Volvulus du grêle sur mésentère commun incomplet une redoutable complication rare chez l’adulte: à propos de 1 cas

Le mésentère commun résulte d'une anomalie de rotation du tube digestif. Il est caractérisé par la persistance d'une disposition anatomique embryonnaire secondaire à une anomalie de rotation de l'anse ombilicale primitive, constituant ainsi un méso commun à toute l'anse intestinale etune racine du mésentère extrêmement courte. Cette insuffisance de rotation est le plus souvent associée à un défaut d'accolement. Ces  anomalies de rotation intestinale peuvent aboutir à des complications redoutables parfois mortelles, qui surviennent généralement au cours de la période néonatale où à l'âge pédiatrique. On estime que la prévalence de ces malformations congénitales à l'âge adulte est de l'ordre de 0,2% à 0,5% âge auquel elles demeurent très souvent asymptomatiques et donc non diagnostiquées. Le diagnostic de volvulus total du grêle peut se faire dans des circonstances très variées: en urgence devant un tableau  d'occlusion intestinale aiguë, voire un état de choc pouvant conduire au décès, devant un tableau de douleurs abdominales répétées plus ou moins associées à des troubles du transit. Nous rapportons l'observation d'un patient de 18 ans admis pour volvulus total du grêle sur mésentère commun incomplet chez qui l'évolution était favorable

Pancréatite aigüe du post-partum: à propos d’un cas

La pancréatite aigüe est une complication rare durant la grossesse. Son incidence est de 1 pour 1000 à 3000 grossesses. L'origine lithiasique est de loin la plus fréquente. Elle survient le plus souvent au cours du 3ème trimestre ou précocement dans le post-partum. Son pronostic dépend de la rapidité du diagnostic. Nous rapportons un cas de pancréatite aigüe grave d'origine biliaire survenant deux semaines après l'accouchement chez une patiente de 24 ans avec une bonne évolution.Key words: Pancréatite aigüe, grossesse, lithiases, traitemen

Design and Implementation of Wireless Zigbee Sensor Based On Embedded 32-Bits FPGA Processor

Wireless Sensor Networks (WSN) has become an emerging area of research in recent years. Today this wireless sensors are used in many industrial and consumer applications, such as industrial process monitoring and control, machine health monitoring, automotive, home appliance, smart grid applications and so on. In this work, an intelligent wireless sensor system for real time functionality has been suggested. The proposed solution is based on the embedded FPGA design using a new Xilinx MicroBlaze Soft Processor to Increases the performance of the system. The effectiveness of the proposed method is verified by the experimental results. The hardware components include Xilinx FPGA board, XBee Series 2 wireless communication module and end device sensors to capture the physical or environmental quantity, such as temperature, sound or pressure..

Complication rare de la coloscopie chez un patient sous anticoagulant: hemopéritoine par rupture d’un hématome sous capsulaire de la rate, cas clinique

La coloscopie à visée diagnostique et/ou thérapeutique est un examen invasif fréquemment pratiquée de nos jours. La perforation colique et l'hémorragie digestive en sont les principales complications. La survenue d'un  hémopéritoine par rupture d'un hématome sous-capsulaire splénique est une complication extrêmement rare et potentiellement mortelle de la coloscopie. Un traumatisme splénique minime passé inaperçu et la prised'anticoagulant en sont des facteurs favorisants. Nous présentons le cas d'une rupture d'un hématome sous-capsulaire de la rate après une coloscopie, survenue chez un patient de 70 ans porteur d'une valve mitrale mécanique sous acénocoumarol à dose hypocaogulante. La nécessité d'obtention d'une anti coagulation rapidement efficace et l'instabilité hémodynamique avaient justifiée la réalisation d'une splénectomie. L'évolution était favorable. A travers cette observation clinique nous discutons les mécanismes et les modalités de prise en charge devant cette complication

How the Cathedral Embraced the Bazaar, and the Bazaar Became a Cathedral

Peer reviewe

Resuscitation of Newborn Piglets. Short-Term Influence of FiO2 on Matrix Metalloproteinases, Caspase-3 and BDNF

