reactive protein (CRP)

For Peer Review Page 4 sur 23 colitis, but found conflicting results when evaluating procalcitonin as a biological marker of disease activity. 9, 10 Only one study evaluated the diagnostic value of SPL in determining disease activity in IBD, but included a relative small number of patients with Crohn’s disease (CD), which prevents to draw conclusions. 11 Furthermore, none of the aforementioned studies evaluated the correlation of procalcitonin with endoscopic and radiological markers of IBD activity. 9-11 Finally, the additional diagnostic benefit of SPL evaluation to that of C-reactive protein (CRP) has never been evaluated in IBD.

5 INRA, UMR 1019, UNH, CRNH Auvergne, F-63000 Clermont-Ferrand, France (Submitted 23 May 2012 – Final revision received 21 November 2012 – Accepted 21 November 2012 – First published online 10 January 2013) Abstract Inflammation mediates several chronic diseases. Micronutrients can act on inflammation, either through modulating cytokine production or by scavenging by-products of activated white cells. Identifying dietary patterns (DP) reflecting these mechanisms and relating them to inflammation is of interest. The objective of the study was to identify DP specifically associated with intakes of nutrients potentially involved in inflammatory processes in a middle-aged population and investigate long-term associations between these DP and C-reactive protein (CRP) status assessed several years later. Subjects included in the Supplementation in Vitamins and Mineral Antioxidants 2 cohort study, having available data on dietary assessment carried out in 1994 – 5 and CRP measurement in 2007 – 9, were included in the analysis. DP were extracted with reduced rank regression (RRR), using antioxidant micronutrients and PUFA as response variables. Associations between CRP measurements . 3 mg/l and extracted DP were then examined with logistic regression models providing OR and 95 % CI. A total of 2031 subjects (53·2 % women, mean follow-up duration: 12·5 years) were included in the analyses. Of the four extracted DP, a DP with high loading values of vegetables and vegetable oils, leading to high intakes of antioxidant micronutrients and essential fatty acids, was significantly and negatively associated with risk of elevated CRP (OR 0·88; 95 % CI 0·78, 0·98). Conversely, a DP reflecting a high n-6:n-3 fatty acid intake ratio was positively and significantly associated with elevated CRP (adjusted OR 1·15; 95 % CI 1·00, 1·32). DP extracted with RRR provide support for further exploration of relationships between dietary behaviour and inflammation.

Methods: Retrospective study. C-reactive protein concentrations and thoracic radio- graphs were available for each dog. Results: Eleven dogs with Bb infection had alveolar lesions. In all dogs, CRP concentra- tion was mildly increased (14-38 mg/L). In the 5 dogs without alveolar lesions, CRP concentration was within the reference range in all but 1 dog, in which it was slightly increased. Median CRP concentration was significantly higher in dogs with alveolar lesions (20 mg/L) compared with dogs without alveolar lesions (5 mg/L; p < .002). In dogs with Bb infection, median duration of clinical signs was not different between dogs with normal CRP concentration and dogs with increased concentration. In dogs with Bb infection either with or without alveolar lessions, median CRP concentration was significantly lower (20 mg/L) than in dogs with ABP (118 mg/L; p < .001).

In 2001, we performed a new series of biochemical measurements from the plasma samples collected at baseline and kept frozen at –80°C. Plasma albumin, prealbumin, orosomucoid and highly sensitive C-reactive protein (CRP, from 0.5 to 20 mg/l) was determined by latex-enhanced immunoturbidimetric method on a Olympus AU2700 biochemistry analyser (Rungis, France). Serum Protein Multi-calibrator and System Reagent particularly for CRP latex (CRP, OSR 6185) was from Olympus (Rungis, France). Calibration for CRP was performed once a week and once a fortnight respectively. The total intra assay and the total inter assay variation coefficients for serum CRP , the CV intra assay and inter assay were 3.3 % and 2.6 % respectively [13]. According to a previous study on intra-individual variability [14] and to the recommendations of the American Heart Association [15], CRP >10 mg/l were excluded in from the statistical analysis.

Surgeons lack predictive accuracy for anastomotic leakage in gastrointestinal surgery (4). Routine imaging is neither reliable nor cost-effective for the detection of leaks and it carries the drawback of radiation. A serum marker would have great advantages provided that it is cost-effective and sensitive enough to allow safe discharge of the patient. C-reactive protein (CRP) has been used for the diagnosis of intra-abdominal surgical infection (5), as a general marker of an unfavorable postoperative course including surgical and nonsurgical

Figure 1 | Kaplan – Meier estimate of survival in hemodialysis patients with serum C-reactive protein (CRP) levels in the highest quartile, middle two quartiles, and lowest quartile. * P = 0.0015 vs CRP < 2.6  g / ml; * * P = 0.0090 vs CRP < 2.6  g / ml; † P = 0.0028 vs CRP 2. 6 – 5.2  g / ml; ‡ P = 0.0012 vs CRP < 5.3 – 11.5  g / ml; § P = 0.0001 vs CRP < 2.6  g / ml. (Adapted with permission

