[Professional fatigue syndrome (burnout) : Part 2 : from therapeutic management]. / Syndrome de fatigue professionnelle (burnout) 2ème partie : de la prise en charge thérapeutique.

Burnout or professional fatigue syndrome is the result of exposure to a situation in which the strategies of the subject who are supposed to manage the stresses of the environment become outdated and inoperative. An imbalance is created between the demands and the material, operational and psychological resources to cope with them. Many health professions are confronted with the challenge of managing burnout, but the general practitioner is very often on the front line. After a first article devoted to the epidemiology, diagnosis, causes and consequences of the burnout, this second article is focusing on its therapeutic management, through listening, sick leave, dietary supplements, antidepressants, behavioural and cognitive therapy, professional coaching and multidisciplinary approach.

on disponible Résumé : Le burnout ou syndrome de fatigue professionnelle est le résultat de l'exposition à une situation durant laquelle les stratégies du sujet, qui sont censées gérer les stress de l'environnement, deviennent dépassées et inopérantes. Un déséquilibre se crée entre l'exigence des demandes et les ressources matérielles, opérationnelles et psychologiques pour y faire face. De nombreuses professions de santé se trouvent confrontées au défi de la prise en charge du burnout, dont le médecin généraliste. Après un premier article dédié à l'épidémiologie, au diagnostic, aux causes et aux conséquences du burnout, ce second article est consacré à la prise en charge de ce syndrome. Il se centre sur la prise en charge thérapeutique par l'écoute, l'interruption du temps de travail, les compléments alimentaires, les antidépresseurs, la thérapie comportementale et cognitive, le coaching professionnel et l'approche multidisciplinaire.

[Professional fatigue syndrome (burnout). Part 1 : identification by the general practitioner]. / Syndrome de fatigue professionnelle (burnout) 1ère partie : de l'identification par le médecin généraliste.

Burnout or professional fatigue syndrome has never been more talked about than in recent times. It is the result of exposure to a situation in which the strategies of the subject who are supposed to manage the stresses of the environment become outdated and inoperative. An imbalance is created between the demands and the material, operational and psychological resources to cope with them. Many health professions are confronted with the challenge of managing burnout. Among them, the general practitioner is very often on the front line. This paper is dedicated to him in priority. In its first part, it deals successively with the classification of the pathology (ICD-10 and DSM-5), its prevalence, its socio-economic impacts, its clinical picture (three stages), its diagnosis (by clinic and questionnaires), its causes, its evolution (from denial to acceptance), and its long-term consequences in the absence of treatment.

Le burnout ou syndrome de fatigue professionnelle n'a jamais autant fait parler de lui que ces derniers temps. Il est le résultat de l'exposition à une situation durant laquelle les stratégies du sujet, qui sont censées gérer les stress de l'environnement, deviennent dépassées et inopérantes. Un déséquilibre se crée entre l'exigence des demandes et les ressources matérielles, opérationnelles et psychologiques pour y faire face. De nombreuses professions de santé se trouvent confrontées au défi de la prise en charge du burnout. Parmi celles-ci, le médecin généraliste est très souvent en première ligne. Cet article s'adresse à lui en priorité. Dans ce premier volet, il traite successivement de la classification de la pathologie (ICD-10 et DSM-5), de sa prévalence, de ses impacts socio-économiques, de son tableau clinique (trois stades), de son diagnostic (par la clinique et les questionnaires), de ses causes, de son évolution (du déni à l'acceptation) et de ses conséquences à long terme en l'absence de traitement.

Novel post-digest isotope coded protein labeling method for phospho- and glycoproteome analysis.

In the field of proteomics there is an apparent lack of reliable methodology for quantification of posttranslational modifications. Present study offers a novel post-digest ICPL quantification strategy directed towards characterization of phosphorylated and glycosylated proteins. The value of the method is demonstrated based on the comparison of two prostate related metastatic cell lines originating from two distinct metastasis sites (PC3 and LNCaP). The method consists of protein digestion, ICPL labeling, mixing of the samples, PTM enrichment and MS-analysis. Phosphorylated peptides were isolated using TiO(2), whereas the enrichment of glycosylated peptides was performed using hydrazide based chemistry. Isolated PTM peptides were analyzed along with non enriched sample using 2D-(SCX-RP)-Nano-HPLC-MS/MS instrumentation. Taken together the novel ICPL labeling method offered a significant improvement of the number of identified (∼600 individual proteins) and quantified proteins (>95%) in comparison to the classical ICPL method. The results were validated using alternative protein quantification strategies as well as label-free MS quantification method. On the biological level, the comparison of PC3 and LNCaP cells has shown specific modulation of proteins implicated in the fundamental process related to metastasis dissemination. Finally, a preliminary study involving clinically relevant autopsy cases reiterated the potential biological value of the discovered proteins.

Validation of the CALUX bioassay for PCDD/F analyses in human blood plasma and comparison with GC-HRMS.

