Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We included 63 patients with chronic heart failure of ischemic origin (32 with left ventricular ejection fraction less than 40%) into prospective study with average duration of follow-up 27+/-10 months. Relative risk of lethal outcome was significantly increased in patients with initial endsystolic left ventricular dimension >6.0 m, enddiastolic left ventricular dimension >7.0 m, left atrial dimension >5.0 cm, left ventricular ejection fraction <35%, hemoglobin level <120 g/L, with disturbances of rhythm and conduction, and elevation of plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) >1000 mol/ml and interleukin-6 >20 g/ml. Relative risk of combined endpoint significantly increased at same values of echocardiographical parameters, plasma levels of NT-proBNP >500 mol/ml and interleukin-6 >10 g/ml.
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PMID:[Prognostic value of plasma levels of N-terminal pro-brain natriuretic peptide and proinflammatory cytokines in patients with heart failure of ischemic etiology]. 1984 14

The aim of this study was to determine the impact of HRCT-confirmed emphysema on biomarkers evaluating airway and systemic inflammation in COPD patients. Forty-nine consecutive male COPD outpatients with stable COPD were divided in two groups according to the presence or absence of emphysema on HRCT. Patients underwent pulmonary function tests, plus assessment of exercise capacity, body composition and quality of life. Biomarkers were measured in serum (CRP, interleukin-6, TNF-alpha, leptin, adiponectin, osteocalcin, insulin growth factor-1, and systemic oxidative stress), in plasma (fibrinogen and VEGF) and in whole blood (B-type natriuretic peptide). TNF-alpha, 8-isoprostane and pH were additionally measured in exhaled breath condensate. Patients with emphysema had more severe lung function impairment, lower body-mass index and fat-free mass index, and poorer quality of life. Additionally, they presented increased systemic oxidative stress and plasma fibrinogen and lower BNP compared to patients without emphysema. After proper adjustment for disease severity, all differences remained with the exceptions of body-mass index, fat-free mass index and BNP. COPD patients with HRCT-confirmed emphysema present increased systemic oxidative stress and fibrinogen, suggesting that they may be more prone to the systemic consequences of COPD compared to patients without emphysema.
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PMID:Systemic and airway inflammation and the presence of emphysema in patients with COPD. 1985 37

Eleven papers on trauma published in Critical Care during 2008 addressed traumatic brain injury (TBI), burns, diagnostic concerns and immunosuppression. In regard to TBI, preliminary results indicate the utility of either magnetic resonance imaging (MRI) or ultrasound in measuring optic nerve sheath diameter to identify elevated intracranial pressure (ICP) as well as the potential benefit of thiopental for refractory ICP. Another investigation demonstrated that early extubation of TBI patients whose Glasgow Coma Scale score was 8 or less did not result in additional incidence of nosocomial pneumonia. Another study indicated that strict glucose control resulted in worse outcomes during the first week after TBI, but improved outcomes after the second week. Another paper showed the prolonged neuroprotective advantages of progesterone administration in TBI patients. There was also guidance on improved classifications of renal complications in burn patients. Another study found that patients with inhalation injuries and increased interleukin-6 (IL-6) and IL-10 and decreased IL-7 had increased mortality rates. One literature review described the disadvantages of prolonged immobilization or additional use of MRI for ruling out cervical spine injuries in obtunded TBI patients already cleared by computerized tomography scans. Other investigators found that higher N-terminal pro B-type natriuretic peptide (NT-proBNP) levels may be useful markers for post-traumatic cardiac impairment. Finally, an experimental model showed that both splenic apoptosis and lymphocytopenia may occur shortly after severe hemorrhage, thus increasing the threat of immunosuppression in those with severe blood loss.
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PMID:Year in review 2008: Critical Care--trauma. 1986 66

Cytokines play important roles in heart failure (HF). We examined whether cytokine levels are different in acute decompensated heart failure (ADHF) patients between with left ventricular systolic dysfunction (LVSDF) and with preserved LV ejection function (PLVEF). We studied 81 HF patients who were admitted to our hospital with acute decompensation. They were divided into two groups: LVSDF (LVEF)<45% and PLVEF (LVEF45%). Serum interleukin-6 (IL-6), highly sensitive C-reactive protein (hsCRP), tumor necrosis factor alpha (TNF-alpha), and IL-18 and plasma brain natriuretic peptide (BNP) were measured on admission and at discharge. On admission, IL-6 and hsCRP were higher in LVSDF than in PLVEF. IL-6 and hsCRP decreased after treatment in LVSDF, but not in PLVEF, while plasma BNP levels decreased in both HF with treatment. There was no difference in TNF-alpha or in IL-18 level between LVSDF and PLVEF, and they did not change after treatment in either group. In conclusion, cytokine profiles were different in ADHF between those with LVSDF and PLVEF. Activation of IL-6-hsCRP pathway may play a specific role in ADHF with LVSDF.
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PMID:Serum interleukin-6 and C-reactive protein are markedly elevated in acute decompensated heart failure patients with left ventricular systolic dysfunction. 2000 39

