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Horse plasma corticotrophin-releasing hormone (CRH): characterisation and lack of a late gestational rise or a plasma CRH-binding protein.

Immunoreactive corticotrophin-releasing hormone (irCRH) was present in methanolic extracts of equine peripheral blood and showed no elevation in maternal peripheral serum in late gestation (0.54 +/- 0.25 pmol/l; mean +/- S.D.) compared with control horses (0.41 +/- 0.15 pmol/l). The irCRH of methanolic extracts of pituitary venous plasma had a similar elution position following reverse-phase HPLC to synthetic human CRH(1-41) and to irCRH released from horse stalk-median eminence tissue incubated in vitro. Gel chromatographic studies showed no evidence for a plasma CRH-binding protein (CRHBP) analogous to that found in human plasma in either peripheral blood from normal or pregnant horses or in pituitary venous plasma sampled from a cannulated horse. CRH-binding activity was detectable in peripheral plasma from one horse, however the molecular size of this was indicative of a gamma-globulin rather than the 37 kDa CRHBP. These studies suggest that, unlike in the human, CRH does not rise to high values in late gestation nor circulate in a bound form in equine plasma.

Animals↗

Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism.

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.

Adolescent↗

Whole genome amplification of plasma-circulating DNA enables expanded screening for allelic imbalance in plasma.

Apoptotic and necrotic tumor cells release DNA into plasma, providing an accessible tumor biomarker. Tumor-released plasma-circulating DNA can be screened for tumor-specific genetic changes, including mutation, methylation, or allelic imbalance. However, technical problems relating to the quantity and quality of DNA collected from plasma hinder downstream genetic screening and reduce biomarker detection sensitivity. Here, we present a new methodology, blunt-end ligation-mediated whole genome amplification (BL-WGA), that efficiently amplifies small apoptotic fragments (<200 bp) as well as intermediate and large necrotic fragments (>5 kb) and enables reliable high-throughput analysis of plasma-circulating DNA. In a single-tube reaction, purified double-stranded DNA was blunted with T4 DNA polymerase, self-ligated or cross-ligated with T4 DNA ligase and amplified via random primer-initiated multiple displacement amplification. Using plasma DNA from breast cancer patients and normal controls, we demonstrate that BL-WGA amplified the plasma-circulating genome by approximately 1000-fold. Of 25 informative polymorphic sites screened via polymerase chain reaction-denaturating high-performance liquid chromatography, 24 (95%) were correctly determined by BL-WGA to be allelic retention or imbalance compared to 44% by multiple displacement amplification. By enabling target magnification and application of high-throughput genome analysis, BL-WGA improves sensitivity for detection of circulating tumor-specific biomarkers from bodily fluids or for recovery of nucleic acids from suboptimally stored specimens.

Allelic Imbalance↗

Plasma progesterone, serum estriol and plasma HPL determinations during the last trimester to detect changes before spontaneous labor. Comparison of progesterone assay using RIA and CPB.

Conflicting results have been published regarding changes in plasma progesterone during the last trimester of pregnancy. Some have demonstrated a fall in plasma progesterone before labor, and this has been taken as a possible explanation of the onset of labor. It has been suggested that the various results could be due to differences in methods for progesterone determination. In this study the progesterone levels were determined by both RIA and CPB. In 11 women the plasma progesterone, human placenta lactogen, and serum estriol were measured weekly during the last trimester of normal pregnancies and immediately after delivery. All samples were analysed radioimmunologically. In order to compare the radioimmunoassay and competitive protein binding techniques (RIA and CPB), the progesterone levels were determined by both methods. This was also done for 80 successive plasma progesterone routine samples drawn from women who were not pregnant or who were in the early stages of pregnancy. Both methods showed a significant rise in the plasma progesterone level during the last 6 weeks before spontaneous labor. However, the values obtained were lower when assayed by CPB than by RIA, presumably because of a higher specificity and a cross reaction in RIA. Serum estriol exhibited increasing values throughout pregnancy, but without a significant rise during the last few weeks. Plasma HPL settled at a constant level during the last few weeks before labor.

