13 research outputs found

    The Calcium-Looping technology for CO2 capture: On the important roles of energy integration and sorbent behavior

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    The Calcium Looping (CaL) technology, based on the multicyclic carbonation/calcination of CaO in gas-solid fluidized bed reactors at high temperature, has emerged in the last years as a potentially low cost technology for CO capture. In this manuscript a critical review is made on the important roles of energy integration and sorbent behavior in the process efficiency. Firstly, the strategies proposed to reduce the energy demand by internal integration are discussed as well as process modifications aimed at optimizing the overall efficiency by means of external integration. The most important benefit of the high temperature CaL cycles is the possibility of using high temperature streams that could reduce significantly the energy penalty associated to CO capture. The application of the CaL technology in precombustion capture systems and energy integration, and the coupling of the CaL technology with other industrial processes are also described. In particular, the CaL technology has a significant potential to be a feasible CO capture system for cement plants. A precise knowledge of the multicyclic CO capture behavior of the sorbent at the CaL conditions to be expected in practice is of great relevance in order to predict a realistic capture efficiency and energy penalty from process simulations. The second part of this manuscript will be devoted to this issue. Particular emphasis is put on the behavior of natural limestone and dolomite, which would be the only practical choices for the technology to meet its main goal of reducing CO capture costs. Under CaL calcination conditions for CO capture (necessarily implying high CO concentration in the calciner), dolomite seems to be a better alternative to limestone as CaO precursor. The proposed techniques of recarbonation and thermal/mechanical pretreatments to reactivate the sorbent and accelerate calcination will be the final subjects of this review.Financial support by the Spanish Government Agency Ministerio de Economia y Competitividad (contracts CTQ2014-52763-C2-2-R and CTQ2014-52763-C2-1-R) and Andalusian Regional Government (Junta de Andalucia-FEDER contracts FQM-5735 and TEP-7858) is acknowledged

    miRNA-Mediated Epigenetic Regulation of Treatment Response in RA Patients-A Systematic Review.

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    This study aimed to evaluate the role of microRNAs (miRNA) as biomarkers of treatment response in rheumatoid arthritis (RA) patients through a systematic review of the literature. The MEDLINE and Embase databases were searched for studies including RA-diagnosed patients treated with disease-modifying antirheumatic drugs (DMARDs) that identify miRNAs as response predictors. Review inclusion criteria were met by 10 studies. The main outcome of the study was the response to treatment, defined according to EULAR criteria. A total of 839 RA patients and 67 healthy donors were included in the selected studies. RA patients presented seropositivity for the rheumatoid factor of 74.7% and anti-citrullinated C-peptide antibodies of 63.6%. After revision, 15 miRNAs were described as treatment response biomarkers for methotrexate, anti-tumour necrosis factor (TNF), and rituximab. Among treatments, methotrexate presented the highest number of predictor miRNAs: miR-16, miR-22, miR-132, miR-146a and miR-155. The most polyvalent miRNAs were miR-146a, predicting response to methotrexate and anti-TNF, and miR-125b, which predicts response to infliximab and rituximab. Our data support the role of miRNAs as biomarkers of treatment response in RA and point to DMARDs modifying the miRNAs expression. Nevertheless, further studies are needed since a meta-analysis that allows definitive conclusions is not possible due to the lack of studies in this field

    Collinsella is associated with cumulative inflammatory burden in an established rheumatoid arthritis cohort.

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    To analyze the gut microbiota of patients with rheumatoid arthritis (RA) according to disease activity. An observational cross-sectional study of 110 patients with RA and 110 age- and sex-matched controls was performed. Patients were classified according to the disease activity (DAS28 ≥3.2 or DAS28  The mean DAS28 indicated remission/low inflammatory activity in 71 patients (64.5 %) and moderate/high activity in 39 (35.5 %) during follow-up. Alpha and beta diversity analysis revealed differences in gut microbiota between the 3 study groups. In the moderate/high activity RA, we observed a significant change in the abundance of genera compared with the other groups. The abundance of Collinsella and Bifidobacterium was increased in RA patients compared with controls. The metabolic profile of gut microbiota was characterized by differences in pathways related to Biosynthesis, Generation of Precursor Metabolites/Energy, and Degradation/Utilization/Assimilation between the 3 groups. The factors associated with cumulative inflammatory activity in RA were age (OR [95 % CI], 1.065 [1.002-1.131]), obesity (OR [95% CI], 3.829 [1.064-8.785]), HAQ score (OR [95% CI], 2.729 [1.240-5.009]), and expansion of the genus Collinsella (OR [95% CI], 3.000 [1.754-9.940]). The composition of gut microbiota differed between patients with RA and moderate/high activity, patients with remission/low activity, and controls. The genus Collinsella, age, obesity, and physical function were associated with cumulative inflammatory burden in RA

    Inflammatory profile of incident cases of late-onset compared with young-onset rheumatoid arthritis: A nested cohort study.

