Serum Soluble Intercellular Adhesion Molecule-1 Research Articles

Serum procalcitonin, interleukin-6, soluble intercellular adhesin molecule-1 and IgG to shortchain exocellular lipoteichoic acid as predictors of infection in total joint prosthesis revision

The diagnosis of prosthetic joint infection and its differentiation from aseptic loosening remains problematic. The definitive laboratory diagnostic test is the recovery of identical infectious agents from multiple intraoperative tissue samples; however, interpretation of positive cultures is often complex as infection is frequently associated with low numbers of commensal microorganisms, in particular the coagulase-negative staphylococci (CNS). In this investigation, the value of serum procalcitonin (PCT), interleukin-6 (IL-6) and soluble intercellular adhesion molecule-1 (sICAM-1) as predictors of infection in revision hip replacement surgery is assessed. Furthermore, the diagnostic value of serum IgG to short-chain exocellular lipoteichoic acid (sce-LTA) is assessed in patients with infection due to CNS. Presurgical levels of conventional serum markers of infection including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cell count (WBC) is also established. Forty-six patients undergoing revision hip surgery were recruited with a presumptive clinical diagnosis of either septic (16 patients) or aseptic loosening (30 patients). The diagnosis was confirmed microbiologically and levels of serum markers were determined. Serum levels of IL-6 and sICAM-1 were significantly raised in patients with septic loosening (P=0.001 and P=0.0002, respectively). Serum IgG to sce-LTA was elevated in three out of four patients with infection due to CNS. In contrast, PCT was not found to be of value in differentiating septic and aseptic loosening. Furthermore, CRP, ESR and WBC were significantly higher (P=0.0001, P=0.0001 and P=0.003, respectively) in patients with septic loosening. Serum levels of IL-6, sICAM-1 and IgG to sce-LTA may provide additional information to facilitate the diagnosis of prosthetic joint infection.

Mast cells promote atherosclerosis by inducing both an atherogenic lipid profile and vascular inflammation

Accumulating in vitro and in vivo studies have proposed a role for mast cells in the pathogenesis of atherosclerosis. Here, we studied the role of mast cells in lipoprotein metabolism, a key element in the atherosclerotic disease. Male mice deficient in low-density lipoprotein receptors and mast cells on a Western diet for 26 weeks had significantly less atherosclerotic changes both in aortic sinus (55%, P = 0.0009) and in aorta (31%, P = 0.049), as compared to mast cell-competent littermates. Mast cell-deficient female mice had significantly less atherosclerotic changes in aortic sinus (43%, P = 0.011). Furthermore, we found a significant positive correlation between the extent of atherosclerosis and the number of adventitial/perivascular mast cells in aortic sinus of mast cell-competent mice (r = 0.615, P = 0.015). Serum cholesterol and triglyceride levels were significantly lower in both male (63%, P = 0.0005 and 57%, P = 0.004) and female (73%, P = 0.00009 and 54%, P = 0.007) mast cell-deficient mice, with a concomitant decrease in atherogenic apoB-containing particles and serum prebeta-high-density lipoprotein and phospholipid transfer protein activity in both male (69% and 24%) and female (74% and 54%) mast cell-deficient mice. Serum soluble intercellular adhesion molecule was decreased in both male (32%, P = 0.004) and female (28%, P = 0.003) mast cell-deficient mice, whereas serum amyloid A was similar between mast cell-deficient and competent mice. In conclusion, mast cells participate in the pathogenesis of atherosclerosis in ldlr(-/-) mice by inducing both an atherogenic lipid profile and vascular inflammation.

Circulating adhesion molecules in patients with Keshan disease and their relationship with Coxsackie B virus infection

