271 Studying the effect of long-term dosed exercise on the level of systemic inflammation markers in patients with II-III FC CHF

2007 ◽  
Vol 6 (1) ◽  
pp. 55-55
Author(s):  
G ARUTYUNOV ◽  
T CHERNIAVSKAYA ◽  
O VOLGINA
Keyword(s):  
Systemic Inflammation ◽  
Inflammation Markers

scholarly journals Systemic Inflammation (C-Reactive Protein) in Older Chinese Adults Is Associated with Long-Term Exposure to Ambient Air Pollution

2021 ◽  
Vol 18 (6) ◽  
pp. 3258
Author(s):  
Mona Elbarbary ◽  
Artem Oganesyan ◽  
Trenton Honda ◽  
Geoffrey Morgan ◽  
Yuming Guo ◽  
...  
Keyword(s):  
Air Pollution ◽  
Systemic Inflammation ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Chinese Adults ◽  
Reactive Protein ◽  
Hs Crp ◽  
Older Chinese ◽  
Older Chinese Adults

There is an established association between air pollution and cardiovascular disease (CVD), which is likely to be mediated by systemic inflammation. The present study evaluated links between long-term exposure to ambient air pollution and high-sensitivity C reactive protein (hs-CRP) in an older Chinese adult cohort (n = 7915) enrolled in the World Health Organization (WHO) study on global aging and adult health (SAGE) China Wave 1 in 2008–2010. Multilevel linear and logistic regression models were used to assess the associations of particulate matter (PM) and nitrogen dioxide (NO2) on log-transformed hs-CRP levels and odds ratios of CVD risk derived from CRP levels adjusted for confounders. A satellite-based spatial statistical model was applied to estimate the average community exposure to outdoor air pollutants (PM with an aerodynamic diameter of 10 μm or less (PM10), 2.5 μm or less (PM2.5), and 1 μm or less (PM1) and NO2) for each participant of the study. hs-CRP levels were drawn from dried blood spots of each participant. Each 10 μg/m3 increment in PM10, PM2.5, PM1, and NO2 was associated with 12.8% (95% confidence interval; (CI): 9.1, 16.6), 15.7% (95% CI: 10.9, 20.8), 10.2% (95% CI: 7.3, 13.2), and 11.8% (95% CI: 7.9, 15.8) higher serum levels of hs-CRP, respectively. Our findings suggest that air pollution may be an important factor in increasing systemic inflammation in older Chinese adults.

scholarly journals Prognostic role of lymphocyte-to-monocyte ratio in pancreatic neuroendocrine neoplasms

2020 ◽  
Vol 9 (4) ◽  
pp. 289-298 ◽  
Author(s):  
Wentao Zhou ◽  
Tiantao Kuang ◽  
Xu Han ◽  
Wenqi Chen ◽  
Xuefeng Xu ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Systemic Inflammation ◽  
Lymphocyte Count ◽  
Neuroendocrine Neoplasms ◽  
Inflammation Markers ◽  
Clinical Value ◽  
Term Survival ◽  
Pancreatic Neuroendocrine Neoplasms ◽  
Lymphocyte Ratio ◽  
Lymphocyte To Monocyte Ratio

Objectives Systemic inflammation markers have been demonstrated to be associated with prognosis in various tumors. In this study, we aimed to assess the value of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index and the counts of lymphocyte, monocyte and neutrophil in predicting prognosis among patients with resected pancreatic neuroendocrine neoplasms (pNENs). Methods A total of 174 patients were included in the study. Univariate and multivariate analyses were performed to evaluate the predictive roles of inflammation markers for relapse-free survival (RFS) and overall survival (OS) in pNEN patients. Results The optimal cut-off values of NLR, LMR and lymphocyte count were 1.9, 5.0 and 1.4 × 109/L, respectively, determined by the X-tile software. RFS was found to be significantly longer in patients with NLR ≤1.9 (P = 0.041), LMR >5.0 (P < 0.001) and lymphocyte count >1.4 × 109/L (P = 0.002) in comparison to those with NLR >1.9, LMR ≤5.0 and lymphocyte count ≤1.4 × 109/L, respectively. Multivariate analysis revealed that LMR (hazard ratio 0.30, 95% CI 0.11–0.85, P = 0.023) was an independent predictor for RFS, but not NLR or lymphocyte count. For long-term survival analysis, patients with NLR ≤1.9 (P = 0.016) were found to be associated with favorable OS, but NLR was not an independent factor validated by multivariate analysis. Conclusions Preoperative LMR is an independent systemic inflammation marker to predict relapses in pNEN patients who underwent curative resections, whose clinical value needs to be verified in further large sample-based prospective studies.

