Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (1/189)New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. 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. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction. (+info)
A thymidine to cytosine substitution for codon 26 of exon 3 of apolipoprotein C-II gene in a patient with apolipoprotein C-II deficiency. (2/189)A 52-year-old Japanese woman was evaluated for severe hypertriglyceridemia and recurrent acute pancreatitis. This hypertriglyceridemia was found to be due to the absence of serum apolipoprotein C-II (apo C-II) which was identified by Western blotting using polyclonal anti-apo C-II antiserum. DNA sequence analysis of the apo C-II gene from the patient revealed a homozygous nucleotide change: a thymidine (T) to cytosine (C) substitution in codon 26 (TGG->CGG) at the third exon of the apo C-II gene, that resulted in a Trp26 to Arg substitution. The mutation was also confirmed by restriction fragment length polymorphism (RFLP) analysis with the restriction enzyme Hpa II. The same mutation has been found in a case previously reported in Japan, and was named apo C-II Wakayama. However, the case in Wakayama prefecture showed two concomitant point mutations at the 5'-flanking region upstream from the first exon, which were not identified in our case by RFLP analysis with the restriction enzyme BstXI. Considering that the prefectures of these two cases, Nara and Wakayama, are next to each other, the mutation in our case may be a genetic forebear of apo C-II Wakayama. However, no familial relationship between the two cases has been documented. (+info)
Protective effect of apolipoprotein A I, A II, C I and C II on endothelial cells injury induced by low density lipoprotein. (3/189)OBJECTIVE: To investigate the protective effect of apo-lipoprotein (apo) A I, A II, C I and C II, the main proteins in high density lipoprotein (HDL), on the morphology and function of human umbilical vein endothelial cells injured with low density lipoprotein (LDL) in vitro. METHODS: Cultured human endothelial cells derived from umbilical veins were exposed to LDL, HDL, and apoA I, A II, C I and C II. The morphology of endothelial cells was examined with phase contrast and transmission electron microscope. The released amount of lactate dehydrogenase (LDH) and 6-keto-prostaglandin F1 alpha (PGF1 alpha) was also measured. RESULTS: Endothelial cells after being injured by LDL showed cell contraction, increased release of LDH and decreased secrection of prostacyclin (PGI2). However, the addition of HDL, and apoA I, A II, C I and C II before incubation with LDL inhibited the cellular injury induced by LDL as demonstrated by lowered LDH release, increased level of PGF1 alpha and prevention of morphological changes. CONCLUSION: The results indicate that apoA I, A II, C I and C II, as well as HDL, may play an important role in combating atherogenesis by protecting endothelial cells from damages induced by LDL. (+info)
Fibrinolytic factors, serum lipid and C-reactive protein predicting cardiac events in Japanese patients with coronary atherosclerotic lesions. (4/189)Although disturbances of the fibrinolytic system and serum lipid, and the presence of inflammation, may be risk factors for coronary artery disease (CAD), few reports have investigated these relationships in Japanese patients. Data on 106 patients (79 men and 27 women, mean age 62.3 years) with atherosclerotic lesions on the coronary angiogram were evaluated prospectively to identify whether the factors were useful in predicting the risk of coronary events during a follow-up of 50+/-4 months. Of the 106 patients who were followed, 11 patients had coronary events (4 acute myocardial infarction and 7 unstable angina pectoris). In univariate Cox analyses, a high level of tissue-plasminogen activator (t-PA), apolipoprotein CII, C-reactive protein (CRP), and a low level of high-density lipoprotein-cholesterol (HDL-C) was each associated with a significant increase in the risk of future cardiac events. The stepwise model of Cox proportional hazards analysis selected only a high level of t-PA and CRP as predictors of cardiac events. Controlling for any risk factor did not lower the relation between t-PA and the risk of cardiac events, whereas the relative risk of cardiac events in CRP was not significant when controlled for HDL-C. Thus, in prospective data obtained from a cohort of Japanese patients with coronary atherosclerotic lesions, the elevation of t-PA was an independent predictor of subsequent cardiac events. The prognostic role of CRP in cardiac events was related to a low level of HDL-C. (+info)