This study determined the levels of serum soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecular-1 (sVCAM-1) in patients with different types of Keshan disease (KD), examined the relationship between Coxsackie B virus-specific IgM antibody (CBV-IgM) and sICAM-1 or sVCAM-1 in KD patients, and investigated the role of these adhesion molecules in the pathogenesis of KD and their clinical implications. The levels of serum sICAM-1, sVCAM-1 and CBV-IgM were measured by using enzyme-linked immunosorbent assay in 22 patients with chronic Keshan disease (CKD), 27 with latent Keshan disease (LKD) and 28 healthy controls. The subjects in different groups were adjusted for sex and age. Echocardiography was adopted to determine left ventricular ejection fraction (LVEF) in 22 patients with CKD. The results showed that CKD patients had significantly higher levels of sICAM-1 and sVCAM-1 than LKD patients and healthy controls (P<0.01 for all). And there was significant difference in the levels of the 2 adhesion molecules between LKD patients and healthy controls (P<0.05). A negative correlation was found between LVEF and sICAM-1 or sVCAM-1 in CKD patients. The percentage of CBV-specific IgM positive individuals in KD patients was significantly higher than that of healthy controls. In CVB-specific IgM positive patients, the levels of serum sICAM-1 and sVCAM-1 were significantly greater than those in CBV-specific IgM negative counterpart. It was concluded that the increase in the levels of sICAM-1 and sVCAM-1 suggests the progression of inflammation in KD. sICAM-1 and sVCAM-1 can promote the development of myocardial pathology and lead to poor myocardial function. The increased serum sICAM-1 and sVCAM-1 in KD patients may be related to CBV infection.

The Impact of Oral L-Arginine Supplementation on Acute Smoking-Induced Endothelial Injury and Arterial Performance

Smoking is associated with endothelial dysfunction and increased inflammatory status. The amino acid L-arginine, improves endothelial function in patients with cardiovascular risk factors. We investigated the effect of L-arginine on vascular function and inflammatory process in healthy smokers at rest and after acute smoking. We studied the effect of L-arginine and/or placebo in 12 healthy young smokers on three occasions (day 0, day 1, and day 3). The study was carried out on two separate arms, one with L-arginine (3 x 7 g/day) and one with placebo, according to a randomized, placebo-controlled, double-blind, cross-over design. Measurements were carried out before, immediately after, and 20 min after cigarette smoking. Endothelial function was evaluated by flow-mediated dilation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) and as a measure of arterial wave reflections. Serum soluble intercellular adhesion molecule-1 (sICAM-1) was measured. Compared to placebo, L-arginine improved FMD (P < 0.01 at day 1 and P < 0.05 at day 3). L-Arginine reduced PWV and AIx at both days 1 and 3 (P < 0.05 vs. baseline). L-Arginine blunted the acute smoking-induced increase of AIx at both day 1 (P < 0.05) and day 3 (P < 0.01), and prevented the smoking-induced elevation of PWV at day 3 (P < 0.05). Importantly, L-arginine reduced sICAM-1 at days 1 and 3 (P < 0.05 for both vs. baseline). Oral L-arginine improves endothelial function and vascular elastic properties of the arterial tree during the acute phase of smoking, an effect accompanied by reduced sICAM-1 levels in these subjects.

Soluble intercellular adhesion molecule-1, D-lactate and diamine oxidase in patients with inflammatory bowel disease

To study the levels of serum soluble intercellular adhesion molecule-1 (sICAM-1), plasma D-lactate and diamine oxidase (DAO) in patients with inflammatory bowel disease (IBD), and the potential clinical significance. Sixty-nine patients with IBD and 30 healthy controls were included in this study. The concentration of sICAM-1 was detected with enzyme-linked immunosorbent assay, the level of D-lactate and DAO was measured by spectroscopic analysis, and the number of white blood cells (WBC) was determined by routine procedure. The levels of sICAM-l, DAO, and WBC in IBD patients were significantly higher than those in the control group (P < 0.01). sICAM-l in IBD patients was found to be closely related to the levels of DAO and D-lactate (212.94 +/- 69.89 vs 6.35 +/- 2.35, P = 0.000), DAO 212.94 +/- 69.89 vs 8.65 +/- 3.54, P = 0.000) and WBC (212.94 +/- 69.89 vs 7.40 +/- 2.61, P = 0.000), but no significant difference was observed between patients with ulcerative colitis and patients with Crohn's disease. The post-treatment levels of sICAM-l, D-lactate and WBC were significantly lower than before treatment (sICAM-l 206.57 +/- 79.21 vs 146.21 +/- 64.43, P = 0.000), (D-lactate 1.46 +/- 0.94 vs 0.52 +/- 0.32, P = 0.000) and (WBC 7.24 +/- 0.2.33 vs 5.21 +/- 3.21, P = 0.000). sICAM-1, D-lactate and DAO are closely related to the specific conditions of IBD, and thus could be used as a major diagnostic index.

