Biomedical subjects

Mehdi Rasouli

Publications and source records attributed to Mehdi Rasouli.

9 recordsLinked to original sources

PubMed2006

Total and differential leukocytes counts, but not hsCRP, ESR, and five fractioned serum proteins have significant potency to predict stable coronary artery disease.

BACKGROUND: The role and diagnostic value of markers of inflammation is well recognized in acute coronary syndromes but it is uncertain in patients with stable coronary artery disease (CAD). This study was done to investigate the association of markers of inflammation with the occurrence and severity of CAD and to evaluate their predictive values. METHODS: Markers of inflammation, electrophoresis serum protein fractions, serum (apo)lipoproteins and classical risk factors were determined in 270 angiographically documented subjects. The subjects were classified as CAD cases and controls according to angiography. The severity of CAD was scored on the basis of the number and extent of lesions. RESULTS: The counts of total leukocytes (7.14+/-1.86 cell/nl vs. 6.58+/-1.62, p<or=0.02), neutrophils (3.95+/-1.42 vs. 3.59+/-1.07, p<or=0.05) and eosinophils (0.25+/-0.28 vs. 0.19+/-0.24, p<or=0.03) were increased significantly, whereas the concentrations of high-sensitivity C-reactive protein (hsCRP, 2.03 (0.0-32.0) mg/l vs.1.72 (0.09-11.36), p<or=0.07) changed modestly in CAD patients relative to controls. There were no significant differences in the counts of monocytes and lymphocytes and the concentrations of erythrocyte sedimentation rate (ESR) and any five fractions of serum proteins between two groups. The counts of total leukocytes, neutrophils and eosinophils, but not hsCRP and ESR exhibited significant associations with the severity of CAD. In univariate logistic regression analysis, leukocytes count associated significantly (OR=1.97, p<or=0.01) whereas hsCRP modestly (OR=1.76, p<or=0.06) with the occurrence of CAD. The association was lessened by diabetes mellitus in multivariable adjustment. Receiver operating characteristic (ROC) analysis showed that, only total leukocyte and differential counts had significant potency to predict CAD (area under curve, AUC=0.60+/-0.04, p<or=0.02). CONCLUSIONS: The total leukocytes count and its subgroups are associated with the presence and severity of CAD, but the associations were not independent. The efficiency was questioned for hsCRP, ESR and five fractioned serum proteins to identify stable CAD.

Adult↗

PubMed2006

Interactions of serum hsCRP with apoB, apoB/AI ratio and some components of metabolic syndrome amplify the predictive values for coronary artery disease.

BACKGROUND: Plasma high-sensitivity CRP (hsCRP) is a marker of inflammation, and it is reported to link with coronary artery disease (CAD). Interactions between elevated serum hsCRP and other unfavorable risk factors have been proposed to cause high risk for CAD. OBJECTIVES: To examine the potential interactions between serum hsCRP and lipids and non-lipidic risk factors. METHODS: Markers of inflammation, the profiles of serum (apo)(lipo) proteins as well as classical risk factors were determined in 270 clinically stable angiographically documented subjects. The patients were stratified into tertiles according to hsCRP distribution. RESULTS: The Framingham CAD scores, relative and absolute risk for CAD and the prevalence of diabetes mellitus and hypertension were significantly higher in 3rd relative to 1st tertile of hsCRP. Subjects with hsCRP levels in the upper tertile had significant higher levels of serum glucose, triglyceride, apolipoprotein (apo)B, apoB/apoAI ratio and the counts of total leukocyte and neutrophil and lower levels of HDL-C, albumin and the ratio of albumin/globulins. Analyses by bivariate correlation as well as linear regression showed that serum hsCRP was associated positively with the occurrence of diabetes and hypertension, the counts of total leukocyte and neutrophil and the levels of serum glucose, uric acid, apoB, apoB/apoAI ratio, alpha1- and alpha2-globulins and inversely with albumin, albumin/globulin ratio and HDL-C. By constructing dummy combined variables, elevated hsCRP accompanied with male sex, diabetes, hypertension and high levels of serum glucose, apoB, apoB/apoAI ratio and cholesterol exhibited amplified high risk for CAD. CONCLUSIONS: The results show that hsCRP does interact multiplicatively with apoB and some variables of metabolic syndrome. The simultaneous assessment of hsCRP and interactive risk factors enhances discriminating value for CAD. It is suggested to use hsCRP in conjunction with apoB or apoB/apoAI ratio instead of cholesterol ratios in global risk assessment.

