Home About us Contact
|
Home About us Contact | ||
|
|
||
Systemic Markers (systemic + marker)
Selected AbstractsMRI of atherosclerosis in clinical trialsNMR IN BIOMEDICINE, Issue 6 2006Chun Yuan Abstract Magnetic resonance imaging (MRI) of the arterial wall has emerged as a viable technology for characterizing atherosclerotic lesions in vivo, especially within carotid arteries and other large vessels. This capability has facilitated the use of carotid MRI in clinical trials to evaluate therapeutic effects on atherosclerotic lesions themselves. MRI is specifically able to characterize three important aspects of the lesion: size, composition and biological activity. Lesion size, expressed as a total wall volume, may be more sensitive than maximal vessel narrowing (stenosis) as a measure of therapeutic effects, as it reflects changes along the entire length of the lesion and accounts for vessel remodeling. Lesion composition (e.g. lipid, fibrous and calcified content) may reflect therapeutic effects that do not alter lesion size or stenosis, but cause a transition from a vulnerable plaque composition to a more stable one. Biological activity, most notably inflammation, is an emerging target for imaging that is thought to destabilize plaque and which may be a systemic marker of vulnerability. The ability of MRI to characterize each of these features in carotid atherosclerotic lesions gives it the potential, under certain circumstances, to replace traditional trials involving large numbers of subjects and hard end-points , heart attacks and strokes , with smaller, shorter trials involving imaging end-points. In this review, the state of the art in MRI of atherosclerosis is presented in terms of hardware, image acquisition protocols and post-processing. Also, the results of validation studies for measuring lesion size, composition and inflammation will be summarized. Finally, the status of several clinical trials involving MRI of atherosclerosis will be reviewed. Copyright © 2006 John Wiley & Sons, Ltd. [source] Imbalance between interleukin-1 agonists and antagonists: relationship to severity of inflammatory bowel diseaseCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2004O. LUDWICZEK SUMMARY Interleukin (IL)-1 is a key mediator in the pathogenesis of inflammatory bowel disease (IBD). Naturally occurring IL-1 modulators include IL-1 receptor antagonist (IL-1Ra), IL-1 soluble receptor Type I (IL-1sRI), IL-1sRII and IL-1 receptor accessory protein (AcP). Systemic and mucosal levels of IL-1 soluble receptors remain unknown in IBD. Plasma or colonic tissues were obtained from 185 consecutive unselected patients with Crohn's disease (CD) or ulcerative colitis (UC) and from 52 control subjects. Plasma and colonic explant culture supernatants were assessed for IL-1,, IL-1,, IL-1Ra, IL-1sRI and IL-1sRII. Plasma IL-1Ra levels were higher in UC (+93%) than in healthy subjects. IL-1, and IL-1, were not detected. IL-1sRII levels were marginally lower in CD (,10%) and UC (,9%), whereas IL-1sRI levels were elevated in CD (+28%) only. Plasma IL-1sRI levels correlated positively (P < 0·01) with Crohn's disease activity index (r = 0·53), C-reactive protein (r = 0·46) and ,1-acid glycoprotein (r = 0·42). In colonic explant cultures, IL-1, and IL-1Ra levels were elevated in non-lesional (+233% and +185% respectively) and lesional CD (+353% and +1069%), lesional UC (+604% and +1138%), but not in non-lesional UC. IL-1, was elevated in lesional UC (+152%) and CD (+128%). In contrast, IL-1sRII levels were elevated in non-lesional CD (+65%), but remained unchanged in lesional CD, non-lesional and lesional UC. IL-1sRI levels did not differ between patient and control groups. These results indicate that (i) the proinflammatory moiety IL-1sRI is a systemic marker of inflammation and activity in CD and (ii) local shedding of the functional antagonist IL-1sRII may dampen colonic inflammation in CD, but not in UC. [source] Evaluation of t-PA, PAI-2, IL-1, and PGE2 in gingival crevicular fluid of rheumatoid arthritis patients with periodontal diseaseJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 9 2006Abstract Aims: This study was undertaken to compare periodontal conditions, gingival crevicular fluid (GCF) levels of tissue-type plasminogen activator (t-PA), its inhibitor plasminogen activator inhibitor-2 (PAI-2), interleukin-1, (IL-1,), prostaglandin E2 (PGE2) in rheumatoid arthritis (RA) patients and control groups. Methods: Twenty-three RA patients, 17 systemically healthy patients with periodontal disease (PD), and 17 systemically and periodontally healthy subjects were recruited. GCF samples were obtained from two single-rooted teeth. Full-mouth clinical periodontal measurements were recorded at six sites/tooth. GCF samples were analysed using relevant ELISA kits. Data were tested statistically by appropriate tests. Results: Total amounts of t-PA, PAI-2 and PGE2 in GCF samples of the healthy control group were significantly lower than the other groups (p<0.05). The RA group exhibited a higher total amount of t-PA in GCF samples than the PD group (p<0.05). PAI-2, IL-1, and PGE2 total amounts were similar in RA and PD groups (p>0.05). Conclusion: The coexistence of RA and periodontitis does not seem to affect clinical periodontal findings or systemic markers of RA. Similar inflammatory mediator levels in RA and PD groups, despite the long-term usage of corticosteroids, non-steroidal anti-inflammatory