Structure of a biologically active fragment of human serum apolipoprotein C-II in the presence of sodium dodecyl sulfate and dodecylphosphocholine. (5/189)We have studied the three-dimensional structure of a biologically active peptide of apolipoprotein C-II (apoC-II) in the presence of lipid mimetics by CD and NMR spectroscopy. This peptide, corresponding to residues 44-79 of apoC-II, has been shown to reverse the symptoms of genetic apoC-II deficiency in a human subject. A comparison of alpha-proton secondary shifts and CD spectroscopic data indicates that the structure of apoC-II(44-79) is similar in the presence of dodecylphosphocholine and sodium dodecyl sulfate. The three-dimensional structure of apoC-II(44-79) in the presence of sodium dodecyl sulfate, determined by relaxation matrix calculations, contains two amphipathic helical domains formed by residues 50-58 and 67-75, separated by a non-helical linker centered at Tyr63. The C-terminal helix is terminated by a loop formed by residues 76-79. The C-terminal helix is better defined and has a larger hydrophobic face than the N-terminal helix, which leads us to propose that the C-terminal helix together with the non-helical Ile66 constitute the primary lipid binding domain of apoC-II(44-79). Based on our structure we suggest a new mechanism of lipoprotein lipase activation in which both helices of apoC-II(44-79) remain lipid bound, while the seven-residue interhelical linker extends away from the lipid surface in order to project Tyr63 into the apoC-II binding site of lipoprotein lipase. (+info)
In addition to the high-density lipoprotein fraction, apolipoprotein C-III is detected in chylomicrons and the very low-density lipoprotein fraction from serum of normolipidemic cows. (6/189)Apolipoprotein (apo) C-III is a low-molecular-mass protein that is involved in the regulation of the triglyceride metabolism. Except for the hyperlipidemic calf, cattle apoC-III is mainly detected in the high-density lipoprotein (HDL) fraction, and the distribution in chylomicrons (CM) and the very low-density lipoprotein (VLDL) fraction has not yet been clarified. The purpose of the present study was to detect apoC-III in concentrated CM and VLDL fractions to examine whether apoC-III is distributed in the two fractions even in normolipidemic cattle. ApoC-III could be detected by immunoblot analysis in both concentrated cow CM and VLDL fractions, but not in the corresponding calf fractions. These results suggest that apoC-III is distributed in the CM and VLDL fractions, at least in cows, although the concentrations in these fractions are considerably lower than in the HDL fraction. (+info)
Expression of the apolipoprotein C-II gene during myelomonocytic differentiation of human leukemic cells. (7/189)Apolipoprotein C-II (apoC-II), which is known to activate lipoprotein lipase (LPL), was identified by ordered differential display (ODD)-polymerase chain reaction (PCR) as a cDNA fragment exhibiting a distinct increase in expression during 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced differentiation of promonocytic U937 cells into monocytes and macrophages. The amount of apoC-II mRNA expression detectable in U937 cells significantly increased and reached a maximum 24-48 h after treatment with 32 nM TPA. apoC-II mRNA was also detected in monocytic THP-1 cells but was not detected in promyelocytic HL-60 cells. In healthy human tissues, the most significant expression of apoC-II mRNA was in the liver. Although apoC-II mRNA expression was markedly up-regulated during the induced differentiation of HL-60 cells into monocytes and macrophages with 32 nM TPA, such expression was not induced during the differentiation of HL-60 cells into granulocytes with 1.25% dimethyl sulfoxide. These results suggest that human apoC-II expression is induced at the transcription level during myelomonocytic differentiation and may confer an important role to macrophages involved in normal lipid metabolism and atherosclerosis. (+info)
Sub-micellar phospholipid accelerates amyloid formation by apolipoprotein C-II. (8/189)Lipid-free human apolipoprotein C-II (apoC-II) forms amyloid fibrils with characteristic beta-structure. This conformation is distinct from the alpha-helical fold of lipid-bound apoC-II. We have investigated the effect of the short-chain phospholipid, dihexanoylphosphatidylcholine (DHPC) on amyloid formation by apoC-II. The alpha-helical content of apoC-II increases in the presence of micellar DHPC (16 mM) and amyloid formation is inhibited. However, at sub-micellar DHPC concentrations (below 8 mM) amyloid formation is accelerated 6 fold. These results suggest that individual phospholipid molecules in vivo may exert significant effects on amyloid folding pathways. (+info)
The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.
The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.
Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.
Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.
In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.
Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.
There are several types of arteriosclerosis, including:
1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.
Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.
