Neutron induced reactions on 26Al, 36Cl and 41Ca and their astrophysical implications

Neutron induced reactions on 26Al, 36Cl and 41Ca and their astrophysical implications In this work (n,p) and (n,alpha) reactions on 26Al, 36Cl and 41Ca are studied as a function of the neutron energy. The measurements were performed at the high resolution GELINA time-of-flight facility of the IRMM in Geel, Belgium. Besides the nuclear physics information obtained from the resonance analysis of the reaction cross sections, these reactions are of importance in the understanding of the observed 36S and 26Al solar abundances. In the case of 26Al, the 26Al(n,alpha)23Na cross section up to 45 keV has been determined. Six resonances are observed. For three of them, the total level width and the spin could be calculated. For most of the resonances the obtained resonance parameters are in agreement with previous data. The calculated Maxwellian Averaged Cross Section values (MACS) used in stellar model calculations confirm that 26Al is indeed severely depleted by neutron captures in AGB stars. In the (n,p) and (n,alpha) measurements on 36Cl, eighteen resonances are observed in the energy region up to 250 keV, whereas eight were identified before. Only the lowest energy resonance shows a significant (n,alpha)-contribution of (76+-7)%, which is in perfect agreement with the value reported before. Furthermore, for four resonances, the resonance strength, spin, total and partial width Gamma_p could be determined. They are in good agreement with previous data, but the achieved accuracy is better. The calculated MACS values are used in stellar model calculations to trace the origin of 36S and reveal that the weak component of the s-process occurring in massive stars accounts for almost the entire production of solar 36S. The 41Ca(n,alpha)38Ar measurement is the first ever reported in the resonance region and affects the 36S abundance through 41Ca(n,alpha)38Ar(n,gamma)39Ar(n,alpha)36S. Twelve resonances are observed in the energy region up to 45 keV. For most of them the area, the total width, the spin and a value for Gamma_n/Gamma_p could be determined. After extension of the energy range, with a complementary measurement at the GELINA facility, the calculated MACS values will be used in stellar models

Chronic smoke exposure is associated with autophagy in murine Peyer's patches

INTRODUCTION: Cigarette smoke causes oxidative stress, leading to smoke-induced autophagy in several organs. Autophagy is a homeostatic process regulating the turnover of proteins and cytoplasmatic organelles. However, recently it has also been associated with many autoimmune and inflammatory disorders, among which Crohn’s disease. The purpose of the present study was to investigate whether cigarette smoke exposure is associated with increased autophagy in Peyer’s patches and its epithelium. AIMS & METHODS: C57BL/6 mice were exposed to cigarette smoke or air. After 24 weeks, the animals were sacrificied and Peyer’s patches were collected. m RNA expression of autophagy-related genes was determined by RT-PCR. Transmission electron microscopy (TEM) was used to evaluate the presence of autophagic vesicles in the follicleassociated epithelium of Peyer’s patches. RESULTS: Expression of Beclin-1, a protein involved in the nucleation of autophagosomes, and of Atg5 and Atg7, which both play a role in the autophagosome vesicle elongation and completion, increased after chronic smoke exposure. Furthermore, electron microscopy of the follicle-associated epithelium demonstrated that the mean area of autophagic vesicles per epithelial cell increased considerably from 1.1 μm2 ± 0.4 μm2 in the air group to 2.4 μm2 ± 0.4 μm2 in the smoke group (p < 0.05). Epithelial cells had a significantly higher number of autophagic vesicles after smoke exposure (1.1 ± 0.1 after smoke exposure versus 0.5 ± 0.1 vesicles per cell after air exposure, p < 0.05), but the size of the vesicles did not differ between both groups. CONCLUSION: Here we provide the first evidence that chronic exposure to cigarette smoke is associated with autophagy in murine Peyer’s patches, and more in particular in the follicle-associated epithelium covering Peyer’s patches. Our findings can help to understand the role of smoking in the pathogenesis of inflammatory bowel disease, such as Crohn’s disease