Estriol↗

Studies on the plasma kallikrein-kinin system in peritoneal exudate and plasma during experimental acute pancreatitis in pigs.

Acute pancreatitis was induced in pigs by retrograde injection of Na-taurocholate into the pancreatic duct. By means of chromogenic peptide substrate assays, increased plasma kallikrein activity, parallel with a reduction of plasma prekallikrein and functional kallikrein inhibition values, was found in peritoneal exudate. In plasma, however, no changes in the kallikrein-kinin system were found during the 6-h observation time. The study demonstrates the presence of components of the plasma kallikrein-kinin system in peritoneal fluid and suggests that the peritoneal cavity to a great extent is a functionally separate compartment from plasma. Activation of the plasma kallikrein-kinin system in peritoneal exudate during acute experimental pancreatitis appears to be of importance for the initial symptoms and the development of shock seen during this condition.

Acute Disease↗

Effect on days of lactation and methionine hydroxy analog on incorporation of plasma fatty acids into plasma triglycerides.

Methionine hydroxy analog has been proposed to stimulate hepatic lipoprotein synthesis and incorporation of plasma fatty acids into plasma triglyceride. Seven cows were fed diets containing 0 or 30 g analog/d starting 14 d prepartum. At approximately 30 and 60 d postpartum, cows were continuously infused intravenously with 1-[14C] palmitic acid for 160 min to achieve steady-state labeling of plasma fatty acid and triglyceride. Turnover of fatty acid and transfer quotients for triglyceride and CO2 were 3.3 and 2.7 mmol min-1; 13.0 and 10.0%; and 8.0 and 5.0%, for control and analog, respectively. Proportion of fatty acid turnover incorporated into triglyceride and CO2 were 14.0 and 15.0%; and 21.0 and 18.0, respectively, for control and analog. Analog increased 14C recovered in milk fat (52 vs. 36%). Plasma concentration of fatty acids, percent oxidized to CO2, and percent of CO2 from fatty acids decreased with increasing lactation days. Milk fat percent and yield, fatty acid turnover, and oxidation were positively correlated with concentration of plasma fatty acids, whereas fatty acid incorporated into plasma triglyceride was negatively correlated with fatty acid concentration. The data suggest that hepatic triglyceride secretion is not increased in early lactation; further, no effects of analog on lipid metabolism were detected.

Animals↗

Plasma fractionation by dead-end membrane filtration: effects of membrane properties and plasma flux.

Plasma fractionation by membrane filtration permits the reinfusion of the patient with his own albumin. In this study, the influence of membrane nature and plasma flux on plasma fractionation in dead-end mode is investigated with acetate hollow fiber filters. It is found that transmembrane pressure TMP rises exponentially with time, the rate of increase being proportional to plasma flux. The faster TMP rises, the faster the drop in sieving coefficient SC. It is also found that albumin SC is a function of TMP and not of plasma flux. Theoretical analysis of the dead-end filtration was performed. This theoretical model indicates that the observed variation of TMP with time is consistent with the assumptions that pore volume decreases proportionally to the filtrate plasma volume.

Blood Component Removal↗

Relationships between fatty acid status of sow plasma and that of umbilical cord, plasma and tissues of newborn piglets when sows were fed on diets containing tuna oil or soyabean oil in late pregnancy.