scholarly journals Acute transient cognitive dysfunction and acute brain injury induced by systemic inflammation occur by dissociable IL-1-dependent mechanisms

2017 ◽  
Author(s):  
Donal T. Skelly ◽  
Éadaoin W. Griffin ◽  
Carol L. Murray ◽  
Sarah Harney ◽  
Conor O’Boyle ◽  
...  
Keyword(s):  
Working Memory ◽  
Brain Injury ◽  
Cognitive Dysfunction ◽  
Systemic Inflammation ◽  
De Novo ◽  
Hippocampal Slices ◽  
Memory Deficits ◽  
Acute Brain Injury ◽  
Contextual Fear Conditioning

AbstractSystemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. Acute episodes of delirium also contribute significantly to rates of long-term cognitive decline, implying that de novo pathology occurs during these acute episodes. Whether systemic inflammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mechanisms has not been investigated. Here we show that systemic inflammation, induced by bacterial LPS, produces both working memory deficits and acute brain injury in the degenerating brain and that these occur by dissociable IL-1-dependent processes. In normal C57BL/6 mice, LPS (100μg/kg) did not affect working memory but robustly impaired contextual fear conditioning (CFC). However prior hippocampal synaptic loss left mice selectively vulnerable to LPS-induced working memory deficits. Systemically administered IL-1 receptor antagonist (IL-1RA) was protective against, and systemic IL-1β replicated, these working memory deficits. Although LPS-induced deficits still occured in IL-1RI-/- mice, systemic TNF-α was sufficient to induce similar deficits, indicating redundancy among these cytokines. Dexamethasone abolished systemic cytokine synthesis and was protective against working memory deficits despite failing to block brain IL-1β synthesis. Direct application of IL-1β to ex vivo hippocampal slices induced non-synaptic depolarisation and irrevesible loss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in the degenerating brain, in an IL-1RI-/- dependent-fashion. The data suggest that LPS induces working memory dysfunction via circulating IL-1β but dysfunction leading to neuronal death is mediated by hippocampal IL-1β. The data suggest that acute systemic inflammation produces both reversible cognitive deficits, resembling delirium, and acute brain injury that may lead to long-term cognitive impairment but that these events are mechanistically dissociable. This would have significant implications for management of cognitive dysfunction and decline during acute illness.

Abstract P075: Influence of Systemic Interleukin-6 on the Inverse Association between Your-Choice American Heart Diet and a 41-Year Mortality Risk from Coronary Heart Disease among Men

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Jun Dai ◽  
Anthony J Acton ◽  
Robert V Considine ◽  
Ruth E Krasnow ◽  
Terry Reed
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Systemic Inflammation ◽  
Mortality Risk ◽  
Interleukin 6 ◽  
Reactive Protein ◽  
Chd Risk ◽  
Long Term Mortality