Adult↗

PubMed2006

Suppression of VLDL associated triacylglycerol secretion by both alpha- and beta-adrenoceptor agonists in isolated rat hepatocytes.

The signal transduction pathways of intracellular calcium and adenosin 3',5'-cyclic monophosphate (cAMP) participate in the regulation of intrahepatic metabolism of very low density lipoproteins (VLDL). The adrenoceptors are linked to calcium and cAMP signal transduction pathways so it is proposed that they may be involved in the regulation of VLDL secretion. The current study is designed to test the effects of alpha- and beta-adrenoceptor agonists and antagonists on triacylglycerol secretion in freshly isolated rat hepatocytes. The inhibitory effect of epinephrine appeared at concentrations of more than 1 microM and reached a plateau at 100 microM. Epinephrine concentration for the half of the maximal bio-effect (EC(50)) was about 10 microM. Epinephrine at a concentration of 10 microM suppressed the secretion of triacylglycerol by 33% (P<or=0.01) and increased cellular content of triacylglycerol (18%, P<or=0.05) and total phospholipids (20%, P<or=0.05). Time course experiments for triacylglycerol secretion exhibited a linear relationship with a slope of 8.2+/-0.6 mug triacylglycerol/3 h mg cell protein. In the presence of epinephrine, cellular triacylglycerol and total phospholipids were slightly but significantly higher than the respective control at all points of time examined. The inhibitory effect elicited by epinephrine (10 microM) was abolished by the inclusion of the general alpha-adrenoceptor antagonist phentolamine (10 microM) and the specific alpha(1)-antagonist prazosin (1 microM) but not with the nonselective beta-antagonist propranolol (10 microM). Trifluoperazine an alpha-adrenoceptor antagonist and anticalmodulin agent, concealed the inhibitory effect of epinephrine in a concentration dependent manner, whereas theobromine a cAMP-phosphodiestrase inhibitor did not have any significant effect. The secretion of triacylglycerol was decreased not only by the alpha-adrenoceptor agonist phenylephrine (10 microM) but also by the beta-agonist isoproterenol (10 microM). Dibutyryl-cAMP (0.1 mM) also inhibited the secretion of triacylglycerol by 30% (P<or=0.01). The results suggest that epinephrine inhibits the secretion of triacylglycerol from rat hepatocytes via the alpha(1)-adrenoceptor while stimulation of beta- as well as alpha-adrenoceptors can also exert a similar effect.

Adrenergic alpha-Agonists↗

PubMed2006

Serum calcium and phosphorus associate with the occurrence and severity of angiographically documented coronary heart disease, possibly through correlation with atherogenic (apo)lipoproteins.

The associations of serum calcium and phosphorus concentrations as well as other cardiovascular risk factors were investigated in relation to the existence and severity of coronary heart disease (CHD) in 260 clinically stable, angiographically defined CHD patients aged 40-70 years. The subjects were classified as CHD(+) cases if one or more coronary arteries had a significant stenosis (> or =70%) and CHD(-) controls if there was no stenosis (< or =10%) in any artery. The severity of coronary occlusion was scored on the basis of the number and extent of lesions, as normal, mild, moderate or severe. Fasting serum concentrations of electrolytes, lipids and (apo)lipoproteins were determined. The concentrations of serum total calcium (2.41 +/-0.14 vs. 2.33 +/- 0.22 mmol/L, p < or = 0.05), albumin-corrected calcium (2.33 +/- 0.25 vs. 2.23 +/- 0.25 mmol/L, p < or = 0.01), phosphorus (1.32 +/-0.21 vs. 1.25 +/- 0.17 mmol/L, p < or = 0.007) and the ion product of calcium and phosphorus (3.16 +/- 0.58 vs. 2.91 +/- 0.50, p < or =0.0001) were significantly higher in the CHD(+) compared to the CHD(-) group. Patients with CHD compared with controls had increased serum levels of triglyceride, total cholesterol, low-density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), lipoprotein(a) [Lp(a)] and decreased serum levels of high-density lipoprotein (HDL)-C and apoAI. Multiple logistic regression analysis showed strong and significant association between diabetes mellitus (odds ratio, OR = 5.24, p < or = 0.0001), male gender (OR = 8.84, p < or =0.0001), Lp(a) (OR = 1.014, p < or =0.006), hypertension (OR = 2.61, p < or =0.02), apoB (OR = 1.031, p < or =0.001), age (OR = 1.055, p < or =0.003), phosphorus (OR = 2.438, p < or =0.01), albumin-adjusted calcium (OR = 1.532, p < or =0.05), cholesterol (OR = 1.009, p < or =0.05) and the occurrence of CHD. On the basis of bivariate correlation analysis, serum-adjusted calcium was positively correlated with the levels of cholesterol (r = 0.285, p < or =0.0001), LDL-C (r = 0.320, p < or =0.0001), Lp(a) (r = 0.173, p < or = 0.005), apoB (r = 0.237, p < or =0.0001), LDL-C/apoB ratio (r = 0.180, p < or= 0.007), apoAI (r = 0.181, p < or =0.003) and inversely to HDL-C (r = -0.146, p < or =0.02) and HDL-C/apoAI ratio (r = -0.263, p < or =0.0001). Serum phosphorus concentration was a significant correlate of triglyceride (r = 0.199, p < or =0.001) and Lp(a) (r = 0.129, p < or =0.04). The results demonstrated that serum calcium and phosphorus are associated with the prevalence and severity of CHD, probably through correlation with atherogenic lipids and (apo)lipoproteins. Serum calcium and phosphorus and their ion product were also independent risk factors for CHD.