Measurement of the U-236(n, f) cross section in the neutron energy range from 0.5 eV up to 25 keV

The U-236(n,f) cross section has been measured in the energy range from 0.5 eV to 25 keV at the Geel Electron Linear Accelerator neutron time-of-flight facility of the Institute for Reference Materials and Measurements in Geel, Belgium. A highly enriched U-236 sample was mounted back-to-back with a B-10 sample in the center of a Frisch-gridded ionization chamber, hence realizing a 2 pi detection geometry. A U-235(n,f) cross-section control measurement was performed in the same experimental conditions. Special attention has been given to the fission resonance integral I-f and to the strongest resonance at 5.45 eV, for which a resonance analysis has been performed yielding Gamma(f) = 1.7 mu eV Both values are highly overestimated in the literature

Comparison of methods to estimate the affected body surface area and the dosage of topical treatments in psoriasis and atopic dermatitis : the advantage of a picture‐based tool

Background: The accurate determination of the dosage of topical treatments is important given its repercussions on patient adherence and therapeutic efficacy. Up till now, the fingertip unit calculated by the rule of hands is considered the gold standard, although its use is associated with several drawbacks. Objective: To compare different methods to estimate the affected body surface area (BSA) and dosage of topical treatments in atopic dermatitis and psoriasis and investigate its reliability, user-friendliness and timing. Methods: In this study, we compared the reliability of three different methods: (i) the fingertip unit calculated by the 1% hand rule; (ii) a picture-based tool [termed Cutaneous Inflammatory Disease Extent Score (CIDES)]; and (iii) a digital drawing tool. Eleven observers scored 40 patients with psoriasis and eczema to assess the inter-rater and intrarater reliability. Timing was automatically recorded, and user-friendliness was investigated by a questionnaire. Results: An excellent intraclass correlation (ICC) was found for both inter-rater agreement and intrarater agreement for the picture-based tool (ICC = 0.92 and ICC = 0.96, respectively). The ICCs for drawing the area of involvement on a silhouette were 0.89 and 0.93, respectively. Finally, the rule of hands was associated with an increased inter-rater variability although an excellent intrarater agreement was found (ICC = 0.79 and 0.95, respectively). Automated calculation of the amount of topical treatment improved reliability, and CIDES was associated with the least variation. CIDES was considered the preferred method by all observers and was fast to perform (median: 30 s). Conclusion: A picture-based method offered the most advantages (in terms of reliability, speed and user-friendliness) to estimate the affected BSA and calculate the dosage of topical treatments

Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease

Crohn's disease is a pathological condition of the gastro-intestinal tract, causing severe transmural inflammation in the ileum and/or colon. Cigarette smoking is one of the best known environmental risk factors for the development of Crohn's disease. Nevertheless, very little is known about the effect of prolonged cigarette smoke exposure on inflammatory modulators in the gut. We examined the effect of cigarette smoke on cytokine profiles in the healthy and inflamed gut of human subjects and in the trinitrobenzene sulphonic acid mouse model, which mimics distal Crohn-like colitis. In addition, the effect of cigarette smoke on epithelial expression of transient receptor potential channels and their concurrent increase with cigarette smoke-augmented cytokine production was investigated. Active smoking was associated with increasedIL-8transcription in ileum of controls (p < 0,001; n = 18-20/group). In the ileum, TRPV1 mRNA levels were decreased in never smoking Crohn's disease patients compared to healthy subjects (p <0,001; n = 20/group). In the colon, TRPV1 mRNA levels were decreased (p = 0,046) in smoking healthy controls (n = 20/group). Likewise, healthy mice chronically exposed to cigarette smoke (n = 10/group) showed elevated ilealCxcl2(p = 0,0075) and colonicKcmRNA levels (p = 0,0186), whereas TRPV1 mRNA and protein levels were elevated in the ileum (p = 0,0315). Although cigarette smoke exposure prior to trinitrobenzene sulphonic acid administration did not alter disease activity, increased pro-inflammatory cytokine production was observed in the distal colon (Kc: p = 0,0273; Cxcl2: p = 0,104; Il1-beta: p = 0,0796), in parallel with the increase ofTrpv1mRNA (p < 0,001). We infer that CS affects pro-inflammatory cytokine expression in healthy and inflamed gut, and that the simultaneous modulation of TRPV1 may point to a potential involvement of TRPV1 in cigarette smoke-induced production of inflammatory mediators