To investigate the relationships between maternal, umbilical cord and piglet fatty acid status, multiparous sows (six per diet) were fed on diets containing supplements (30 g/kg) of either soyabean oil or tuna oil for the last 21 d of pregnancy. The proportions of most fatty acids differed between diets: in particular, the tuna-oil-containing diet supplied more 22:6n-3 and less 18:2n-6 fatty acids than the soyabean-oil-containing diet. Maternal plasma fatty acid concentrations (mg/l) were greater than those in umbilical plasma and 20:4n-6 and 22:6n-3 fatty acids were present in higher proportions (g/100 g fatty acids) in umbilical than maternal plasma. Feeding tuna oil increased the proportionate amounts (g/100 g fatty acids) of total n-3 fatty acids (particularly 22:6n-3) in umbilical cord, plasma and piglet tissues compared with feeding soyabean oil: in contrast, the proportion of 20:4n-6 was decreased by feeding tuna oil. Changes in piglet fatty acid proportions as a result of oil feeding were not influenced by piglet weight. While proportions of the long-chain n-3 and n-6 polyunsaturated fatty acids in piglet liver, spleen and reproductive tract (ovaries plus uterus of the female, testes of the male) correlated well with those of umbilical plasma, those in brain and retina were poorly correlated. Therefore umbilical plasma cannot be used to predict the fatty acid status of piglet brain.

Animal Nutritional Physiological Phenomena↗

How to minimize missing those subjects with high 2HR plasma glucose but 'normal' fasting plasma glucose levels?

Among the subjects with 'normal' fasting plasma glucose (PG) levels (< 7.0 mmol/L), some of them are actually suffering from impaired glucose tolerance and diabetes, which can only be diagnosed by 2hr PG levels. We aim to find out a proper clinical approach in order to minimize missing those subjects with high 2hr PG but 'normal' fasting PG levels. We analyzed data collected from a previously published population-based prevalence survey for glucose intolerance in 1486 Hong Kong Chinese subjects who had no past history of diabetes. Of the 1468 subjects, there were 138 subjects (9.4%) having "missed glucose intolerance". Compared to the diabetic subjects (fasting plasma glucose > or = 7.0 mmol/L) after adjustment for age, the subjects with missed glucose intolerance had similar characteristics except lower glycemic level. Compared to the normal subjects (fasting plasma glucose < 7.0 mmol/L) after adjustment for age, subjects with missed glucose intolerance had more obesity (both general and central), more hypertension, worse glycemic status and lipid profile in both men and women. There were 38 subjects (2.6%) having impaired fasting glucose. Of these 38 subjects, 24 (63.2%) had missed glucose intolerance. The detection of missed glucose intolerance increased from 9.7% of overall male subjects to 23.1% in men with hypertension to 52.9% in men with both hypertension and family history of diabetes. Similarly, the detection of missed glucose intolerance increased from 9.0% of overall female subjects to 25.7% in women with obesity to 45.2% in women with both obesity and hypertension. If only fasting plasma glucose is performed, 4% of subjects will be diagnosed to have diabetes or impaired fasting glucose while up to 10% of subjects having impaired glucose tolerance or diabetes will be missed in Hong Kong Chinese. The latter 2 groups of subjects have similar cardiovascular risk factors to those with fasting PG > or = 7.0 mmol/L. We recommend that for those with a family history of diabetes, hypertension or obesity, an oral glucose tolerance test instead of fasting plasma glucose should be used in the first place for the diagnosis of glucose intolerance. For those with impaired fasting glucose, a routine follow-up oral glucose tolerance test should also be performed. This clinical approach may improve the detection of those subjects with glucose intolerance, who will be otherwise missed by using fasting plasma glucose alone.

Adult↗

[Effects of lovastatin on plasma lipid, plasma glucose and insulin metabolism of patients with type II B hyperlipemia].