Inhibition of circulating immune cell activation: a molecular antiinflammatory effect of the Mediterranean diet

BackgroundAdherence to the Mediterranean diet (Med-Diet) is associated with a reduced risk of cardiovascular disease (CVD). However, the molecular mechanisms involved are not fully understood. ObjectiveThe objective was to compare the effects of 2 Med-Diets with those of a low-fat diet on immune cell activation and soluble inflammatory biomarkers related to atherogenesis in subjects at high risk of CVD. DesignIn a controlled study, we randomly assigned 112 older subjects with diabetes or ≥3 CVD risk factors to 3 dietary intervention groups: Med-Diet with supplemental virgin olive oil (VOO), Med-Diet with supplemental nuts, and low-fat diet. Changes from baseline in cellular and serum inflammatory biomarkers were assessed at 3 mo. ResultsOne hundred six participants (43% women; average age: 68 y) completed the study. At 3 mo, monocyte expression of CD49d, an adhesion molecule crucial for leukocyte homing, and of CD40, a proinflammatory ligand, decreased (P < 0.05) after both Med-Diets but not after the low-fat diet. Serum interleukin-6 and soluble intercellular adhesion molecule-1, inflammatory mediators crucial in firm adhesion of leukocytes to endothelial surfaces, decreased (P < 0.05) in both Med-Diet groups. Soluble vascular cellular adhesion molecule-1 and C-reactive protein decreased only after the Med-Diet with VOO (P < 0.05), whereas interleukin-6, soluble vascular cellular adhesion molecule-1, and soluble intercellular adhesion molecule-1 increased (P < 0.05) after the low-fat diet. ConclusionsMed-Diets supplemented with VOO or nuts down-regulate cellular and circulating inflammatory biomarkers related to atherogenesis in subjects at high risk of CVD. The results support the recommendation of the Med-Diet as a useful tool against CVD.

Effect of raisin consumption on oxidative stress and inflammation in obesity

Oxidative stress can initiate increased inflammation that elevates risk for cardiovascular disease. The objective of this study was to determine the effects of daily consumption of raisins on markers of oxidative stress, inflammation and endothelial activation in response to an acute high-fat meal in overweight individuals. Seventeen overweight men and women consumed 90 g raisins or isocaloric placebo (264 kcal/day) for 14 days in a randomized, crossover design while following a low-flavonoid diet. The oxidative [urinary 8-iso-prostaglandin-F(2alpha) (8-epi PGF(2alpha)) and serum oxygen radical absorbance capacity (ORAC)], inflammatory (serum C-reactive protein and interleukin-6), endothelial (serum soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1, sVCAM-1) and metabolic [free fatty acids (FFAs), triacylglycerol, glucose and insulin] response to four high-fat (53%) meals was tested pre- and postintervention. Urinary 8-epi PGF(2alpha) decreased (-22%) and fasting ORAC increased (+3%) after both interventions combined. Fasting protein-free ORAC was modestly (+3.5%) higher during the raisin than the placebo intervention. Neither the meals nor the raisins consistently induced fasted markers of inflammation or endothelial dysfunction. Gender influenced postprandial metabolic responses in that males responded with higher serum FFAs, sVCAM-1 and glucose compared with females. Serum antioxidant capacity was modestly increased by daily raisin consumption, but this did not alter fasted or postprandial inflammatory response in these relatively healthy but overweight individuals. Providing all food in regular pattern reduced measures of oxidative stress.

Early Induction of Moderate Hypothermia Suppresses Systemic Inflammatory Cytokines and Intracellular Adhesion Molecule-1 in Rats With Caerulein-Induced Pancreatitis and Endotoxemia

To evaluate the systemic effects of moderate hypothermia (MH) and the timing of induction on acute pancreatitis (AP) and endotoxemia in rats. The effects of MH were compared in 4 groups, that is, sham group (38 degrees C), control group (38 degrees C), early MH group (32 degrees C on administration of lipopolysaccharide [LPS]), and delayed MH group (32 degrees C 1 hour after LPS). AP and endotoxemia were induced by intramuscular injection of caerulein and intraperitoneal injection of LPS. Serum interleukin 6 (IL-6) in both MH groups was significantly lower than that in the control group at 3 hours. Serum interleukin 10 (IL-10) in the early MH group was significantly higher than those in the other 3 groups at 1 hour. IL-10/IL-6 ratios in both MH groups were significantly higher than that in the control group at 3 hours. Serum soluble intercellular adhesion molecule (sICAM-1) in both MH groups was significantly lower than that in the control group at 3 hours. Serum sICAM-1 in the early MH group was significantly lower than that in the delayed MH group. The tendency of pancreatic ICAM-1 was similar to that of serum sICAM-1. Early induction of MH might be protective against pancreatic injury and systemic inflammation in AP and endotoxemia.

Elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and sE-selectin levels in bronchial asthma.

Adhesion molecules such as ICAM-1 and E-selectin have been shown to play important roles in the production of allergic inflammation. In the present study, we measured serum soluble ICAM-1 (sICAM-1) and soluble E-selectin (sE-selectin) levels by ELISA in 42 patients with bronchial asthma (22 atopic and 20 non-atopic) during asthma attacks and in stable conditions in order to assess the state of ICAM-1 and E-selectin in allergic inflammation. Both serum sICAM-1 levels and serum sE-selectin levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These findings were observed regardless of atopic status. To examine the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels, serum tumour necrosis factor-alpha (TNF-alpha) levels were measured by ELISA. TNF-alpha levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. There was a correlation between the nature of change in serum TNF-alpha levels and the nature of change in serum sICAM-1 levels or serum sE-selectin levels, though serum TNF-alpha levels did not correlate with serum sICAM-1 levels or serum sE-selectin levels. These results suggest that higher levels of sICAM-1 and sE-selectin during asthma attacks may reflect the up-regulation of ICAM-1 and E-selectin expression in allergic inflammation, and that the soluble form of these adhesion molecules may be useful markers for the presence of allergic inflammation. TNF-alpha is shown to enhance the expression and release of ICAM-1 and E-selectin in vitro, however; the regulatory mechanism in the elevation of serum sICAM-1 and sE-selectin levels remains to be clarified.

Elevation of serum soluble vascular cell adhesion molecule-1 (sVCAM-1) levels in bronchial asthma.

We have previously shown the elevation of serum soluble intercellular adhesion molecule-1 (sICAM-1) and soluble E-selectin (sE-selectin) in patients with bronchial asthma during asthma attacks. In the present study, we extended our earlier study by measuring serum sVCAM-1 levels by ELISA in 45 patients with bronchial asthma (23 atopic and 22 non-atopic) during asthma attacks and in stable conditions in order to assess further the state of adhesion molecules in allergic inflammation of bronchial asthma. The levels of sVCAM-1 in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These findings were observed regardless of atopic status. To examine the regulatory mechanism in the elevation of serum sVCAM-1 levels, serum tumor necrosis factor-alpha (TNF-alpha) levels were measured by ELISA. TNF-alpha levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. The nature of change in serum TNF-alpha levels correlated with the nature of change in serum sVCAM-1 levels, but serum TNF-alpha levels did not correlate with serum sVCAM-1 levels. These results suggest that higher levels of sVCAM-1 during asthma attacks may reflect the up-regulation of VCAM-1 expression in allergic inflammation, and that a soluble form of VCAM-1 molecules may be useful markers for the presence of allergic inflammation. TNF-alpha is shown to enhance the expression and release of VCAM-1 in vitro, however; the regulatory mechanism in the elevation of serum sVCAM-1 levels remains to be clarified.

Inflammatory Markers and Progression of Subclinical Atherosclerosis in Healthy Postmenopausal Women (from the Estrogen in the Prevention of Atherosclerosis Trial)

The objective of this study was to determine whether high-sensitivity C-reactive protein (hs-CRP) and serum soluble intercellular adhesion molecule-1 (sICAM-1) correlate with progression of subclinical atherosclerosis. Secondarily, the long-term effect of oral estradiol on hs-CRP and sICAM-1 were determined. Data were analyzed from 180 healthy postmenopausal women aged 45 to 80 years randomly assigned to either unopposed micronized 17beta-estradiol 1 mg/day or placebo in the Estrogen in the Prevention of Atherosclerosis Trial (EPAT). Carotid artery intima-media thickness (CIMT), hs-CRP, and sICAM-1 were measured at baseline and every 6 months thereafter for 2 years. Unopposed 17beta-estradiol significantly increased hs-CRP (p = 0.01) and decreased sICAM-1 compared with placebo (p = 0.04). Changes in hs-CRP and sICAM-1 did not correlate with changes in carotid artery intima-media thickness. In conclusion, although unopposed 17beta-estradiol significantly altered hs-CRP and sICAM-1, neither marker was associated with progression of subclinical atherosclerosis.