EULAR definition of arthralgia suspicious for progression to rheumatoid arthritis

Copyright © 2017 BMJ Publishing Group Ltd & European League Against Rheumatism. All rights reserved.Background: During the transition to rheumatoid arthritis (RA) many patients pass through a phase characterised by the presence of symptoms without clinically apparent synovitis. These symptoms are not well-characterised. This taskforce aimed to define the clinical characteristics of patients with arthralgia who are considered at risk for RA by experts based on their clinical experience. Methods: The taskforce consisted of 18 rheumatologists, 1 methodologist, 2 patients, 3 health professionals and 1 research fellow. The process had three phases. In phase I, a list of parameters considered characteristic for clinically suspect arthralgia (CSA) was derived; the most important parameters were selected by a three-phased Delphi approach. In phase II, the experts evaluated 50 existing patients on paper, classified them as CSA/no-CSA and indicated their level of confidence. A provisional set of parameters was derived. This was studied for validation in phase III, where all rheumatologists collected patients with and without CSA from their outpatient clinics. Results: The comprehensive list consisted of 55 parameters, of which 16 were considered most important. A multivariable model based on the data from phase II identified seven relevant parameters: symptom duration <1 year, symptoms of metacarpophalangeal (MCP) joints, morning stiffness duration ≥60 min, most severe symptoms in early morning, first-degree relative with RA, difficulty with making a fist and positive squeeze test of MCP joints. In phase III, the combination of these parameters was accurate in identifying patients with arthralgia who were considered at risk of developing RA (area under the receiver operating characteristic curve 0.92, 95% CI 0.87 to 0.96). Test characteristics for different cut-off points were determined. Conclusions: A set of clinical characteristics for patients with arthralgia who are at risk of progression to RA was established.info:eu-repo/semantics/publishedVersio

The effect of cigarette smoke exposure on the development of inflammation in lungs, gut and joints of TNFΔARE mice

The inflammatory cytokine TNF-alpha is a central mediator in many immune-mediated diseases, such as Crohn's disease (CD), spondyloarthritis (SpA) and chronic obstructive pulmonary disease (COPD). Epidemiologic studies have shown that cigarette smoking (CS) is a prominent common risk factor in these TNF-dependent diseases. We exposed TNF Delta ARE mice; in which a systemic TNF-alpha overexpression leads to the development of inflammation; to 2 or 4 weeks of air or CS. We investigated the effect of deregulated TNF expression on CS-induced pulmonary inflammation and the effect of CS exposure on the initiation and progression of gut and joint inflammation. Upon 2 weeks of CS exposure, inflammation in lungs of TNF Delta ARE mice was significantly aggravated. However, upon 4 weeks of CS-exposure, this aggravation was no longer observed. TNF Delta ARE mice have no increases in CD4+ and CD8+ T cells and a diminished neutrophil response in the lungs after 4 weeks of CS exposure. In the gut and joints of TNF Delta ARE mice, 2 or 4 weeks of CS exposure did not modulate the development of inflammation. In conclusion, CS exposure does not modulate gut and joint inflammation in TNF Delta ARE mice. The lung responses towards CS in TNF Delta ARE mice however depend on the duration of CS exposure

Pediatric burns in Brussels: The use of a new scar scoring system and its clinical applications in the evaluation of long term results

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Post-irradiation Sarcoma.

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