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- See the reference protein sequence for apolipoprotein E isoform b precursor (NP_000032.1). (nih.gov)
- Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of tubular malfunction. (bmj.com)
- Apolipoprotein B is the main protein component of LDL and accounts for approximately 95% of the total protein content of LDL. (cdc.gov)
- LpA-I exhibited significantly more protein diversity than LpA-I/A-II when isolated directly from plasma . (bvsalud.org)
- This effect was independent of the accessory protein signature suggesting that apoA-II induces a structural change in apoA-I in HDLs. (bvsalud.org)
- Apolipoprotein A1 (apoA1) is the major protein of high-density lipoprotein (HDL), and apoB is among the major proteins of very low-, low- (LDL), and intermediate-density lipoproteins. (cdc.gov)
- Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. (medlineplus.gov)
- Protein kinase C (PKC) inhibitors suppressed both ABCA1 stabilization and cellular lipid release mediated by apolipoprotein A-I (apoA-I) but not ABCA1 increase by calpain inhibitors. (nih.gov)
- 1. We hypothesized that differences within genes whose protein products are involved in apolipoprotein B metabolism could influence the response of plasma apolipoprotein B-containing lipoprotein concentrations to increases in dietary fibre. (portlandpress.com)
- Plasticity in structure and assembly of SARS-CoV-2 nucleocapsid protein. (nih.gov)
- The analyst should use the special sampling weights in this file to analyze Apolipoprotein B (ApoB). (cdc.gov)
- Because of their associations with the respective lipoproteins, apoA1 is inversely and apoB is positively associated with cardiovascular risk (2). (cdc.gov)
- Linear regression models conducted in each cycle were used to perform a meta-analysis to investigate associations between urinary BPA and serum levels of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), triglycerides (TG) and apolipoprotein B (ApoB). (bmj.com)
- Apolipoprotein E (ApoE) ε4 Genotype (ApoE rs429358-ApoE rs7412 Polymorphisms) Is Not Associated with Long COVID Symptoms in Previously Hospitalized COVID-19 Survivors. (nih.gov)
- We studied the association of HDL cholesterol (HDL-C), apoA1, apoCIII, apoD, and apoE as well as the ratios of apolipoproteins with apoA1 with the risk of T2D. (eur.nl)
- Tissue samples from temporal lobes resected from epilepsy patients carrying two APOE ε3 alleles were examined regarding an association between inheritance of these alleles and determinants of neuronal resilience. (biomedcentral.com)
- Apolipoprotein E ( APOE ) is a gene that influences Alzheimer's risk. (nih.gov)
- People who carry two copies of APOE ε4 and are of European descent have a higher risk than those who are of African, Hispanic, or Japanese descent. (nih.gov)
- The increased risk was only observed when the APOE ε3 [R145C] variant was paired with APOE ε4 and the risk was similar to that associated with carrying two copies of APOE ε4 . (nih.gov)
- We herein investigated the properties of macrophages that contribute to amyloid degradation and disease progression using inducible apolipoprotein A-II amyloidosis model mice. (qxmd.com)
- Sixty percent of women were at increased cardiovascular risk because of low apolipoprotein A1 (apoA1) levels, compared with 35% of men. (cdc.gov)
- Apolipoprotein A-II alters the proteome of human lipoproteins and enhances cholesterol efflux from ABCA1. (bvsalud.org)
- Apolipoproteins may also offer advantages over lipoprotein cholesterol measurements because they are direct measurements, whereas LDL, for example, is calculated from other lipoproteins from a fasting blood sample. (cdc.gov)
- Regulation and clearance of apolipoprotein B-containing lipoproteins. (medlineplus.gov)
- 1. Abnormal activation of lipoprotein lipase by non-equilibrating apoC-II: further evidence for the presence of non-equilibrating pools of apolipoproteins C-II and C-III in plasma lipoproteins. (nih.gov)
- 4. Lipoprotein distribution of apolipoprotein C-III and its relationship to the presence in plasma of triglyceride-rich remnant lipoproteins. (nih.gov)
- 5. Lipoprotein lipase-catalyzed hydrolysis of phosphatidylcholine of guinea pig very low density lipoproteins and discoidal complexes of phospholipid and apolipoprotein: effect of apolipoprotein C-II on the catalytic mechanism. (nih.gov)