drugs, suggest that RA patients may have a propensity to overproduce these inflammatory mediators. [source] Periodontal health improves systemic inflammatory and haemostatic status in subjects with coronary heart diseaseJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2 2005L. Montebugnoli Abstract Objectives: A relationship between poor oral health and coronary heart disease (CHD) and systemic inflammatory and haemostatic factors has been recently documented in an Italian population. The present study was performed to assess whether intensive dental care may produce a periodontal improvement along with a change in systemic inflammatory and haemostatic factors. Material and Methods: The study population consisted of 18 males aged 40,65 years with proven CHD and elevated values of systemic inflammatory and haemostatic factors. A detailed description of their oral status was given by using two different dental indices (clinical periodontal sum score and clinical and radiographic sum score). Blood samples were taken for measurement of the following systemic markers of inflammation [(C-reactive protein (CRP), leucocytes, fibrinogen)] and haemostatic factors [(von Willebrand factor, fibrin D-dimer and oxidized-low density lipoprotein (Ox-LDL)]. All parameters were determined in each subject at baseline, after 4 months as a control and 3 months after an intensive protocol of scaling and root planing. anova for repeated measures was used for the statistical analysis. Results: No statistical difference was found between values at baseline and at the 4-month-control. All oral indexes showed a significant decrease (p<.01) 3 months after periodontal treatment. All systemic inflammatory indexes decreased but only the decrease in CRP reached statistical significance (p<.05). A significant decrease (p<.01) was also found as regards Ox-LDL among haemostatic factors. Conclusions: Preliminary results from the present study suggest an association between poor oral status and CHD, and provide evidence that the improvement of periodontal status may influence the systemic inflammatory and haemostatic situation. [source] Relationship between induced sputum cytology and inflammatory status with lung structural and functional abnormalities in asbestosisAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2008José Henrique Setta MD Abstract Background Asbestosis is associated with lung cellular and immunological abnormalities. Induced sputum cytology and local and systemic markers of inflammation may be helpful to characterize disease status and progression in these patients. Methods Thirty-nine ex-workers with asbestosis on high-resolution CT (HRCT) and 21 non-exposed controls were evaluated. Sputum cytology and IL-8 in serum and sputum were related to lung function impairment. Results Subjects with asbestosis had reduced sputum cellularity but higher macrophage/neutrophil ratio and % macrophage as compared with controls. Sputum and serum IL-8 were also higher in patients with asbestosis (P,<,0.05). In addition, evidence of lung architectural distorption on HRCT was associated with increased levels of serum IL-8. Interestingly, absolute macrophage number was negatively correlated with total lung capacity (r,=,,0.40; P,=,0.04) and serum IL-8 to lung diffusing capacity (r,=,,0.45; P,=,0.01). Conclusions Occupationally exposed subjects with asbestosis on HRCT have cytologic abnormalities in induced sputum and increased local and systemic pro-inflammatory status which are correlated to functional impairment. Am. J. Ind. Med. 51:186,194, 2008. © 2008 Wiley-Liss, Inc. [source] 2424: Pulsatile haemodynamics: potential for end-organ damage?ACTA OPHTHALMOLOGICA, Issue 2010C HUDSON Purpose Increases in velocity pulse wave amplitude, or max:min velocity ratio, represent early haemodynamic disturbances associated with diabetic retinopathy (DR) and age-related macular degeneration. This change reflects an increase in vessel wall rigidity that is generally accepted to occur in the central vasculature but the peripheral vasculature is also implicated in this process. This presentation will highlight the implications of these changes in terms of end-organ damage in DR. Methods The sample comprised 4 groups: Group 1: 50 non-diabetic control subjects. Group 2: 56 diabetic patients without clinically visible DR. Group 3: 54 diabetic patients with micro-aneurysms and / or hard exudates within 2 disc diameters of the fovea in the absence of clinically manifest diabetic macular edema (DME). Group 4: 40 patients with clinically manifest DME. The diabetic patients were predominantly type 2. Retinal hemodynamics were assessed in the superior temporal retinal arteriole using the Canon Laser Blood Flowmeter. Intraocular pressure, blood pressure and relevant systemic markers of diabetes control and complications were also assessed. Results The velocity pulse wave amplitude was elevated with increasing risk of DME (p<0.0001). No significant differences were found between the groups with respect to diameter, velocity or flow. Pulse wave amplitude was correlated to age, duration of diabetes, blood pressure, pulse rate, IOP and serum potassium levels. Conclusion The increase in velocity pulse wave amplitude will induce excessive pressure pulsatility in the retinal arterioles and capillaries, changes in vascular function (e.g. loss of vascular regulation) and changes in vessel structure. Commercial interest [source] | ||||||||||