Introduction: Whole diet evaluated using dietary pattern is associated with systemic inflammation and coronary heart disease (CHD). Systemic inflammation also contributes to CHD risk. Genetic factors explain variations in whole diet, systemic inflammation, and CHD. However, it is unknown whether systemic inflammation is a mechanism linking whole diet to the long-term mortality risk from coronary heart disease independent of genes. Hypothesis: Systemic inflammation measured as plasma interleukin-6 levels medicates the association between whole diet and long-term mortality risk from coronary heart disease independent of genes. Methods: From the National Heart, Lung, and Blood Institute Twin Study, we included 554 white, middle-aged, veteran male twins (105 monozygotic and 109 dizygotic twin pairs; 65 monozygotic and 61 dizygotic unpaired twins). The twins were not on antihypertensive medication and had diastolic blood pressure below 105 mmHg at baseline (1969-1973) and did not have suspected acute inflammation [plasma levels of interleukin-6 (IL-6) above 10 pg/mL or C-reactive protein above 30 mg/L)]. Usual dietary data at baseline were collected through nutritionist-administered dietary history interview. Your-Choice American Heart Diet (YCARD) score was devised to quantitatively evaluate whole diet. Plasma interleukin-6 and C-reactive protein levels were measured with ELISA. Data on vital status and death causes were collected through death certificates until Dec 31, 2010. A frailty survival model was used to estimate various associations: overall (equivalent to the association in the general population), within-pair (independent of genes and environment common to co-twins), and between-pair (indicating influence of the common factors). We controlled for total caloric intake and known CHD risk factors including body mass index and modified Framingham Risk Score. Results: There were 75 CHD deaths during a 41-year follow-up (median follow-up of 34 years). The adjusted overall association between YCARD score and the CHD mortality risk was negative [partial coefficient for a 10-unit increment in the YCARD score: βo (95% confidence interval (CI)): -0.13 (-0.24, -0.02); hazard ratio (95% CI): 0.88 (0.78, 0.98)]. The partial regression coefficient was -0.02 [95% CI (-0.23, 0.19)] for the within-pair effect of YCARD (βw) and -0.12 [95% CI (-0.26, 0)] for the between-pair effect of YCARD (βb) in relation to CHD mortality risk. Additional adjustment for IL-6 led to a 15.4% reduction in the βo, a 100% increment in the βw, and a 16.7% reduction in the βb. Conclusions: Systemic inflammation measured as interleukin-6 mediates the association between whole diet and long-term coronary heart mortality risk, which is largely through genetic and environmental factors shared between co-twins.

scholarly journals Long-Term Effect of Continuous Positive Airway Pressure Therapy on Inflammation Markers of Patients with Obstructive Sleep Apnea Syndrome

SLEEP ◽  
2009 ◽  
Vol 32 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Paschalis Steiropoulos ◽  
Ioannis Kotsianidis ◽  
Evangelia Nena ◽  
Venetia Tsara ◽  
Evdoxia Gounari ◽  
...  
Keyword(s):  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Sleep Apnea Syndrome ◽  
Term Effect ◽  
Inflammation Markers ◽  
Pressure Therapy ◽  
Long Term Effect ◽  
Obstructive Sleep ◽  
Apnea Syndrome

Longitudinal effects of systemic inflammation markers on periodontitis

2015 ◽  
Vol 42 (11) ◽  
pp. 988-997 ◽  
Author(s):  
Christiane Pink ◽  
Thomas Kocher ◽  
Peter Meisel ◽  
Marcus Dörr ◽  
Marcello R. P. Markus ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Inflammation Markers ◽  
Longitudinal Effects

scholarly journals Prolonged, 24-h Delayed Peripheral Inflammation Increases Short- and Long-Term Functional Impairment and Histopathological Damage after Focal Ischemia in the Rat

2010 ◽  
Vol 30 (8) ◽  
pp. 1450-1459 ◽  
Author(s):  
Kristopher D Langdon ◽  
Crystal L MacLellan ◽  
Dale Corbett
Keyword(s):  
Systemic Inflammation ◽  
Clinical Data ◽  
Experimental Studies ◽  
Artery Occlusion ◽  
Febrile Response ◽  
Behavioral Assessments ◽  
Short And Long Term ◽  
Systemic Infections ◽  
Cerebral Artery Occlusion

The incidence of infection among stroke patients is alarmingly high and both acute and delayed infections increase morbidity and mortality. Experimental studies support the acute clinical data, but little attention has focused on delayed systemic infections. Here, we investigated the effects of prolonged systemic inflammation either before or 24-h after ischemia. Systemic inflammation was induced by injecting rats with three separate doses of lipopolysaccharide (LPS; 50 μg/kg, i.p.) with core temperature monitoring for 48-h after middle cerebral artery occlusion (MCAo). Lipopolysaccharide injected before MCAo increased injury by ∼30%, whereas delayed injection increased injury by ∼85% (30-day survival). Proinflammatory cytokines assessed repeatedly for 72 h were significantly and persistently elevated with inflammation. This was accompanied by increases in microglia/macrophage and infiltrating leukocyte numbers in delayed LPS-treated animals. Behavioral assessments at 7 and 30 days revealed ∼15% deficit in hindlimb function in animals treated with LPS 24-h after ischemia. Clearly, delayed and prolonged postischemic systemic inflammation has devastating effects on stroke outcome, in the absence of a prolonged febrile response. These findings, together with corroborative clinical data, emphasize the importance of early intervention to counteract the deleterious consequences of stroke-associated inflammation and infection.

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