- 6. Guinea pig apolipoprotein C-II: expression in E. coli, functional studies of recombinant wild-type and mutated variants, and distribution on plasma lipoproteins. (nih.gov)
- 8. Evidence for non-equilibrating pools of apolipoprotein C-III in plasma lipoproteins. (nih.gov)
- 12. Independent regulation of plasma apolipoprotein C-II and C-III concentrations in very low density and high density lipoproteins: implications for the regulation of the catabolism of these lipoproteins. (nih.gov)
- 14. Effects of dietary carbohydrate and fat on plasma lipoproteins and apolipoproteins C-II and C-III in healthy men. (nih.gov)
- The apo E gene is polymorphic with 3 common alleles (2, (3 and (4. (europa.eu)
- This study aimed to demonstrate whether lipoprotein lipase enzyme (LPL) and Apolipoprotein CII (APOCII) gene polymorphisms can be considered as independent genetic risk factors for dyslipidaemia among smokers with various smoking durations. (who.int)
- Genotypes were determined using DNA markers for the low-density lipoprotein receptor, apolipoprotein B, apolipoprotein CIII and hepatic lipase gene loci. (portlandpress.com)
- Both proapolipoprotein C-II and apolipoprotein C-II can activate lipoprotein lipase. (enquirebio.com)
- 2. Lipoprotein ApoC-II activation of lipoprotein lipase. (nih.gov)
- 3. Effects of plasma apolipoproteins on lipoprotein lipase-mediated lipolysis of small and large lipid emulsions. (nih.gov)
- 7. Modulation of lipoprotein lipase activity by apolipoproteins. (nih.gov)
- 17. Human apolipoprotein A-II determines plasma triglycerides by regulating lipoprotein lipase activity and high-density lipoprotein proteome. (nih.gov)
- Serum levels of an isoform of apolipoprotein A-II as a potential marker for prostate cancer. (nih.gov)
- SELDI-based immunoassay revealed that an 8.9-kDa isoform of ApoA-II is specifically overexpressed in serum from individuals with prostate cancer. (nih.gov)
- ApoA-II was also overexpressed in the serum of individuals with prostate cancer who have normal prostate-specific antigen (0-4.0 ng/mL). (nih.gov)
- In an immunochemical reaction, Apolipoprotein B in the human serum sample form immune complexes with specific antibodies. (cdc.gov)
- Apolipoprotein C3 (APOC3) mutations carriers typically display high plasma high-density lipoprotein cholesterol (HDL-C) and low triglycerides (TGs). (nih.gov)
- Apolipoprotein and lipid profiles in this First Nation population suggest high cardiovascular risk. (cdc.gov)
- Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. (nih.gov)
- ForAPO CII-Ava II polymorphisms, compared with those of the A2A2 genotype group, the total cholesterol TC, TG, low-density lipoprotein cholesterol LDL-C and VLDL-C concentrations were significantly increased in the A1A2 genotype group, while the HDL-C concentration was significantly decreased. (who.int)
- There was no significant variation in the reduction of plasma total cholesterol, low-density lipoprotein cholesterol or apolipoprotein B concentrations for alleles of other genes tested. (portlandpress.com)
- [ 2 ] The revisions and update have reflected the results of randomized placebo controlled clinical trials that have demonstrated reduced morbidity and mortality in subjects with moderate hypercholesterolemia treated with cholesterol-lowering agents, particularly (though not exclusively) statins. (medscape.com)
- Concentrations of low density lipoprotein cholesterol and apolipoprotein B were about 10% lower with margarine than with butter. (bmj.com)
- Lp(a) lipoprotein and high density lipoprotein cholesterol concentrations were similar with the two diets. (bmj.com)
- 1 2 A major justification for this recommendation is the association between saturated fatty acids and total and low density lipoprotein cholesterol. (bmj.com)
- The structure of most HDLs is maintained by two scaffold proteins , apoA-I and apoA-II , but up to 95 other "accessory" proteins have been found associated with the particles. (bvsalud.org)
- Most LpA-I/A-II accessory proteins were associated with lipid transport pathways, whereas those in LpA-I were associated with inflammatory response, hemostasis , immune response , metal ion binding, and protease inhibition. (bvsalud.org)
- Among them, apolipoprotein C-II (apoC-II) was found to have the highest abundance among the CKD patients with hypertension. (frontiersin.org)
- As such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in children suffering from mild-to-moderate CKD. (frontiersin.org)