Anika Alberts 1 , Annika Klingberg 1 , Anne Kathrin Wessig 1 , Christèle Combes 2 , torsten Witte 3 , Korbinian Brand 1 , Andreas Pich 4 & Konstantin neumann 1* Gout is caused by crystallization of uric acid in the form of monosodium urate (MSU) crystals, which induce a sterile inflammatory response that is hardly distinguishable from microbe-induced inflammatory responses. It is unclear, if MSU crystals (like microbes) are recognized by specific pattern recognition receptors. To identify possible soluble pattern recognition molecules for MSU crystals, we purified MSU-binding proteins from human body fluids. We identified C-reactive protein (CRP) as a major MSU-binding protein. Binding of CRP was strong enough to specifically deplete CRP from human serum. We found that CRP was required for fixation of complement components C1q, C1r, C1s and MASP1. Thus, we have identified a pattern recognition molecule for MSU crystals that links to the activation of complement. Notably, CRP does not show an even binding to the complete surface of the crystals. It rather binds to edges or distinct faces of the crystals.

ANOVA to examine differences in baseline characteristics between non-medicated and medicated groups. C-reactive protein was log transformed to normalise the data and we excluded any participants reporting an acute infection (bronchitis, influenza, etc) in the 3 weeks prior to the nurse visit since this may contribute to elevated levels of CRP.

Gout is caused by crystallization of uric acid in the form of monosodium urate (MSU) crystals, which induce a sterile inflammatory response that is hardly distinguishable from microbe-induced inflammatory responses. It is unclear, if MSU crystals (like microbes) are recognized by specific pattern recognition receptors. To identify possible soluble pattern recognition molecules for MSU crystals, we purified MSU-binding proteins from human body fluids. We identified C-reactive protein (CRP) as a major MSU-binding protein. Binding of CRP was strong enough to specifically deplete CRP from human serum. We found that CRP was required for fixation of complement components C1q, C1r, C1s and MASP1. Thus, we have identified a pattern recognition molecule for MSU crystals that links to the activation of complement. Notably, CRP does not show an even binding to the complete surface of the crystals. It rather binds to edges or distinct faces of the crystals.

Changqin Chen, Molei Yan, Caibao Hu, Xiaochun Lv, Huihui Zhang, Shangzhong Chen > Objective: The aim of this study was to evaluate the diagnostic efficacy of serum procalcitonin (PCT), c-reactive protein (CRP) concentration and clinical pulmonary infection score(CPIS) in ventila- tor-associated pneumonia(VAP). Methods: Forty- nine patients who were admitted to the intensive care unit (ICU) of Zhejiang Hospital with suspected VAP were recruited in this study. The serum level of PCT and CRP of all patients were measured and CPIS was calculated at the time of VAP suspected diagnosis. Of the included 49 patients, 24 were finally confirmed of VAP by microbiology assay. And the other 25 patients were considered as cli- nical suspected VAP without microbiology confir- mation. The diagnostic sensitivity, specificity and area under the receiver operating characteristic (ROC) curve (AUC) were calculated using the serum PCT, CRP concentration and CPIS. The correlation among serum PCT, CRP concentration and CPIS were also evaluated by Spearson correlation test. Results: A total of 100 bronchoscopic aspira- tion sputum specimen were examined in bacterial culture. 30 samples were found with suspected pathogenic bacteria. Six samples were found with 2 types of suspected pathogenic bacteria. PCT serum concentration and CPIS score were significantly different (P<0.05) between the patient group [1.4 (0.68 ∼ 2.24), 6.0 (4.25 ∼ 8.00)] and the control group [0.4 (0.17 ∼ 1.39), 3.0 (1.00 ∼ 5.00)] ; However, the serum CRP [102.8(66.75 ∼ 130.90) vs 86.1(66.95 ∼ 110.10)] was not statistically dif- ferent between the two groups (P>0.05). A signi- ficant correlation was found between serum PCT and CRP concentrations (r=0.55, P<0.01), but not between PCT vs CPIS and CRP vs CPIS (p>0.05). The diagnostic sensitivity, specificity and AUC were 72.0%, 75.0%, 0.81 (0.69 ∼ 0.93) for CPIS; 60.0%, 87.5%, 0.76 (0.62 ∼ 0.90) for PCT and 68.0%,

stimulates neuro-inflammatory processes with neurotoxic effects that exacerbate neuronal damage. There is also evidence that circulating levels of inflammatory markers are raised before clinical onset of dementia; for instance, in nondemented persons, interleukin-6 (IL-6) and C- reactive protein (CRP) have been shown to predict dementia.(4-6) However, given the long preclinical phase of dementia(7) it is unclear whether peripheral inflammation is a by-product of neuropathology or whether it contributes to neuronal damage.