Serum Soluble ICAM-1, VCAM-1, L-Selectin, and P-Selectin Levels as Markers of Infection and their Relation to Clinical Severity in Neonatal Sepsis

Adhesion molecules may play a role in the evolution and severity of neonatal sepsis. The purposes of this study were to determine whether serum soluble intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, L-selectin, and P-selectin levels are useful tools in the diagnosis of proven sepsis in newborn infants, and whether their levels are related to the clinical severity of the disease. A cohort of 25 consecutive newborns meeting criteria for clinical sepsis, 10 hemoculture-negative (HC - ) and 15 hemoculture-positive (HC + ), were prospectively followed and compared with 12 healthy newborns (six </= 38 weeks of gestational age and six >/= 39 weeks). Serum soluble (s)ICAM-1, sVCAM-1, sL-selectin, and sP-selectin concentrations were measured at the time of the septic workup, then followed by up to three determinations in each newborn every third day. The Score for Neonatal Acute Physiology (SNAP)-II severity was assessed at the moment of highest clinical severity of the disease. At the beginning of sepsis, sICAM-1 levels increased in both groups, being higher in HC + sepsis than in HC - ; sVCAM-1 only increased slightly in HC + sepsis. Soluble ICAM-1 levels were independently related to group of sepsis, and not to days of life. The best initial sICAM-1 cutoff level for diagnosing HC + neonatal sepsis was 274 microg/L. The highest sICAM-1 levels were positively correlated with SNAP-II scores. Soluble L-selectin and sP-selectin did not change. Soluble ICAM-1 levels increased in HC - and HC + sepsis, but concentrations > 274 microg/L suggest HC + sepsis. These levels were related to the clinical severity of the disease. Soluble VCAM-1 levels increased only slightly in HC + sepsis. Soluble L-selectin and sP-selectin did not change.

Circulating vascular endothelial growth factor is unaffected by acute hyperglycemia and hyperinsulinemia in type 1 diabetes mellitus

Background Circulating levels of vascular endothelial growth factor (VEGF) may predict microvascular complications in type 1 diabetes mellitus and are elevated when metabolic control is poor. We tested whether serum VEGF is influenced by prevailing glucose and insulin levels. Methods In 15 type 1 diabetic patients, serum VEGF, plasma von Willebrand factor antigen (vWF-Ag), and serum soluble intercellular adhesion molecule-1 (s-ICAM) levels were measured after 210 min of hyperglycemia (blood glucose target 12.0 mmol/l) and hyperinsulinemia (insulin infused at 120 mU/kg/h), alone and in combination. These were then compared with the levels obtained at the end of a 210-min normoglycemic (blood glucose target 5.0 mmol/l) standard insulin clamp (insulin infused at 30 mU/kg/h). Results VEGF ( p > 0.60) as well as vWF-AG ( p > 0.80) and s-ICAM ( p > 0.20) remained unchanged at the end of the three intervention periods. Conclusion These findings suggest that no special precautions, in terms of concurrent measurement of glucose or timing of insulin administration, are necessary when interpreting circulating VEGF in this patient category.

Risk for Nonalcoholic Fatty Liver Disease in Hispanic Youth With BMI ≥95th Percentile