This study was directed at the effects of lovastatin on plasma glucose and insulin metabolism of patients with Type II B hyperlipemia. Thirty patients with Type II B hyperlipemia were observed. At the beginning, We detected the patients' TC, TG, HDL-C, VLDL-C with enzyme assay, calculated their LDL-C with formula, determined their plasmaglucose(PG) with oxidase assay and plasma insulin(PI) with immunoradioassay, and then we performed OGTT and insulin release test, these indices were detected again after the administration of 8 weeks' lovastatin therapy (20 mg per day). The results showed that, aftert the therapy, TC and LDL-C decreased significantly(P < 0.05), TG, HDL-C and VLDL-C had no significant change(P > 0.05). Fasting plasma glucose(FPG) and fasting plasma insulin(FPI) increased (the former, P < 0.05). Two hours after administration of glucose, the level of plasma glucose(2hPG) and plasma insulin(2hPI)increased(the latter, P < 0.05). 1/(FPG x FPI) had no significant change, but 1/(2hPG x 2hPI) decreased (P < 0.05). These data indicate that long-period use of lavastatin may cause insulin resistance. So we advise patients with Type II B hyperlipemia treated by statin to limit their glucose intake in case of hyperinsulinemia and insulin resistance.

Aged↗

Studies on activator formation in human plasma with streptokinase. III. Investigation of activator kinetics in undiluted plasma in terms of urokinase equivalents.

A new method is presented for estimating the activator (plasminogen-streptokinase complex) concentration in native plasma of patients undergoing streptokinase infusion. The principle of the method is based on clot lysis time as recorded by the thromboelastograph. The test clot constituents were bovine fibrinogen, bovine plasminogen, EDTA, human plasma (with unknown activator concentrations), and thrombin. In order to obtain a standardization line, urokinase dissolved in NaCl solution was substituted for patients' plasma. Thus, each lysis time could easily be converted into urokinase equivalent (CTA-u/ml). Streptokinase and plasminogen molecules in undiluted patients' plasma were found to exist both in an activator-bound (equimolar plasminogen-streptokinase complex) and in a freely circulating form. This result is in agreement with earlier findings where the activator complex was demonstrated to be a widely dissociated complex in highly diluted plasma of patients, thus displaying an ample proportion of free streptokinase and plasminogen and molecules. Streptokinase treatment using dosage schemes of 100,000 u SK/h, and 200,000 u/h were monitored by quantitative activator, streptokinase, and plasminogen measurements. An average activator concentration of 50-100 CTA-u/ml and a SK-concentration of 7-16 u/ml were recorded during streptokinase infusion. Plasminogen values averaged 0.25%, independent of the amount of streptokinase infused. Each drop in streptokinase was accompanied by a drop in activator during the infusion, and each rise in streptokinase by a rise in activator. There was a strong correlation between streptokinase and activator concentrations in that, on the average, 1 u streptokinase equalled 8.4 CTA-u/ml activator (correlation coefficient r = 0.9) It is concluded that the activator concentration in the plasma of patients undergoing fibrinolytic treatment can easily be adjusted by regulating the hourly streptokinase influx.

Endopeptidases↗

Plasma exudation by activated plasma kallikrein after intraperitoneal injection of lambda-carrageenin or endotoxin in rats.

The experimental study was carried out to examine whether intraperitoneal injection of carrageenin or endotoxin activates plasma kallikrein-kinin system to induce plasma exudation in rats. Intraperitoneal injection of 2% lambda-carrageenin induced plasma exudation in the peritoneal cavity by activation of plasma prekallikrein. Intraperitoneal injection of endotoxin (3mg/kg) also resulted in intraperitoneal plasma exudation, but plasma kallikrein-kinin system did not seem to be involved.

Animals↗

[Plasma concentration of big endothelin-1 and its relation with plasma NT-proBNP and ventricular function in heart failure patients].

