Renal effects of adenosine A1-receptor blockade with 8-cyclopentyl-1,3-dipropylxanthine in hypoxemic newborn rabbits.

The key role of intrarenal adenosine in mediating the hypoxemic acute renal insufficiency in newborn rabbits has been well demonstrated using the nonspecific adenosine antagonist theophylline. The present study was designed to define the role of adenosine A1 receptors during systemic hypoxemia by using the specific A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Renal function parameters were assessed in 31 anesthetized and mechanically ventilated newborn rabbits. In normoxia, DPCPX infusion induced a significant increase in diuresis (+44%) and GFR (+19%), despite a significant decrease in renal blood flow (RBF) (-22%) and an increase in renal vascular resistance (RVR) (+37%). In hypoxemic conditions, diuresis (-19%), GFR (-26%), and RBF (-35%) were decreased, whereas RVR increased (+33%). DPCPX administration hindered the hypoxemia-induced decrease in GFR and diuresis. However, RBF was still significantly decreased (-27%), whereas RVR increased (+22%). In all groups, the filtration fraction increased significantly. The overall results support the hypothesis that, in physiologic conditions, intrarenal adenosine plays a key role in regulating glomerular filtration in the neonatal period through preferential A1-mediated afferent vasoconstriction. During a hypoxemic stress, the A1-specific antagonist DPCPX only partially prevented the hypoxemia-induced changes, as illustrated by the elevated RVR and drop in RBF. These findings imply that the contribution of intrarenal adenosine to the acute adverse effects of hypoxemia might not be solely mediated via the A1 receptor.

MRI newsletter 8: Georeferenced biological databases - A tool for understanding mountain biodiversity

The Mountain Research Initiative invited Dr Eva Spehn, Director of the Global Mountain Biodiversity Assessment (GMBA), and Dr Antoine Guisan, head of the Spatial Ecology Group at the University of Lausanne, to introduce the reader to their coordinated efforts to advance understanding and prediction of mountain biodiversity. Antoine Guisan's EUROMONT project is one of the many scientific projects that may potentially provide data for the new GMBA initiative for a GIS mountain biodiversity database.

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Objective: To assess the factorial validity of the Portuguese version of the Maslach Burnout Inventory - Human Services Survey (MBI-HSS). Methods: Between November 2010 and November 2011 a Portuguese version of the MBI-HSS was applied to 151 Portuguese family doctors (55% women, median age 54 years). The factorial structure of the MBI-HSS was examined by principal component analysis (PCA) and confirmatory factor analysis (CFA). Internal consistency estimates of the MBI-HSS were determined with Cronbach's alpha. Results: The fit of the hypothesized three-factor model to the data was superior to the alternative two-factor and four-factor models. CFA supported MBI-HSS as an acceptable measure to evaluate burnout and deletion of items 12 and 16 improved the goodness of fit of the model. In PCA, the three-factor model explained 50.58% of the variance and the four-factor model did not lead to understandable components. Item 12 was also found to be problematic in PCA. The Cronbach's alpha was satisfactory for emotional exhaustion (alpha=0.90), lack of personal accomplishment (alpha=0.73), and depersonalization (alpha=0.64). Conclusion: The Portuguese version of the MBI-HSS was found to be reliable to measure burnout among Portuguese medical doctors. We also recommend the deletion of items 12 and 16 from the MBI-HSS.

Gastric outlet obstruction by Brunner's gland hyperplasia in an 8-year-old child.

Several cases of Brunner's gland hyperplasia causing hemorrhage, obstruction, or intussusception have been published in the adult literature. Similar cases in the pediatric population are very rare and have only been described twice, always associated with chronic renal failure. We report the third and youngest case of gastric outlet obstruction because of Brunner's gland hyperplasia focusing on histopathologic condition and treatment based on a review of the literature.

Evaluation of C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as diagnostic parameters in sepsis-related fatalities.

