Intercellular Adhesion Molecule-1 and Interleukin-6 Gene Polymorphisms in Patients with Advanced-Stage Endometriosis

2010 ◽  
Vol 70 (1) ◽  
pp. 34-39 ◽  
Author(s):  
Soo Jin Chae ◽  
Gyoung Hoon Lee ◽  
Young Min Choi ◽  
Min A Hong ◽  
Jong Mee Kim ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Interleukin 6 ◽  
Gene Polymorphisms ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Advanced Stage ◽  
Intercellular Adhesion Molecule 1

Interaction between interleukin?6 and intercellular adhesion molecule?1 genes and Alzheimer?s disease risk

2005 ◽  
Vol 252 (4) ◽  
pp. 485-487 ◽  
Author(s):  
Onofre Combarros ◽  
J. Infante ◽  
J. Llorca ◽  
N. Pe�a ◽  
C. Fern�ndez-Viadero ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Interleukin 6 ◽  
Disease Risk ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Effects of NF-κB inhibition on mesenteric ischemia-reperfusion injury

2003 ◽  
Vol 284 (4) ◽  
pp. G713-G721 ◽  
Author(s):  
Lei Zou ◽  
Bashir Attuwaybi ◽  
Bruce C. Kone
Keyword(s):  
Reperfusion Injury ◽  
Tyrosine Phosphorylation ◽  
Adhesion Molecule ◽  
Interleukin 6 ◽  
Mesenteric Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Mesenteric ischemia-reperfusion injury is a serious complication of shock. Because activation of nuclear factor-κB (NF-κB) has been implicated in this process, we treated rats with vehicle or the IκB-α inhibitor BAY 11-7085 (25 mg/kg ip) 1 h before mesenteric ischemia-reperfusion (45 min of ischemia followed by reperfusion at 30 min or 6 h) and examined the ileal injury response. Vehicle-treated rats subjected to ischemia-reperfusion exhibited severe mucosal injury, increased myeloperoxidase (MPO) activity, increased expression of interleukin-6 and intercellular adhesion molecule 1 protein, and a biphasic peak of NF-κB DNA-binding activity during the 30-min and 6-h reperfusion courses. In contrast, BAY 11-7085-pretreated rats subjected to ischemia-reperfusion exhibited less histological injury and less interleukin-6 and intercellular adhesion molecule 1 protein expression at 30 min of reperfusion but more histological injury at 6 h of reperfusion than vehicle-treated rats subjected to ischemia-reperfusion. Studies with phosphorylation site-specific antibodies demonstrated that IκB-α phosphorylation at Ser32,Ser36 was induced at 30 min of reperfusion, whereas tyrosine phosphorylation of IκB-α was induced at 6 h of reperfusion. BAY 11-7085 inhibited the former, but not the latter, phosphorylation pathway, whereas α-melanocyte-stimulating hormone, which is effective in limiting late ischemia-reperfusion injury to the intestine, inhibited tyrosine phosphorylation of IκB-α. Thus NF-κB appears to play an important role in the generation and resolution of intestinal ischemia-reperfusion injury through different activation pathways.

Predictive Value of Soluble Immunological Mediators in Neonatal Infection

1994 ◽  
Vol 87 (2) ◽  
pp. 165-171 ◽  
Author(s):  
J. D. M. Edgar ◽  
D. C. Wilson ◽  
S. A. McMillan ◽  
A. D. Crockard ◽  
M. I. Halliday ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Interleukin 6 ◽  
Predictive Value ◽  
Neonatal Infection ◽  
Intercellular Adhesion ◽  
Interleukin 8 ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Reactive Protein ◽  
Factor Α

1. Infection in the neonatal period is difficult to diagnose and is a significant cause of morbidity and mortality in preterm infants. 2. We investigated prospectively the predictive value of plasma measurement of bacterial endotoxin (lipo-polysaccharide), tumour necrosis factor-α, interleukin-6, interleukin-8, intercellular adhesion molecule-1 and C-reactive protein in 60 consecutive newborn infants suspected of having neonatal infection. Plasma samples were taken at the time of acute clinical deterioration. Sixty-two cord blood samples were studied as controls taken at elective Caesarean section. 3. Forty-three infants had confirmed infections, 25 with positive blood cultures. Tumour necrosis factor-α and bacterial endotoxin levels were not significantly elevated over controls, whereas interleukin-6, interleukin-8 and intercellular adhesion molecule-1 levels were all significantly increased in the infected group compared with controls (all P < 0.001). 4. Increased plasma intercellular adhesion molecule-1 levels were a highly sensitive (88%) indicator of clinical infection and were independent of C-reactive protein. Use of these two assays in combination improved the diagnostic sensitivity to 95% and gave a negative predictive value of 97%. Addition of interleukin-6 or interleukin-8 measurements failed to further significantly enhance the prediction of infection. 5. Measurement of intercellular adhesion molecule-1 level may have a clinical role in rapidly confirming, or predicting, the likely diagnosis in cases of suspected neonatal infection.

Effect of acute sleep deprivation on vascular function in healthy subjects

2010 ◽  
Vol 108 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Fabien Sauvet ◽  
Georges Leftheriotis ◽  
Danièlle Gomez-Merino ◽  
Christophe Langrume ◽  
Catherine Drogou ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Adhesion Molecule ◽  
Interleukin 6 ◽  
Vascular Function ◽  
Sympathetic Activity ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Doppler Flowmetry ◽  
Acute Sleep Deprivation

Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 ± 3 yr). The days before [ day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 ( P < 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD ( P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04–0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD ( P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP.

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