To characterize children at risk for nonalcoholic fatty liver disease (NAFLD) and to explore possible mechanisms underlying the development of NAFLD in Hispanic youth with a body mass index > or =95th percentile. Hispanic nonoverweight (n = 475) and overweight (n = 517) children, ages 4 to 19 y, were characterized in terms of body composition (dual-energy x-ray absorptiometry), maturation (Tanner stage), diet (24-h recall), physical activity (accelerometry), fitness (maximal oxygen uptake), and biochemical profile (fasting alanine aminotransferase [ALT], glucose, insulin, and lipids; inflammation markers such as adiponectin, leptin, C-reactive protein, and soluble intercellular adhesion molecule-1; and total antioxidants) using standard laboratory techniques. Risk for NAFLD was defined by fasting serum ALT values >97.5th percentile for age- and sex-specific reference values. Fasting serum ALT was elevated in 24% of overweight children and in only 4% of nonoverweight children. Therefore, to identify risk factors associated with elevated ALT, the remaining statistical analysis was restricted to the overweight group. The percentage of overweight children with elevated ALT did not differ by sex, age, or Tanner stage. Weight, body mass index, z score, waist-to-hip ratio, fat-free mass, fat mass, and percent truncal fat mass were higher in the overweight children with elevated ALT. Fasting insulin, glucose, and homeostasis model-insulin resistance were higher in the overweight children with elevated ALT, as were triglycerides, total cholesterol, low-density lipoprotein, thyroid-stimulating hormone, and triiodothyronine. Fasting serum leptin, C-reactive protein, and soluble intercellular adhesion molecule-1 were significantly higher and adiponectin was lower in the overweight children with elevated ALT. The risk for developing NAFLD was high in the overweight Hispanic children. The proportion of "at risk" children was not influenced by gender, age, or maturation. The risk for elevated ALT was predicted by the severity of obesity, central adiposity, hyperinsulinemia, hypertriglyceridemia, elevated thyroid-stimulating hormone, and systemic inflammation.

Serum soluble intercellular adhesion molecule-1 in children with severe pneumonia

目的 探讨重症肺炎患儿血清可溶性细胞间黏附分子-1(sICAM-1)水平的变化,以及不同病原体所致重症肺炎血清sICAM-1的水平及其临床意义.方法 采用双抗体夹心酶联免疫吸附法测定40例重症肺炎患儿和43例普通肺炎患儿急性期、恢复期、以及48例健康对照组小儿血清sICAM-1水平.结果 重症肺炎急性期血清sICAM-1水平明显高于重症肺炎恢复期,差异有非常显著性(P＜0.01);与普通肺炎急性期与健康对照组比较,差异有非常显著性(P＜0.01);重症肺炎恢复期血清sICAM-1水平与普通肺炎恢复期及健康对照组比较,则差异均无显著性(P＞0.05);重症细菌性肺炎、病毒性肺炎、支原体肺炎、病毒与细菌混合感染性肺炎急性期血清sICAM-1水平比较,差异均无显著性(P＞0.05).结论 重症肺炎患儿急性期血清sICAM-1水平较普通肺炎急性期明显增高,但不同病原体所致重症肺炎血清sICAM-1水平变化无统计学意义;sICAM-1参与了重症肺炎的炎症过程,其水平的高低可以作为肺炎病情轻重的判断指标之一。

Influence of Scalp Point-to-Point Acupuncture on Serum sICAM1 in Patients with Acute Cerebral Infarction

Objective: To study the influence of different methods on serum soluble intercellular adhesion molecule1 (sICAM1) in patients with acute cerebral infarction.Methods: Double antibody enzyme-linked immunoadsorbent assay was used.Results and Conclusion: Scalp point-to-point acupuncture has a significant reducing effect on abnormally elevated serum sICAM1 in patients with acute cerebral infarction. Its curative effect is superior to that of simple Western medicine. There is a significant difference between them (P<0.05).

Are Inflammatory Factors Related to Retinal Vessel Caliber?

To examine the relationship of systemic markers of inflammation, endothelial dysfunction, and serum folate level to retinal vessel diameter. Cross-sectional analyses were completed for data from a random sample of 396 persons aged 50 to 86 years who underwent a baseline examination from 1988 to 1990. Standardized protocols for blood collection and measurement of markers were used. Diameters of arterioles and venules were measured from digitized photographs. Standard univariate and multivariate analyses were performed. While controlling for age, smoking status, diabetes status, serum high-density lipoprotein cholesterol, and hematocrit, wider retinal venular diameters were associated with higher serum high-sensitivity C-reactive protein, interleukin 6, and amyloid A levels. While controlling for age, systolic and diastolic blood pressure, smoking, serum high-density lipoprotein cholesterol level, and gout, smaller arteriolar diameters were associated with higher serum amyloid A and lower serum albumin and folate levels but not high-sensitivity C-reactive protein or interleukin 6 levels. Levels of serum soluble intercellular adhesion molecule-1 and serum soluble E-selectin, markers of endothelial dysfunction, were not associated with retinal arteriolar or venular diameters. These data show an association of inflammatory markers with larger retinal venular diameter, suggesting that retinal venular caliber may be a marker of systemic inflammation.