Sympathetic activation after subarachnoid hemorrhage (SAH) can induce tachycardia as well as cardiac and brain injury. We examined the effects of beta1 receptor antagonist landiolol on hemodynamics and the levels of tissue injury markers in patients with SAH. Fifty-six SAH patients undergoing intracranial aneurysm surgery with tachycardia (>or=90 beats per minute) randomly allocated to landiolol (L) or control (C) group were examined. In L group, landiolol was continuously administered during anesthesia. In C group, landiolol was not administered except bolus dose used in cases that exhibited uncontrolled tachycardia. Hemodynamics, the incidence of electrocardiographic abnormality, and levels of B-type natriuretic peptide, troponin T, S-100beta, 8-Hydroxy-2'-deoxyguanosine, interleukin-6 (IL-6), and IL-1 receptor antagonist were compared. Heart rate values from time of intubation to the end of anesthesia were significantly lower in L group than in C group, whereas blood pressure was similar between the groups. Although the incidence of bradycardia (<60 beats per minute) was significantly higher in L group than in C group (57% vs. 18%, respectively), bradycardia could be recovered without any adverse effects. The serum S-100beta levels 24 hours after operation were significantly lower in L group than in C group, whereas there were no significant differences in the incidence of electrocardiographic abnormality and levels of B-type natriuretic peptide, troponin T, 8-Hydroxy-2'-deoxyguanosine, IL-6, and IL-1 receptor antagonist between groups. We conclude that landiolol can be effectively used in the treatment of tachycardia in SAH patients and significantly reduced the serum S-100beta levels 24 hours after the operation.
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PMID:Effects of a short-acting [beta]1 receptor antagonist landiolol on hemodynamics and tissue injury markers in patients with subarachnoid hemorrhage undergoing intracranial aneurysm surgery. 2011 92

Several previous studies have suggested that n-3 polyunsaturated fatty acids (n-3 PUFA) can exert favourable effects in patients with heart failure, but the mechanisms involved are not fully understood. This study was designed to investigate the effects of n-3 PUFA on circulating inflammatory markers and N-terminal pro-brain natriuretic peptide (NT-proBNP) in patients with heart failure. Seventy-six patients with heart failure were randomly assigned to receive 2 g/day of n-3 PUFA or placebo for 3 months. Treatment with n-3 PUFA significantly decreased plasma levels of tumour necrosis factor, interleukin-6, intercellular adhesion molecule 1 and NT-proBNP. Left ventricular ejection fraction showed a small, non-significant improvement. High-sensitivity C-reactive protein levels decreased significantly in smokers after n-3 PUFA treatment. Thus, n-3 PUFA can reduce levels of plasma inflammatory markers and NT-proBNP as biomarkers of risk stratification in patients with heart failure. n-3 PUFA may offer a novel therapy for heart failure.
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PMID:Effects of n-3 polyunsaturated fatty acid therapy on plasma inflammatory markers and N-terminal pro-brain natriuretic peptide in elderly patients with chronic heart failure. 2014 81

Adrenomedullin (AM) is located in the zona glomerulosa of the adrenal cortex and is considered to suppress aldosterone release. To determine the effect of AM in primary aldosteronism (PA), we infused AM (2.5 pmol kg(-1) min(-1)) for 27 h, followed by a 15-h recovery period, in a control group (essential hypertensives with plasma aldosterone levels <or=100 pg ml(-1), n=7) and in a PA group (n=5). The control group was also infused with vehicle. Hemodynamic, hormonal, oxidative and inflammatory responses were studied. AM infusion caused similar and steady decreases in blood pressure and several markers for arteriosclerosis (for example, pulse wave velocity) in both groups. Interestingly, AM infusion suppressed aldosterone release to values within the normal range in the PA group (300.0+/-58.4 to 111.6+/-13.5 pg ml(-1), P<0.01). In the control group, aldosterone release suppression was significant but limited (81.7+/-9.1 to 47.9+/-9.9 pg ml(-1), P<0.01). The adrenocorticotropic hormone-cortisol system was not changed by AM infusion. Brain natriuretic peptide was cumulatively increased by prolonged AM infusion in both groups, probably because of cardiac overload. AM did not affect oxidative markers. In addition, a mild but significant increase in C-reactive protein (CRP) mediated by interleukin-6 was observed during AM infusion in every participant, without exception. This pathway might participate in CRP elevation in cardiovascular disease. In summary, AM seems to have an essential role in the suppression of aldosterone release in PA. AM may be an important modulator in PA, and intermediate-term (3 h) AM infusion could be used as an alternative renin-stimulating/aldosterone-suppressing test for PA detection.
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PMID:Aldosterone antisecretagogue and antihypertensive actions of adrenomedullin in patients with primary aldosteronism. 2015 Sep 11