Angiography↗

PubMed2006

The ratio of apoB/apoAI, apoB and lipoprotein(a) are the best predictors of stable coronary artery disease.

BACKGROUND: The ratio of low- to high-density lipoprotein-cholesterol (LDL-C/HDL-C) conventionally represents the balance of proatherogenic and anti-atherogenic lipids. However, growing evidence supports the idea that the ratio of apolipoprotein (apo) B/apoAI is a better index for risk assessment of coronary artery disease (CAD). The aim of this study was to evaluate the efficiency of advanced profile of serum (apo)lipoproteins for predicting stable CAD in secondary prevention. METHODS: The study subjects, 138 men and 126 women aged 40-70 years, were classified as CAD cases or controls, according to the results of coronary angiography. The severity of CAD was scored on the basis of the number and extent of lesions in coronary arteries. Serum (apo)lipoproteins were measured by immunoturbidometric and electrophoresis methods. RESULTS: Patients with CAD compared with controls had increased serum levels of triglycerides (2.6+/-2.0 vs. 2.0+/-1.2 mmol/L, p< or =0.005), apoB (1.36+/-0.31 vs. 1.19+/-0.24 g/L, p< or =0.0001), lipoprotein(a) [Lp(a)] (0.69+/-0.60 vs. 0.43+/-0.31 g/L, p< or =0.0001) and apoB/apoAI ratio (1.07+/-0.32 vs. 0.87+/-0.18, p< or =0.0001), and decreased serum levels of HDL-C (1.02+/-0.29 vs. 1.11+/-0.34 mmol/L, p< or =0.03), apoAI (1.32+/-0.22 vs. 1.37+/-0.19 g/L, p< or =0.04) and LDL-C/apoB ratio (0.91+/-0.32 vs. 1.02+/-0.25 mmol/g, p< or =0.01). Multiple logistic regression analysis after adjusting for major risk factors showed that the apoB/apoAI ratio, apoB and Lp(a) were among seven significant and independent determinants of CAD. The area under the receiver operating characteristic (ROC) curves (AUC) as a relative measure of test efficiency was highest and significant for the apoB/apoAI ratio (AUC=0.71, p< or =0.0001), apoB (0.67, p< or =0.0001), Lp(a) (0.63, p< or =0.001), the LDL-C/apoB ratio (0.62, p< or =0.006), triglycerides (0.62, p< or =0.004) and apoAI (0.58, p< or =0.05). ANOVA analysis showed significant association for the apoB/apoAI ratio, apoB, Lp(a) and triglycerides, and moderate association for total cholesterol and its subfractions, with the severity of CAD. CONCLUSIONS: The results indicate that the apoB/apoAI ratio, apoB and Lp(a) are independent risk factors for CAD and are superior to any of the cholesterol ratios. We suggest using the apoB/apoAI ratio as the best marker of CAD in clinical practice.