INTRODUCTION AND OBJECTIVES: Elevated plasma concentrations of big endothelin-1 (big ET-1) are related with severity and prognosis in patients with heart failure, and N-terminal pro-brain natriuretic peptide (NT-proBNP) is a marker of ventricular remodeling. The purpose of this study was to investigate the relationship between plasma levels of big ET-1 and NT-proBNP, and between the former and ventricular function. PATIENTS AND METHOD: We studied 103 patients with heart failure (75 men, mean age 63 [13] years). Each participant completed a questionnaire and underwent Doppler echocardiographic study to measure ejection fraction (EF), mitral flow propagation velocity (Vp) and atrioventricular plane displacement (AVPD). Blood samples were also taken to determine plasma levels of big ET-1, aldosterone and NT-proBNP. RESULTS: For the whole population big ET-1 concentration was 1.03 [0.75] fmol/m, NT-proBNP 619 (307-1328) pg/mL, aldosterone 168 [102] pg/mL, EF 37 [10], Vp 37 [11] cm/s, and AVPD 8.0 [1.7] mm. Plasma big ET-1 correlated positively with plasma NT-proBNP (r=0.50, P<.0001). However, a negative correlation was found between big ET-1 and EF (r=-0.30, P<.01), Vp, (r=-0.30, P<.01) and AVPD (r=-0.21, P<.05). When ET-1 levels were divided into quartiles and the corresponding NT-proBNP, EF, Vp and AVPD values were compared, we found significant differences (ANOVA P<.0001, P<.01, P<.05 and P<.05, respectively). CONCLUSIONS: Plasma levels of big ET-1 correlated positively with NT-proBNP levels and inversely with EF, Vp and AVPD. These findings help clarify the relationships between ventricular function and the neurohormonal activation involved in heart failure, and may aid the search for therapeutic interventions.

Endothelin-1↗

Influence of phospholipid fatty acid composition of plasma membrane on sensitivity of plasma membrane ATPase of a self-flocculating yeast to in vivo ethanol activation and its relationship to ethanol tolerance.

Although alterations in fatty acid composition of phospholipids in plasma membranes had no effect on activities of plasma membrane ATPases of a self-flocculating fusant of Schizosaccharomyces pombe and Saccharomyces cerevisiae cells grown in the absence of ethanol (basal enzymes), they significantly affected the susceptibilities of the enzymes to in vivo activation induced by ethanol: the maximal values for the activated enzymes in cells pregrown with 0.6 mmol/L palmitic, linoleic or linolenic acid respectively were 3.6, 1.5 and 1.2-fold higher than their respective basal levels (in cells grown without ethanol), whereas the corresponding value for cells pregrown in the absence of fatty acid was 2.3-fold, with the concentrations of ethanol for the above maximal in vivo activation of enzymes being 7%, 6%, 6% and 7% (V/V) respectively. The Km values for ATP, the pH profiles, and the sensitivities to orthovanadate of the basal and the activated plasma membrane ATPases were essentially identical; however, the v(max) values of activated enzymes increased significantly. It was found that the characteristics of phospholipid fatty acid composition of plasma membrane leading to the enhanced ethanol tolerance of this strain, were also efficacious to increase the percentage of activation of plasma membrane ATPase per unit of ethanol. These data support a close correlation between the ethanol tolerance of this strain and the sensitivity of its plasma membrane ATPase to the in vivo ethanol-induced activation.

Adenosine Triphosphatases↗

Photochemical inactivation of viruses and bacteriophage in plasma and plasma fractions.

Transfusion-associated transmission of viral diseases remains a problem. A number of methods have been developed to inactivate viral pathogens in plasma and plasma fractions, including: dry heating, wet heating, solvent-detergent treatment, and immunoaffinity purification. While some of these methods successfully inactivate pathogenic viruses, inactivation may be incomplete or result in damage to labile plasma proteins. We have developed a method of photochemical decontamination (PCD) using psoralens and long wavelength ultraviolet light to inactivate pathogenic viruses. In the present study, a spectrum of model viruses have been added to plasma and plasma fractions to examine the efficiency of photochemical decontamination and the effects on labile plasma coagulation factors. Both RNA and DNA viruses have been inactivated under conditions which permit preservation of coagulation protein function. PCD technology appears to offer a promising solution to decontamination of blood products.

Bacteriophages↗

Chronic black tea administration protects plasma proteins, plasma, liver and kidney lipids against oxidation.