The sympathetic nervous system and pro-inflammatory cytokines play key roles in numerous cardiovascular disorders. Chronic beta-adrenergic receptor (beta-AR) stimulation in myocardium induces expression of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), which contribute to cardiac hypertrophy and failure. To evaluate the relationship between beta-AR stimulation and pro-inflammatory cytokines, we studied the effects of the beta-AR agonist isoprenaline (ISO) on IL-1-induced IL-6 production in adult rat ventricular myocytes (ARVMs). We report that ISO and IL-1 synergistically enhanced IL-6 gene expression and secretion. The synergistic effect of ISO was mimicked by cAMP elevating agents and involved the G(s) protein/cAMP/PKA signalling pathway, but not the exchange factor EPAC. To evaluate the contribution of IL-6 to cellular hypertrophy, we examined the signalling pathways stimulated by the membrane-bound IL-6 receptor (IL-6R), and the IL-6 soluble receptor (sIL-6R) involved in the mechanism named IL-6 trans-signalling. The IL-6/sIL-6R complex promoted a rapid and persistent phosphorylation of STAT3(Tyr705) in ARVMs. Moreover, IL-6 trans-signalling increased protein synthesis, c-fos gene expression and B-type natriuretic peptide secretion, three markers of cardiac hypertrophy. IL-6 trans-signalling also increased cell size. In contrast, IL-6 alone had no significant effect on either cell size or STAT3 phosphorylation although it induced phosphorylation of ERK1/2, AKT and S6K, demonstrating the presence of a functional IL-6R in ARVMs. Taken together, these results demonstrate that beta-AR stimulation synergises with IL-1 for IL-6 secretion in adult ventricular myocytes and indicate that IL-6 induces cardiac hypertrophy only via IL-6 trans-signalling. The IL-6 soluble receptor may thus serve as a switch for IL-6 to activate STAT3 phosphorylation and hypertrophy.
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PMID:A new regulation of IL-6 production in adult cardiomyocytes by beta-adrenergic and IL-1 beta receptors and induction of cellular hypertrophy by IL-6 trans-signalling. 2022 92

beta2-Microglobulin (beta2M) is an independent predictor of outcome for hemodialysis (HD) patients and a representative substance of middle molecules. We tested the relationship among serum beta2M levels and cardiovascular disease (CVD) risk factors in HD patients. A total of 132 HD patients were divided according to the dialysis membrane used [property; cellulose and synthetic or beta2M clearance; low filtration (LF), middle filtration (MF), and high filtration (HF)]. There was no significant difference in CVD risk factors between cellulose and synthetic groups. On the other hand, serum beta2M, highly-sensitive C-reactive protein (hCRP), troponin-T (TnT), and myeloperoxidase (MPO) levels of LF were significantly higher and those of prealbumin (PA) were lower than the MF and HF. Serum beta2M level was positively correlated with hCRP, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), MPO, TnT, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and inversely correlated with PA and ankle-brachial index (ABI). There was a significant correlation between serum beta2M levels and various CVD risk factors in HD. Cardiovascular disease risk factors in HD patients were dependent on the beta2M clearance but not membrane property.
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PMID:The impact of beta2-microglobulin clearance on the risk factors of cardiovascular disease in hemodialysis patients. 2043 82

Peroxisome proliferator-activated receptor (PPAR)-gamma modulators, a class of antidiabetic drugs, have been associated with cardiovascular risks in type 2 diabetes in humans. The objective of this study was to explore possible cardiovascular risk biomarkers associated with PPAR-gamma in rodents that could provide an alert for risk to humans. Normal, myocardial infarction-induced heart failure (HF) or Zucker diabetic fatty (ZDF) rats were used. Rats (n = 5-6) were treated with either vehicle or rosiglitazone (RGZ; 3 or 45 mg/kg/day p.o.) for 4 weeks. Biomarkers for potential cardiovascular risks were assessed, including 1) ultrasound for cardiac structure and function; 2) neuroendocrine and hormonal plasma biomarkers of cardiovascular risk; 3) pharmacogenomic profiling of cardiac and renal tissue by targeted tissue low-density gene array representing ion channels and transporters, and components of the renin-angiotensin-aldosterone system; and 4) immunohistochemistry for cardiac fibrosis, hypertrophy, and inflammation (macrophages and tumor necrosis factor-alpha). HF was confirmed by increase in cardiac brain natriuretic peptide expression (p < 0.01) and echocardiography. Adequate exposure of RGZ was confirmed by pharmacokinetics (plasma drug levels) and the pharmacodynamic biomarker adiponectin. In normal or HF rats, RGZ had no negative effects on any of the biomarkers investigated. Similarly, RGZ had no significant effects on gene expression except for the increase in interleukin-6 mRNA expression in the heart and decrease in epithelial sodium channel beta in the kidney. In contrast, echocardiography showed improved cardiac structure and function after RGZ in ZDF rats. Taken together, this study suggests a limited predictive power of these preclinical models in respect to observed clinical adverse effects associated with RGZ.
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PMID:Pharmacogenomic, physiological, and biochemical investigations on safety and efficacy biomarkers associated with the peroxisome proliferator-activated receptor-gamma activator rosiglitazone in rodents: a translational medicine investigation. 2051 51


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