- Early evaluations of apoC-II and apoC-III, ABPM, and surrogate markers of CV risk will aid in early preventative interventions to reduce the risk of CV in youths suffering from CKD. (frontiersin.org)
- Two methods are compared for measuring the kinetic parameters of apolipoprotein A-I and A-II metabolism in human plasma. (houstonmethodist.org)
- The 'obesogen hypothesis' and 'metabolism-disrupting hypothesis' suggest that exposure to endocrine-disrupting chemicals (EDCs) found in the environment may predispose some individuals to the development of obesity and associated health conditions, such as type 2 diabetes and cardiovascular diseases. (bmj.com)
- The apoC-III proteoform containing two sialic acid residues (apoC-III2) has different in vitro effects on lipid metabolism compared with asialylated (apoC-III0) or the most abundant monosialylated (apoC-III1) proteoforms. (nih.gov)
- Disialylated apolipoprotein C-III proteoform is associated with improved lipids in prediabetes and type 2 diabetes. (nih.gov)
- Cross-sectional and longitudinal associations between plasma apoC-III proteoforms (by mass spectrometric immunoassay) and plasma lipids were tested in two randomized clinical trials: ACT NOW, a study of pioglitazone in subjects with impaired glucose tolerance (n = 531), and RACED (n = 296), a study of intensive glycemic control and atherosclerosis in type 2 diabetes patients. (nih.gov)
- Epub 2003 Sep 2. (nih.gov)
- Sequence identification by liquid chromatography-MS/MS and subsequent immunoassays verified that an isoform of apolipoprotein A-II (ApoA-II) is the observed 8,946 m/z SELDI peak. (nih.gov)
- We have identified an isoform of ApoA-II giving rise to an 8.9K m/z SELDI 'peak' that is specifically overexpressed in prostate disease. (nih.gov)
- Conclusions: The study revealed that the HþHþ or H þ H-genotype of the LPL-Hind III polymorphism and the A1A1or A1A2 genotype of the APOCII-Ava II polymorphism were at higher risk of developing dyslipidaemia compared to the HeH- genotype of the LPL-Hind III polymorphism and A2A2 genotype of the APOCII-Ava II polymorphism. (who.int)
- 3. Reductions in plasma concentrations of apolipoprotein B were significantly different depending on genotype determined with a low-density lipoprotein receptor DNA marker ( P = 0.03). (portlandpress.com)
- A DNA sequence encoding the Homo sapiens (Human) Apolipoprotein C-II, was expressed in the hosts and tags indicated. (enquirebio.com)
- The intensity of the scattered light is proportional to the concentration of Apolipoprotein B in the sample. (cdc.gov)
- ATP-binding cassette transporter A1 (ABCA1) plays an essential role in the helical apolipoprotein-mediated assembly of high density lipoprotein, and the apolipoporteins stabilize ABCA1 against calpain-mediated degradation during the reaction ((2002) J. Biol. (nih.gov)
- SUMMARY: Notice is hereby given that on April 2, 2018, the Department of Health and Human Services (HHS) Debarring Official, on behalf of the Secretary of HHS, issued a final notice of debarment based on the findings of research misconduct made by the Office of Research Integrity (ORI) against H.M. Krishna Murthy, Ph.D., former Research Associate Professor, Department of Vision Sciences, University of Alabama at Birmingham (UAB). (nih.gov)
- The administrative actions, including ten (10) years of debarment, were implemented beginning on April 2, 2018, and are detailed below. (nih.gov)
- Fasting blood lipid, lipoprotein and apolipoprotein concentrations were measured at the start and end of the 2 week metabolic period. (portlandpress.com)
- 4. Thus, genetic variability is associated with inter-individual differences in the fibre-related reduction in plasma apolipoprotein B and apolipoprotein B-containing lipoprotein concentrations. (portlandpress.com)
- 9. Quantitation of human apolipoprotein C-III and its subspecie by radioimmunoassay and analytical isoelectric focusing: abnormal plasma triglyceride-rich lipoprotein apolipoprotein C-III subspecie concentrations in hypertriglyceridemia. (nih.gov)
- Concentrations of total and low density lipoprotein, Lp(a) lipoprotein, high density lipoprotein, apolipoprotein B 100, and apolipoprotein AI. (bmj.com)
- To begin to address this issue, we separated human plasma and HDL isolated by ultracentrifugation (UC-HDL) into particles with apoA-I and no apoA-II (LpA-I) and those with both apoA-I and apoA-II (LpA-I/A-II). (bvsalud.org)