Perinatal hypoxia-ischemia is a major cause of mortality and cerebral morbidity, and using oxygen during newborn resuscitation may further harm the brain. The aim was to examine how supplementary oxygen used for newborn resuscitation would influence early brain tissue injury, cell death and repair processes and the regulation of genes related to apoptosis, neurodegeneration and neuroprotection.Anesthetized newborn piglets were subjected to global hypoxia and then randomly assigned to resuscitation with 21%, 40% or 100% O(2) for 30 min and followed for 9 h. An additional group received 100% O(2) for 30 min without preceding hypoxia. The left hemisphere was used for histopathology and immunohistochemistry and the right hemisphere was used for in situ zymography in the corpus striatum; gene expression and the activity of various relevant biofactors were measured in the frontal cortex. There was an increase in the net matrix metalloproteinase gelatinolytic activity in the corpus striatum from piglets resuscitated with 100% oxygen vs. 21%. Hematoxylin-eosin (HE) staining revealed no significant changes. Nine hours after oxygen-assisted resuscitation, caspase-3 expression and activity was increased by 30-40% in the 100% O(2) group (n = 9/10) vs. the 21% O(2) group (n = 10; p<0.04), whereas brain-derived neurotrophic factor (BDNF) activity was decreased by 65% p<0.03.The use of 100% oxygen for resuscitation resulted in increased potentially harmful proteolytic activities and attenuated BDNF activity when compared with 21%. Although there were no significant changes in short term cell loss, hyperoxia seems to cause an early imbalance between neuroprotective and neurotoxic mechanisms that might compromise the final pathological outcome

Meta-analysis of heterogeneous Down Syndrome data reveals consistent genome-wide dosage effects related to neurological processes

<p>Abstract</p> <p>Background</p> <p>Down syndrome (DS; trisomy 21) is the most common genetic cause of mental retardation in the human population and key molecular networks dysregulated in DS are still unknown. Many different experimental techniques have been applied to analyse the effects of dosage imbalance at the molecular and phenotypical level, however, currently no integrative approach exists that attempts to extract the common information.</p> <p>Results</p> <p>We have performed a statistical meta-analysis from 45 heterogeneous publicly available DS data sets in order to identify consistent dosage effects from these studies. We identified 324 genes with significant genome-wide dosage effects, including well investigated genes like <it>SOD1</it>, <it>APP</it>, <it>RUNX1 </it>and <it>DYRK1A </it>as well as a large proportion of novel genes (N = 62). Furthermore, we characterized these genes using gene ontology, molecular interactions and promoter sequence analysis. In order to judge relevance of the 324 genes for more general cerebral pathologies we used independent publicly available microarry data from brain studies not related with DS and identified a subset of 79 genes with potential impact for neurocognitive processes. All results have been made available through a web server under <url>http://ds-geneminer.molgen.mpg.de/</url>.</p> <p>Conclusions</p> <p>Our study represents a comprehensive integrative analysis of heterogeneous data including genome-wide transcript levels in the domain of trisomy 21. The detected dosage effects build a resource for further studies of DS pathology and the development of new therapies.</p

Olfactory Stem Cells, a New Cellular Model for Studying Molecular Mechanisms Underlying Familial Dysautonomia

International audienceBackground: Familial dysautonomia (FD) is a hereditary neuropathy caused by mutations in the IKBKAP gene, the most common of which results in variable tissue-specific mRNA splicing with skipping of exon 20. Defective splicing is especially severe in nervous tissue, leading to incomplete development and progressive degeneration of sensory and autonomic neurons. The specificity of neuron loss in FD is poorly understood due to the lack of an appropriate model system. To better understand and modelize the molecular mechanisms of IKBKAP mRNA splicing, we collected human olfactory ecto-mesenchymal stem cells (hOE-MSC) from FD patients. hOE-MSCs have a pluripotent ability to differentiate into various cell lineages, including neurons and glial cells.Methodology/Principal Findings: We confirmed IKBKAP mRNA alternative splicing in FD hOE-MSCs and identified 2 novel spliced isoforms also present in control cells. We observed a significant lower expression of both IKBKAP transcript and IKAP/hELP1 protein in FD cells resulting from the degradation of the transcript isoform skipping exon 20. We localized IKAP/hELP1 in different cell compartments, including the nucleus, which supports multiple roles for that protein. We also investigated cellular pathways altered in FD, at the genome-wide level, and confirmed that cell migration and cytoskeleton reorganization were among the processes altered in FD. Indeed, FD hOE-MSCs exhibit impaired migration compared to control cells. Moreover, we showed that kinetin improved exon 20 inclusion and restores a normal level of IKAP/hELP1 in FD hOE-MSCs. Furthermore, we were able to modify the IKBKAP splicing ratio in FD hOE-MSCs, increasing or reducing the WT (exon 20 inclusion):MU (exon 20 skipping) ratio respectively, either by producing free-floating spheres, or by inducing cells into neural differentiation.Conclusions/Significance: hOE-MSCs isolated from FD patients represent a new approach for modeling FD to better understand genetic expression and possible therapeutic approaches. This model could also be applied to other neurological genetic diseases

Joining S100 proteins and migration:for better or for worse, in sickness and in health

The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used. © 2013 Springer Basel