Adult↗

PubMed2005

Comparison of methods for calculating serum osmolality: multivariate linear regression analysis.

BACKGROUND: There are several methods for calculating serum osmolality, and their accordance with measured osmolality is the subject of controversy. METHODS: The concentrations of sodium, potassium, glucose, blood urea nitrogen (BUN) and osmolalities of 210 serum samples were measured. Two empirical equations were deduced for the calculation of serum osmolality by regression analysis of the data. To choose the best equation, chemical concentrations were also used to calculate osmolalities according to our formulas and 16 different equations were taken from the literature and compared with the measured osmolalities. Correlation and linear regression analyses were performed using Excel and SPSS software. RESULTS: Multiple linear regression analysis showed that serum concentrations of sodium (beta = 0.778, p< or = 0.000), BUN (beta = 0.315, p < or = 0.000), glucose (beta = 0.0.089, p < or = 0.007) and potassium (beta = 0.109, p < or = 0.008) are strong predictors of serum osmolality. The data were also analyzed by manual linear regression to yield the equations: osmolality = 1.897[Na + ]+glucose+BUN+13.5, and osmolality = 1.90[Na+ + K+]+glucose+BUN+5.0. The osmotic coefficient for sodium and potassium solutes was deduced to be 0.949 from the slope of the curves of measured osmolality vs. [Na+] and [Na+ + K+], respectively. The inclusion of a BUN value in the equation for osmolality increased the correlation coefficient by approximately 450% and decreased the SD of difference by approximately 35% (p < or = 0.002). Inclusion of the osmotic coefficient for sodium solutes caused an underestimation of measured osmolality and positive osmolal gap unless an appropriate coefficient, constant value and/or the potassium value were included in the equation. The agreement was not improved when molal chemical concentrations were used instead of molar values. The formula presented by Dorwart and Chalmers gave inferior results to those obtained with our formulas. CONCLUSIONS: Our data suggest use of the Worthley et al. formula Osm = 2[Na +]+glucose+BUN for rapid mental calculation and the formulas of Bhagat et al. or ours for calculation of serum osmolality by equipment linked to a computer.

Blood Glucose↗

PubMed2005

Serum proteins profile as an indicator of malignancy: multivariate logistic regression and ROC analyses.

The electrophoretic pattern of serum proteins of 85 patients carrying different types of neoplasia and 85 matched healthy adults were comparatively studied by agarose gel electrophoresis, to find out if there is a specific protein pattern common to different types of cancer. Each protein fraction was analyzed quantitatively by densitometry. Multivariate logistic regression and receiver operating characteristic (ROC) analyses were performed using SPSS software. When total protein and albumin were measured by colorimetric methods, cancer patients, compared to controls, had a decreased concentration of total protein (66.0+/-11.5 g/L vs. 76.4+/-6.8 g/L, p< or =0.0001) and of albumin (39.0+/-8.1 g/L vs. 46.0+/-4.3 g/L, p< or =0.0001). The electrophoretic data of serum proteins showed that the ratio of albumin to globulin (0.92+/-0.30 vs. 1.21+/-0.16, p< or =0.0001), percent of the fractions albumin (46.7+/-8.5% vs. 54.4+/-3.5%, p< or =0.0001) and beta-globulin (11.6+/-4.4% vs. 13.0+/-1.9%, p< or =0.001) were decreased and alpha(1)- (5.3+/-2.5% vs. 2.9+/-0.8%, p< or =0.0001), alpha(2)- (13.5+/-4.8% vs. 11.3+/-2.1%, p< or =0.0001) and gamma-globulins (23.0+/-7.7% vs. 18.3+/-3.1%, p< or =0.0001) were significantly increased in cancer patients relative to controls. Cancer patients also had higher counts of leukocytes (7.98+/-3.11, x10(9) cells/L vs. 6.33+/-1.68 x10(9) cells/L, p< or =0.0001) and erythrocyte sedimentation rate (35.9+/-23.5 mm/h vs. 14.1+/-9.5 mm/h,p< / =0.0001). On the basis of univariate analysis, a protein profile out of the normal ranges was more prevalent in cancer patients than in controls. Analysis of the data using multiple logistic regression indicated that the prevalence of cancer was strongly associated with the serum proteins' profile, and alpha(1)-globulin, erythrocyte sedimentation rate, total protein and the ratio of albumin to globulin were the best parameters to discriminate between malignant and healthy states. The area under the ROC curves were the same for most components of the serum proteins' profile at about 0.75+/-0.09, p< or =0.001. We conclude that the profile of serum proteins indicates high diagnostic values for discriminating between cancer patients and healthy individuals and may be useful as an adjunct diagnosis for detection of malignancy.