The aims of this study were to investigate the usefulness of serum C-reactive protein, procalcitonin, tumor necrosis factor alpha, interleukin-6, and interleukin-8 as postmortem markers of sepsis and to compare C-reactive protein and procalcitonin values in serum, vitreous humor, and cerebrospinal fluid in a series of sepsis cases and control subjects, in order to determine whether these measurements may be employed for the postmortem diagnosis of sepsis. Two study groups were formed, a sepsis group (eight subjects coming from the intensive care unit of two university hospitals, with a clinical diagnosis of sepsis in vivo) and control group (ten autopsy cases admitted to two university medicolegal centers, deceased from natural and unnatural causes, without elements to presume an underlying sepsis as the cause of death). Serum C-reactive protein and procalcitonin concentrations were significantly different between sepsis cases and control cases, whereas serum tumor necrosis factor alpha, interleukin-6, and interleukin-8 values were not significantly different between the two groups, suggesting that measurement of interleukin-6, interleukin-8, and tumor necrosis factor alpha is non-optimal for postmortem discrimination of cases with sepsis. In the sepsis group, vitreous procalcitonin was detectable in seven out of eight cases. In the control group, vitreous procalcitonin was clearly detectable only in one case, which also showed an increase of all markers in serum and for which the cause of death was myocardial infarction associated with multi-organic failure. According to the results of this study, the determination of vitreous procalcitonin may be an alternative to the serum procalcitonin for the postmortem diagnosis of sepsis.

"La vie et l'oeuvre"? : Recherches sur le biographique : Actes du colloque de relève organisé à l'Université de Lausanne les 8-9 novembre 2007

La réflexion sur la biographie a connu un renouvellement important ces vingt dernières années dans plusieurs disciplines. Florissant sur le marché ditorial, ce genre ancien trouve aujourd'hui des formes nouvelles, nourries de la galaxie des sciences humaines contemporaines, comme en témoigne l'ouvrage de François Dosse, Le Pari biographique (La Découverte, 2005). Genre fondateur en histoire de l'art, la biographie est pratiquée peu ou prou dans la plupart des disciplines des lettres. Bonne raison pour se pencher de manière interdisciplinaire sur le genre et sa pratique. La vogue des éloges académiques au XVIIIe siècle, et la profusion du discours biographique sur les artistes à l'orée du Romantisme ont ouvert la voie à la fameuse «méthode biographique» de Sainte-Beuve, et à sa reconversion dans les programmes d'enseignement, par le biais de Gustave Lanson et de ses émules. Inculqué à des générations d'élèves, devenu une structure invisible de l'entendement universitaire dans les disciplines littéraires, le couple « la vie et l'oeuvre » a été sévèrement reconsidéré, au XXe siècle, par les approches formalistes, structuralistes ou sociologiques. Qu'en est-il de ce genre actuellement? Comment les travaux de littéraires, d'historiens, d'historiens de l'art, de philosophes envisagent-ils les données biographiques?

Reduced development of CD4-8-B220+ T cells but normal autoantibody production in lpr/lpr mice lacking major histocompatibility complex class I molecules.

The lpr gene has recently been shown to encode a functional mutation in the Fas receptor, a molecule involved in transducing apoptotic signals. Mice homozygous for the lpr gene develop an autoimmune syndrome accompanied by massive accumulation of double-negative (DN) CD4-8-B220+ T cell receptor-alpha/beta+ cells. In order to investigate the origin of these DN T cells, we derived lpr/lpr mice lacking major histocompatibility complex (MHC) class I molecules by intercrossing them with beta 2-microglobulin (beta 2m)-deficient mice. Interestingly, these lpr beta 2m-/- mice develop 13-fold fewer DNT cells in lymph nodes as compared to lpr/lpr wild-type (lprWT) mice. Analysis of anti-DNA antibodies and rheumatoid factor in serum demonstrates that lpr beta 2m-/- mice produce comparable levels of autoantibodies to lprWT mice. Collectively our data indicate that MHC class I molecules control the development of DN T cells but not autoantibody production in lpr/lpr mice and support the hypothesis that the majority of DN T cells may be derived from cells of the CD8 lineage.