseline, there was no association between the plasma transferable apolipoproteins with any index of adiposity, insulin sensitivity, lipids, or inflammation, except for apoE with peripheral fat mass (r = 0.18, P < .05), and apoC-II and apoC-III with cholesterol (r = 0.23 and r = 0.20 respectively, P < .05). "
05/01/2010 - "Biological classification of proteins with significant changes revealed functions previously implicated in development of NASH in humans, including immune system regulation and inflammation (orosomucoid 1, serum amyloid P component, paraoxonase 1, protein similar to alpha-2-macroglobulin precursor, beta-2-microglobulin, p101 protein, and complement components 2 and C8G), lipid metabolism (apolipoproteins C-III, E, E precursor, B, and N), structural and extracellular matrix proteins (transthyretin and endopeptidase 24.16 type M2), and coagulation [carboxypeptidase B2 (plasma)]. "
08/01/1979 - "The fatty liver secretes apoE into a recirculating perfusate at a significantly higher rate and produces cholesterol ester-rich, apoC-deficient VLDL with slower electrophoretic mobility than the triacylglycerol-rich VLDL produced by perfused normal livers. "
07/01/2003 - "The unique inborn hypertriglyceridemia seen in FLS (fatty liver Shionogi) mice was relieved by the administration of purified apolipoprotein (apo) C-II. Lipoprotein lipase (LPL) and its cofactor, apoC-II, play a pivotal role in VLDL metabolism. "
|3.||Lipoprotein Lipase (Diacylglycerol Lipase)
|4.||Apolipoprotein C-II (ApoC2)
|7.||Lipase (Acid Lipase)
|9.||Pre-beta High-Density Lipoproteins
|10.||LDL-Receptor Related Protein 1 (LDL-Receptor Related Protein)
|1.||Cardiopulmonary Resuscitation (CPR)
|3.||Drug Therapy (Chemotherapy)