Adult↗

PubMed2004

Calmodulin antagonist W-7 inhibits de novo synthesis of cholesterol and suppresses secretion of de novo synthesized and preformed lipids from cultured hepatocytes.

The effects of a calmodulin antagonist W-7 were studied on the synthesis and secretion of lipids in primary rat hepatocytes and McArdle-RH7777 cells. In time course experiments, W-7 (20 microM) inhibited secretion of newly synthesized triacyl[(3)H]glycerol by 35%. When the cells were pre-treated overnight with W-7 (20 microM), followed by incubation with [(3)H]oleate, a significant decrease in the secretion of triacylglycerol (TG) and cholesteryl ester (CE) was observed. De novo synthesis of cholesterol from acetate or mevalonolactone was inhibited by W-7, but not glycerolipid synthesis from glycerol and oleic acid precursors. Concentration-response curves for the effects of overnight pre-incubation with W-7 followed labeling with [(3)H]glycerol and [(14)C]mevalonolactone revealed that: (1). the inhibitory effect of W-7 was concentration-dependent and appeared even at the lowest concentration examined (1 microM). W-7 at a concentration of 20 microM suppressed secretion of TG by 60% (P<or=0.002), phosphatidylcholine (PC) by 31% (P<or=0.05), CE by 59% (P<or=0.002) and cholesterol by 64% (P<or=0.002). (2). The incorporation of [(14)C]mevalonolactone into cellular cholesterol and CE was decreased significantly, while W-7 did not have any significant effect upon incorporation of [(3)H]glycerol into glycerolipids, except at the highest concentration examined (50 microM), where synthesis of both TG and PC was significantly suppressed. (3). While the percentage of secreted de novo synthesized glycerolipids and CE decreased proportionally with increasing concentration of W-7, the percentage of secreted newly made cholesterol remained unaffected at any concentration of W-7. In the absence of W-7, about 19% of newly formed cholesterol became esterified into CE, whereas W-7 increased cholesterol esterification in a concentration-dependent manner. (4) W-7 (20 microM) also suppressed the secretion of preformed cholesterol by 24% and CE by 55% but did not affect the recruitment of preformed cholesterol for esterification. About 6.5% of pre-labeled cholesterol and 20% of CE were directed to secretion, which was suppressed in the presence of W-7 by 17% (P<or=0.09) and 48% (P<or=0.001), respectively. These results suggest that, W-7 in the range of 1-20 microM inhibited de novo synthesis of cholesterol and the secretion of both de novo synthesized and preformed lipids.

Animals↗

PubMed2003

Inhibitors of hepatic microsomal triacylglycerol hydrolase decrease very low density lipoprotein secretion.

The presence of elevated circulating triacylglycerol (TG)-rich very low density lipoprotein (VLDL) and apolipoprotein B-100 (apoB-100) levels represents an independent risk factor for coronary artery disease. Triacylglycerol hydrolase catalyzes the mobilization of cytoplasmic TG stores. To test the hypothesis that the enzyme plays a role in the provision of core lipids for the assembly of VLDL, we inhibited the lipase activity in primary rat hepatocytes and analyzed lipid and apoB synthesis and secretion. Inhibition of lipolysis resulted in a dramatic decrease in secretion of TGs. In addition, secretion of cholesteryl ester and phosphatidylcholine was substantially decreased. Analysis of secreted apolipoproteins indicated that apoB-100 secretion was much more sensitive to lipase inhibition than was apoB-48 secretion, perhaps because of the ability of apoB-48 to be secreted as a relatively lipid-poor particle. The results agreed with those obtained with hepatoma cells transfected with triacylglycerol hydrolase cDNA, in which preferential lipidation of apoB-100 was observed. Together, our findings provide evidence that inhibition of intracellular TG hydrolysis significantly decreases apoB-100 secretion and suggest that triacylglycerol hydrolase may be a suitable pharmacological target in efforts to lower plasma lipid levels.

Animals↗