Centre for Research on Ageing, Health and Wellbeing, Research School of Population Health, ANU College of Medicine, Biology and Environment at the Australian National University, Canberra, Australia. [Received January 24, 2018; Revised March 13, 2018; Accepted March 29, 2018] ABSTRACT: Chronic systemic low-grade inflammation is associated with aging, but little is known on whether age-related inflammation affects brain structure, particularly white matter. The current study tested the hypothesis that in older adults without dementia, higher serum levels of high-sensitivity C-reactive protein (hs- CRP) are associated with reduced corpus callosum (CC) areas. French community-dwelling subjects (ESPRIT study) aged 65 and older (N=101) underwent hs-CRP testing and structural magnetic resonance imaging (MRI). Multiple linear regression models were carried out. In the unadjusted model, higher hs-CRP level was significantly associated with smaller anterior, mid, and total midsagittal CC areas, but not with the posterior CC area. These associations were independent of demographic characteristics and intracranial volume. After adjustment for body mass index, diabetes, inflammation-related chronic pathologies and white matter lesions (WML), only the associations between hs-CRP level and smaller anterior and total midsagittal CC areas were still significant, although weaker. These findings suggest that low-grade inflammation is associated with CC structural integrity alterations in older adults independently of physical or neuropsychiatric pathologies.

In our analyses adjusted for longstanding illness and major cardiometabolic risk factors, associations between decreased sleep and C-reactive protein and interleukin-6 were reduced, indicating that poor sleep may result in part from disease processes involving in flammation. However, these analyses also suggest a role for interleukin-6 outside the disease pro- cess. Such an effect is biologically plausible, because exper- iments suggest that prolonged sleep deprivation in rats is associated with an evolving proin flammatory state ( 28 ), and studies in humans show that total sleep deprivation is associ- ated speci fically with increasing circulating levels of inter- leukin-6 ( 29 ). More common forms of sleep loss, such as reductions of 25% –50% across consecutive nights, appear to induce an increase in interleukin-6 and C-reactive protein levels ( 30 – 32 ), and increased levels of interleukin-6 are found in patients with primary insomnia ( 33 , 34 ). Morning levels of nuclear-factor kappa beta (a protein complex linked to in flammatory response) activation, are higher after a night of sleep loss, potentially identifying nuclear-factor kappa beta transcription pathways as the molecular mechanism by which sleep in fluences the production of interleukin-6 and other in flammatory cytokines ( 35 ). Although relative increases in in flammatory markers in experimental studies are tiny, small basal shifts are consistent with levels of elevation seen in

c o r r e s p o n d e nc e Rosuvastatin in Patients with Elevated C-Reactive Protein To the Editor: Ridker et al. (Nov. 20 issue) re- port the results of Justification for the Use of Stat- ins in Prevention: an Intervention Trial Evaluat- ing Rosuvastatin (JUPITER), 1 which showed that rosuvastatin significantly reduced cardiovascular events in patients with elevated levels of C-reac- tive protein. However, broad application of their results in primary prevention is premature, since the baseline therapy that many patients in the study were receiving did not meet existing standards. Although about 50% of the patients had interme- diate Framingham risk scores, which would have qualified such men (and possibly women) for as- pirin therapy, 2,3 only 16.6% of the patients were receiving aspirin. One quarter of the patients had a systolic blood pressure of at least 145 mm Hg, indicating that their hypertension was not being treated according to existing national goals. 4 Al- most 16% of the patients were current smokers.

ACS: Acute coronary syndrome; CVD: Cardiovascular disease; CAD: Coronary artery disease; hsCRP: High sensitivity C reactive protein; MDD: Major depression disorder; MINI: Mini-internatio[r]

Taken together, we can hypothesize that the development of low-grade, chronic inflammation in elderly individuals could explain the decrease in the PP anabolic effect of food intake and also explain the development of sarcopenia. However, this has not been demonstrated in elderly humans considered to be healthy and free of any established disease. Furthermore, the inflammatory status is usually assessed by the measurement of CRP in humans. CRP is a homo- pentameric acute-phase protein produced by the liver. Its levels rise dramatically during inflammation. This increase in plasma CRP is the result of a rise in the plasma concentration of IL-6, produced predominantly by macrophages and adipocytes. CRP is a general non-specific marker for inflammation and infection. A large number of studies have shown that the development of chronic, silent, low-level inflammation plays a pivotal role in the increase in the risk of many age-related diseases (Ansar & Ghosh, 2013). The present study aimed to show whether a moderate, chronic increase of CRP may be related to an impaired muscle anabolic effect of food intake and, ultimately, be predictive of sarcopenia in healthy, aged volunteers.

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Patients with blood eosinophilia and systemic manifestations were divided into three study groups for comparison of their respective clinical and biological characteristics: ANCA+ pati[r]

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Abstract Model-driven applications may maintain large networks of structured data mod- els and transformations among them. The development of such applications is complicated by the need to reflect on the whole network any runtime up- date performed on models or transformation logic. If not carefully designed, the execution of such updates may be computationally expensive. In this pa- per we propose a reactive paradigm for programming model transformations, and we implement a reactive model-transformation engine. We argue that this paradigm facilitates the development of autonomous model-driven systems that react to update and request events from the host application by identifying and performing only the needed computation. We implement such approach by pro- viding a reactive engine for the ATL transformation language. We evaluate the usage scenarios that this paradigm supports and we experimentally measure its ability to reduce computation time in transformation-based applications. Keywords: Model-Driven Engineering, Model Transformations, Reactive Programming