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Acute myocardial infarction causing cardiac ischemia is responsible for the majority of cardiac related deaths. Medical interventions that ensure rapid reperfusion, such as percutaneous coronary intervention, are aimed to allow myocardial re-oxygenation. However, this generates reactive oxygen species, resembling ischemia-reperfusion type of injury based on oxidative stress. In the present study we monitored dynamic changes of total serum peroxides, total antioxidant capacity and soluble intercellular adhesion molecule-1 as well as the titer of antibodies against oxidized low-density lipoproteins in the blood during the convalescence period of 32 patients with acute myocardial infarction treated by percutaneous coronary intervention. Samples were taken at admittance and at two hours, four hours, three days and seven days following percutaneous coronary intervention. Total antioxidant capacity dropped to 82% (p < 0.05). The titer of antibodies against oxidized low-density lipoproteins transiently decreased within the first three days, and increased afterwards. The values of serum peroxides and soluble intercellular adhesion molecule-1 increased continuously in respect to the initial levels reaching the maximum at the time of release from hospital. These findings indicate a persistent oxidative stress that might be associated with intravascular inflammation in patients during convalescence and release from hospital.

Serum levels of soluble intercellular adhesion molecule-1 (s-ICAM-1) and soluble endothelial leukocyte adhesion molecule-1(s-ELAM-1) in amyotrophic lateral sclerosis

Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Adhesion molecules are markers of activated endothelial cells up-regulated by action of cytokines. To investigate the activation or inactivation of the vascular cells in ALS, serum soluble intercellular adhesion molecule-1 (s-ICAM-1) and soluble E-selectin (s-ELAM-1) were evaluated (ELISA) in 16 patients with ALS, 30 patients with non-inflammatory neurological diseases (NINDS) and 15 healthy control subjects. Patients with ALS had no higher s-ICAM-1 levels compared with the NINDS patients and the control subjects (pv0.31 and pv0.21, respectively). s-ELAM levels were not statistically significant compared with the NINDS patients and healthy subjects (pv0.21 and pv0.24, respectively). We conclude that the low values of s-ICAM-1 and s-ELAM-1 in the serum of ALS patients do not exclude the presence of immunological abnormality in this disorder. Soluble E-selectin is a glycoprotein which is considered an exclusive marker of endothelial activation. Its low level in our study may suggest a neural rather than an endothelial s-ICAM origin in patients with ALS.

The effects of conjugated linoleic acid supplementation on immune function in healthy volunteers

To assess the effects of dietary supplementation using two isomeric blends of conjugated linoleic acid (CLA) on immune function in healthy human volunteers. Double-blind, randomised, placebo-controlled intervention trial. A total of 55 healthy volunteers (n=20 males, n=35 females) were randomised into one of three study groups who received 3 g/day of a fatty acid blend containing a 50:50 cis-9, trans-11: trans-10, cis-12 CLA isomer blend (2 g CLA), and 80:20 cis-9, trans-11: trans-10, cis-12 (80:20) CLA isomer blend (1.76 g CLA) or linoleic acid (control, 2 g linoleic acid) for 8 weeks. Supplementation with the 80:20 CLA isomer blend significantly (P< or =0.05) enhanced PHA-induced lymphocyte proliferation. CLA decreased basal interleukin (IL)-2 secretion (P< or =0.01) and increased PHA-induced IL-2 and tumor necrosis factor alpha (TNF(alpha)) production (P< or =0.01). However, these effects were not solely attributable to CLA as similar results were observed with linoleic acid. CLA supplementation had no significant effect on peripheral blood mononuclear cells IL-4 production, or on serum-soluble intercellular adhesion molecule-1 (sICAM-1) or plasma prostaglandin E2 (PGE2) or leukotreine B4 (LTB4) concentrations. This study shows that CLA supplementation had a minimal effect on the markers of human immune function. Furthermore, supplementation with CLA had no immunological benefit compared with linoleic acid.