Following the dioxin crisis of 1999, several studies were conducted to assess the impact of this crisis on the dioxin body burden in the Belgian population. The Scientific Institute of Public Health identified a population from whom plasma samples were available and from whom, during the follow up survey, plasma samples were obtained in 2000. In total, 496 samples were collected for GC-HRMS and CALUX analyses to verify statistical assessment conclusions. This study was seen as an opportunity to validate the CALUX bioassay for biological sample analysis and to compare toxic equivalency (TEQ) values obtained by the reference GC-HRMS technique and by the screening method. This article focuses on the validation results of the CALUX bioassay for the analyses of the dioxin fractions of blood plasma. The sample preparation is based on a liquid-liquid extraction, followed by an acid silica in series with an activated carbon clean-up. A good recovery (82%) and reproducibility (coefficient of variation less than 25%) were found for this method. Based on 341 plasma samples, a significant correlation was established between the bioassay and chemical method (R = 0.64). However, a proportional systematic error was observed when the results obtained with the CALUX bioassay were regressed with the results from the GC-HRMS analyses. The limit of quantification (LOQ) used to calculate TEQ values from the GC-HRMS determinations, the use of the relative potency values instead of the toxic equivalent factor and the potential of CALUX bioassay to measure all compounds with affinity for the AhR may partly explain this proportional systematic error. Nevertheless, the present results suggest that the CALUX bioassay could be a promising valid screening method for human blood plasma analyses.

Survey of commercial pasteurised cows' milk in Wallonia (Belgium) for the occurrence of polychlorinated dibenzo-p-dioxins, dibenzofurans and coplanar polychlorinated biphenyls.

Congener-specific analyses of 7 polychlorinated dibenzo-p-dioxins (PCDDs), 10 polychlorinated dibenzofurans (PCDFs) and 4 non-ortho (coplanar) polychlorinated biphenyls (cPCBs) were performed on 35 samples of commercial long-life pasteurised cows' milk issued from eight different brands available in Walloon supermarkets (Belgium). The observed congener profile was characteristic of milk samples issued from industrialised countries with good inter and intra-brand reproducibility's. The PCDDs to PCDFs ratio was equal to 1.8 in concentration. The toxic equivalent (TEQ based on WHO-TEF) value for PCDD/Fs in all analysed milks was 1.09+/-0.30 pg TEQ/g fat (range 0.86-1.59), which is below the recommended EU non-commercialisation threshold value of 3 pg TEQ PCDD/Fs/g of milk fat. The mean TEQ value including cPCBs was 2.23+/-0.55 pg TEQ/g fat. These PCBs actually contributed for 49+/-8.6% of the total TEQ. Among PCDD/Fs and cPCBs, tetrachloro dibenzo-p-dioxin (TCDD), pentachloro dibenzo-p-dioxin (PeCDD), pentachloro dibenzofurans (PeCDFs) and 3,3',4,4',5-pentachloro biphenyl (PCB-126) were the most important contributors to the TEQ. Estimated daily intake (EDI) due to consumption of such milks was 0.34 pg TEQ/kg of body weight/day for PCDD/Fs and 0.69 pg TEQ/kg of body weight/day when cPCBs were included.

Levels and congener distributions of PCDDs, PCDFs and non-ortho PCBs in Belgian foodstuffs--assessment of dietary intake.

Congener-specific analyses of 7 polychlorinated dibenzo-p-dioxins (PCDDs), 10 polychlorinated dibenzofurans (PCDFs) and 4 non-ortho (coplanar) polychlorinated biphenyls (cPCBs) were performed on 197 foodstuffs samples of animal origin from Belgium during years 2000 and 2001. All investigated matrices (except horse) present background levels lower than the Belgian non-commercialization value of 5 pg TEQ/g fat. Pork was the meat containing the lowest concentration of both PCDD/Fs and cPCBs. The mean background concentration of 2,3,7,8-TCDD toxicity equivalent in milk was 1.1 pg/g of fat, with a congener distribution typical of non-contaminated milk. The relative contribution of 2,3,7,8-TCDD, 2,3,7,8-TCDF, 1,2,3,7,8-PeCDD and 2,3,4,7,8-PeCDF to the PCDD/Fs TEQ was 85+/-7.9% for all investigated matrices. The cPCBs contribution to the total TEQ was 47+/-19.0% for products of terrestrial species and 69+/-20.0% for aquatic species. Once the contribution of cPCBs was added to the TEQ, few foodstuffs such as horse, sheep, beef, eggs and cheese presented levels above the future European guidelines that currently only include PCDD/Fs but will be re-evaluated later in order to include 'dioxin-like' PCBs. Based on levels measured in the samples, the estimation of the dietary intake was 65.3 pg WHO-TEQ/day for PCDD/Fs only (1.00 pg WHO-TEQ/kg bw/day, for a 65 kg person) and 132.9 pg WHO-TEQ/day if cPCBs were included (2.04 pg WHO-TEQ/kg bw/day, for a 65 kg person). Meat (mainly beef), dairy products, and fish each account for roughly one third of the intake.