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    To describe the characteristics of patients between late-onset rheumatoid arthritis (LORA) with young-onset (YORA), and analyze their association with cumulative inflammatory burden. We performed a nested cohort study in a prospective cohort comprising 110 patients with rheumatoid arthritis (RA) and 110 age- and sex-matched controls. The main variable was cumulative inflammatory activity according to the 28-joint Disease Activity Score with erythrocyte sedimentation rate (DAS28-ESR). High activity was defined as DAS28 ≥ 3.2 and low activity as DAS28 A total of 22/110 patients (20%) met the criteria for LORA (≥ 60 years). Patients with LORA more frequently had comorbid conditions than patients with YORA and controls. Compared with YORA patients, more LORA patients had cumulative high inflammatory activity from onset [13 (59%) vs. 28 (31%); p = 0.018] and high values for CRP (p = 0.039) and IL-6 (p = 0.045). Cumulative high inflammatory activity in patients with RA was associated with LORA [OR (95% CI) 4.69 (1.49-10.71); p = 0.008], smoking [OR (95% CI) 2.07 (1.13-3.78); p = 0.017], anti-citrullinated peptide antibody [OR (95% CI) 3.24 (1.15-9.13); p = 0.025], average Health Assessment Questionnaire (HAQ) score [OR (95% CI) 2.09 (1.03-14.23); p = 0.034], and physical activity [OR (95% CI) 0.99 (0.99-0.99); p = 0.010]. The second model revealed similar associations with inflammatory activity in patients with LORA. Control of inflammation after diagnosis is poorer and comorbidity more frequent in patients with LORA than in YORA patients and healthy controls

    Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis

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    Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis

    Inflammatory Biomarkers in the Diagnosis and Prognosis of Rheumatoid Arthritis–Associated Interstitial Lung Disease

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    This study aimed to identify inflammatory factors and soluble cytokines that act as biomarkers in the diagnosis and prognosis of rheumatoid arthritis-associated interstitial lung disease (RA-ILD). We performed a nested prospective observational case–control study of patients with RA-ILD matched by sex, age, and time since the diagnosis of RA. All participants underwent pulmonary function testing and high-resolution computed tomography. ILD was defined according to the criteria of the American Thoracic Society/European Respiratory Society; the progression of lung disease was defined as the worsening of FVC > 10% or DLCO > 15%. Inflammation-related variables included the inflammatory activity measured using the DAS28-ESR and a multiplex cytokine assay. Two Cox regression models were run to identify factors associated with ILD and the progression of ILD. The study population comprised 70 patients: 35 patients with RA-ILD (cases) and 35 RA patients without ILD (controls). A greater percentage of cases had higher DAS28-ESR (p = 0.032) and HAQ values (p = 0.003). The variables associated with RA-ILD in the Cox regression analysis were disease activity (DAS28) (HR [95% CI], 2.47 [1.17–5.22]; p = 0.017) and high levels of ACPA (HR [95% CI], 2.90 [1.24–6.78]; p = 0.014), IL-18 in pg/mL (HR [95% CI], 1.06 [1.00–1.12]; p = 0.044), MCP-1/CCL2 in pg/mL (HR [95% CI], 1.03 [1.00–1.06]; p = 0.049), and SDF-1 in pg/mL (HR [95% CI], 1.00 [1.00–1.00]; p = 0.010). The only variable associated with the progression of ILD was IL-18 in pg/mL (HR [95% CI], 1.25 [1.07–1.46]; p = 0.004). Our data support that the inflammatory activity was higher in patients with RA-ILD than RA patients without ILD. Some cytokines were associated with both diagnosis and poorer prognosis in patients with RA-ILD

    Data_Sheet_1_Inflammatory profile of incident cases of late-onset compared with young-onset rheumatoid arthritis: A nested cohort study.docx