- The fractional plasma clearance rates of endogenous apolipoproteins A-I and A-II were the same. (houstonmethodist.org)
- As follow-up care, the patient will receive repeat lumbar punctures every 3 months for 2 years to exclude occult invasion of the central nervous system (CNS). (cdc.gov)
- Second, Cox proportional hazard models were used to examine whether apolipoproteins predict the risk for T2D among individuals free of diabetes at baseline. (eur.nl)
- 10. Identification and metabolic characteristics of an apolipoprotein C-II variant isolated from a hypertriglyceridemic subject. (nih.gov)
- The solution structure of the 16th CCP module from human complement factor H has been determined by a combination of 2-dimensional nuclear magnetic resonance spectroscopy and restrained simulated annealing. (embl.de)
- OBJECTIVE We aimed to investigate the role of serumlevels of various apolipoproteins on the risk for type 2 diabetes (T2D). (eur.nl)
- In order to test whether hyperlipidaemia and glycaemic control can be improved among diabetes patients by dietary supplementation with purified omega-3 fatty acids, we carried out a double-blind, placebo-controlled trial on 50 type 2 diabetes patients randomized to 2 g/day purified omega-3 fatty acids or placebo for 10 weeks. (who.int)
- The prevalence of type 2 diabetes has increased greatly in the past few years, and an even greater increase is foreseen in the next few years . (who.int)
- When additional risk factors were included in the model, including diabetes mellitus, alcohol intake, psychosocial factors, the ratio of apolipoprotein B to A1, and cardiac causes (atrial fibrillation or flutter, previous MI, and valve disease), these 10 risk factors accounted for 90% of the risk of stroke. (medscape.com)
- Our aim was to describe the apolipoprotein profile with respect to cardiovascular risk in a Canadian First Nation community. (cdc.gov)
- Our objective was to describe the apolipoprotein profile and its relationship to cardiovascular risk factors in a Canadian First Nation community. (cdc.gov)
- Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond a lipid panel is unknown. (medlineplus.gov)
- 2. We studied 67 subjects (43 men and 24 women) who had taken part in parallel 2 week metabolic dietary studies involving either wheat bran or oat bran supplementation. (portlandpress.com)
- The LPL-Hind III and APO CII-Ava II polymorphisms were determined using the polymerase reaction-restriction fragment length polymorphisms (RFLP) technique. (who.int)
- All apolipoproteins, ratios, and HDL-C levels were naturally logtransformed to reach normal distribution. (eur.nl)
- The catabolic clearance rate of exogenously labeled apolipoprotein A-I was consistently faster than that of endogenous apolipoprotein A-I. Conversely, endogenously and exogenously labeled apolipoprotein A-II were catabolized at identical rates. (houstonmethodist.org)
- and 2) to evaluate prevention and treatment programs targeting cardiovascular disease in the U.S. (cdc.gov)
- Macrophages in the reticuloendothelial system inhibit early induction stages of mouse apolipoprotein A-II amyloidosis. (qxmd.com)
- The ability of ApoA-II to detect disease in patients with normal prostate-specific antigen suggests potential utility of the marker in identifying indolent disease. (nih.gov)
- In the first, high density lipoprotein apoproteins were radioiodinated in situ in the lipoprotein particle (endogenous apoprotein labeling) while in the second, individually labeled apolipoprotein A-I or A-II was incorporated into the particle by in vitro incubation (exogenous apoprotein labeling). (houstonmethodist.org)
- There is now much evidence implicating apolipoprotein E (apo E) in the pathogenesis of CAD and AD. (europa.eu)
- Nous avons réalisé un essai en double aveugle contre placebo sur 50 patients atteints de diabète de type 2 randomisés pour recevoir 2 g/jour d'acides gras oméga 3 purifiés ou un placebo pendant 10 semaines. (who.int)
- The limitations of this animal model associated with its morphological and physiological differences with humans are minimized by the similarity of the two genomes and by the potential for increased understanding attainable, given that the dietary interventions reported here would have taken 400 years to achieve in humans. (revespcardiol.org)
- After the patient received 2 treatment doses of suramin and analysis of repeat blood films confirmed that parasitemia had cleared, a lumbar puncture was performed. (cdc.gov)