BACKGROUND: Black tea is known to have protective effects against plasma lipid and lipoprotein oxidation, but its influence on lipid peroxidation in tissue has been less studied. The effect of oral black tea consumption on protein oxidation has also not been demonstrated. The present study investigated the antioxidant effects of oral black tea consumption. MATERIAL/METHODS: Male Sprague-Dawley rats were fed a regular murine chow diet. The controls were supplied with water ad libitum, while the black tea group received aqueous black tea extract as the sole source of liquids. At the end of the ten-week experimental period, intestinal brush border, liver and kidney reduced-glutathione concentrations were evaluated as an index of cellular antioxidant defence. Plasma and tissue malondialdehyde concentrations and plasma protein carbonyl content were measured to evaluate lipid peroxidation and protein oxidation, respectively. RESULTS: The plasma malondialdehyde and protein carbonyl contents of rats consuming the black tea were significantly less than in controls. Similarly, liver and kidney malondialdehyde concentrations were significantly lower in the experimental group, while jejunoileal mucosa were not affected. Ten weeks of black tea administration caused significantly higher reduced-glutathione levels in the kidneys of black tea-administered rats, and a significant negative correlation was observed between kidney malondialdehyde and glutathione concentrations. CONCLUSIONS: These findings provide evidence that long term black tea supplementation is capable of protecting both plasma proteins and plasma lipids from oxidative injury, and demonstrate that chronic black tea administration protects both liver and kidney tissues - but not the jejunoileal mucosa - against oxidation.

Administration, Oral↗

Supplementation of difructose anhydride III enhanced elevation of plasma equol concentrations and lowered plasma total cholesterol in isoflavone-fed rats.

Equol, a derivative of daidzein produced by enterobacteria, has greater activity as a phyto-oestrogen compared with daidzein. Difructose anhydride III (DFAIII) is a newly manufactured non-digestible disaccharide with unique fermentation properties. The present study evaluated the prebiotic effects of DFAIII on equol production and on plasma cholesterol concentrations related to the changes in equol production. We compared plasma equol concentrations at 10.00 and 18.00 hours and faecal isoflavone excretion in three groups of seven rats (male Wistar-ST strain, 6 weeks old) fed a basal diet or a DFAIII or fructooligosaccharide (15 g/kg diet) diet containing 1 g soya isoflavones/kg diet for 20 d. Equol concentrations in the DFAIII group were higher than in the control and fructooligosaccharides groups, especially in the later phase of the light period (18.00 hours) throughout the experiment. Daizein and genistein concentrations did not change between the diet groups. The faecal ratios of equol:daidzein were very high in all groups, but the ratios were higher in the DFAIII group than the control and fructooligosaccharide groups on day 3, and this tendency continued throughout the experiment. On day 20, the plasma total cholesterol concentration was lowest in the DFAIII group. Additionally, the cholesterol concentrations were inversely correlated to plasma equol concentration in all the rats. In conclusion, DFAIII efficiently enhanced plasma equol concentrations, which may be associated with an increase in equol production and a decrease in equol degradation by enterobacteria. Higher plasma equol concentrations may contribute to the hypocholesterolaemic effect of DFAIII feeding.

Animals↗

Rapid labeling of lipoproteins in plasma with radioactive cholesterol. Application for measurement of plasma cholesterol esterification.

In order to efficiently and rapidly label lipoproteins in plasma with [3H]cholesterol, micelles consisting of lysophosphatidylcholine (lysoPC) and [3H]cholesterol (molar ratio, 50:1) were prepared. When trace amounts of these micelles were injected into plasma, [3H]cholesterol rapidly equilibrated among the plasma lipoproteins, as compared to [3H]cholesterol from an albumin-stabilized emulsion. The distributions of both [3H]cholesterol and unlabeled free cholesterol in plasma lipoproteins were similar in labeled plasma samples. This method of labeling can be used for the measurement of cholesterol esterification, or lecithin:cholesterol acyltransferase activity, in small amounts (20-40 microliters) of plasma samples.

Cholesterol↗