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    ObjectivesTo describe the characteristics of patients between late-onset rheumatoid arthritis (LORA) with young-onset (YORA), and analyze their association with cumulative inflammatory burden.MethodsWe performed a nested cohort study in a prospective cohort comprising 110 patients with rheumatoid arthritis (RA) and 110 age- and sex-matched controls. The main variable was cumulative inflammatory activity according to the 28-joint Disease Activity Score with erythrocyte sedimentation rate (DAS28-ESR). High activity was defined as DAS28 ≥ 3.2 and low activity as DAS28 ResultsA total of 22/110 patients (20%) met the criteria for LORA (≥ 60 years). Patients with LORA more frequently had comorbid conditions than patients with YORA and controls. Compared with YORA patients, more LORA patients had cumulative high inflammatory activity from onset [13 (59%) vs. 28 (31%); p = 0.018] and high values for CRP (p = 0.039) and IL-6 (p = 0.045). Cumulative high inflammatory activity in patients with RA was associated with LORA [OR (95% CI) 4.69 (1.49–10.71); p = 0.008], smoking [OR (95% CI) 2.07 (1.13–3.78); p = 0.017], anti–citrullinated peptide antibody [OR (95% CI) 3.24 (1.15–9.13); p = 0.025], average Health Assessment Questionnaire (HAQ) score [OR (95% CI) 2.09 (1.03–14.23); p = 0.034], and physical activity [OR (95% CI) 0.99 (0.99–0.99); p = 0.010]. The second model revealed similar associations with inflammatory activity in patients with LORA.ConclusionControl of inflammation after diagnosis is poorer and comorbidity more frequent in patients with LORA than in YORA patients and healthy controls.</p

    Longitudinal Study of Cognitive Functioning in Adults with Juvenile Idiopathic Arthritis

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    Objective: To prospectively evaluate possible decline of cognitive functions in adult patients with juvenile idiopathic arthritis (JIA) and identify associated factors. Patients and methods: We performed a 24-month prospective observational study of adults (&ge;16 years) with JIA. The primary outcome measure was decline in cognitive function defined as a worsening of &ge;2 points on the scales of the subsets administered to evaluate the different cognitive areas using the Wechsler Adult Intelligence Scale (WAIS) after 24 months: attention/concentration (digit span); verbal function (vocabulary); visual-spatial organization (block design); working memory (letter-number sequencing); and problem solving (similarities). Other variables included average inflammatory activity using C-reactive protein and composite activity indexes, comorbidity, and treatment. Logistic regression was performed to identify factors associated with cognitive decline. Results: The study population comprised 52 patients with JIA. Of these, 15 (28.8%) had cognitive decline at V24. The most affected functions were working memory (17.3%), attention/concentration (9.6%), verbal function (7.7%), visual-spatial organization (7.7%), and problem solving (3.8%). There were no significant differences in the median direct or scale scores for the cognitive functions evaluated between V0 and V24 for the whole sample. The factors associated with cognitive decline in patients with JIA were average C-reactive protein (OR [95% CI], 1.377 [1.060&ndash;1.921]; p = 0.039), depression (OR [95% CI], 3.691 [1.294&ndash;10.534]; p = 0.015), and treatment with biologics (OR [95% CI], 0.188 [0.039&ndash;0.998]; p = 0.046). Conclusion: Cognitive decline was detected in almost one third of adults with JIA after 24 months of follow-up. Systemic inflammatory activity in JIA patients was related to cognitive decline. Patients treated with biologics had a lower risk of decline in cognitive functions

    Preconditioning by portal vein embolization modulates hepatic hemodynamics and improves liver function in pigs with extended hepatectomy

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    Background. Portal vein embolization is performed weeks before extended hepatic resections to increase the future liver remnant and prevent posthepatectomy liver failure. Portal vein embolization performed closer to the operation also could be protective, but worsening of portal hyper-perfusion is a major concern. We determined the hepatic hemodynamic effects of a portal vein embolization performed 24 hours prior to hepatic operation. Methods. An extended (90%) hepatectomy was performed in swine undergoing (portal vein embolization) or not undergoing (control) a portal vein embolization 24 hours earlier (n = 10/group). Blood tests, hepatic and systemic hemodynamics, hepatic function (plasma disappearance rate of indocyanine green), liver histology, and volumetry (computed tomographic scanning) were assessed before and after the hepatectomy. Hepatocyte proliferating cell nuclear antigen expression and hepatic gene expression also were evaluated. Results. Swine in the control and portal vein embolization groups maintained stable systemic hemodynamics and developed similar increases of portal blood flow (302 ± 72% vs 486 ± 92%, P = .13). Portal pressure drastically increased in Controls (from 9.4 ± 1.3 mm Hg to 20.9 ± 1.4 mm Hg, P < .001), while being markedly attenuated in the portal vein embolization group (from 11.4 ± 1.5 mm Hg to 16.1 ± 1.3 mm Hg, P = .061). The procedure also improved the preservation of the hepatic artery blood flow, liver function, and periportal edema. These effects occurred in the absence of hepatocyte proliferation or hepatic growth and were associated with the induction of the vasoprotective gene Klf2. Conclusion. Portal vein embolization preconditioning represents a potential hepato-protective strategy for extended hepatic resections. Further preclinical studies should assess its medium-term effects, including survival. Our study also supports the relevance of hepatic hemodynamics as the main pathogenetic factor of post-hepatectomy liver failure.MinecoISCIII-Fondos FEDERSociedad Española de Trasplante HepáticoDepto. de Farmacología y ToxicologíaFac. de VeterinariaTRUEpu
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